---
_id: '570'
abstract:
- lang: eng
text: 'Most phenotypes are determined by molecular systems composed of specifically
interacting molecules. However, unlike for individual components, little is known
about the distributions of mutational effects of molecular systems as a whole.
We ask how the distribution of mutational effects of a transcriptional regulatory
system differs from the distributions of its components, by first independently,
and then simultaneously, mutating a transcription factor and the associated promoter
it represses. We find that the system distribution exhibits increased phenotypic
variation compared to individual component distributions - an effect arising from
intermolecular epistasis between the transcription factor and its DNA-binding
site. In large part, this epistasis can be qualitatively attributed to the structure
of the transcriptional regulatory system and could therefore be a common feature
in prokaryotes. Counter-intuitively, intermolecular epistasis can alleviate the
constraints of individual components, thereby increasing phenotypic variation
that selection could act on and facilitating adaptive evolution. '
article_number: e28921
author:
- first_name: Mato
full_name: Lagator, Mato
id: 345D25EC-F248-11E8-B48F-1D18A9856A87
last_name: Lagator
- first_name: Srdjan
full_name: Sarikas, Srdjan
id: 35F0286E-F248-11E8-B48F-1D18A9856A87
last_name: Sarikas
- first_name: Hande
full_name: Acar, Hande
id: 2DDF136A-F248-11E8-B48F-1D18A9856A87
last_name: Acar
orcid: 0000-0003-1986-9753
- first_name: Jonathan P
full_name: Bollback, Jonathan P
id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
last_name: Bollback
orcid: 0000-0002-4624-4612
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Lagator M, Sarikas S, Acar H, Bollback JP, Guet CC. Regulatory network structure
determines patterns of intermolecular epistasis. eLife. 2017;6. doi:10.7554/eLife.28921
apa: Lagator, M., Sarikas, S., Acar, H., Bollback, J. P., & Guet, C. C. (2017).
Regulatory network structure determines patterns of intermolecular epistasis.
ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.28921
chicago: Lagator, Mato, Srdjan Sarikas, Hande Acar, Jonathan P Bollback, and Calin
C Guet. “Regulatory Network Structure Determines Patterns of Intermolecular Epistasis.”
ELife. eLife Sciences Publications, 2017. https://doi.org/10.7554/eLife.28921.
ieee: M. Lagator, S. Sarikas, H. Acar, J. P. Bollback, and C. C. Guet, “Regulatory
network structure determines patterns of intermolecular epistasis,” eLife,
vol. 6. eLife Sciences Publications, 2017.
ista: Lagator M, Sarikas S, Acar H, Bollback JP, Guet CC. 2017. Regulatory network
structure determines patterns of intermolecular epistasis. eLife. 6, e28921.
mla: Lagator, Mato, et al. “Regulatory Network Structure Determines Patterns of
Intermolecular Epistasis.” ELife, vol. 6, e28921, eLife Sciences Publications,
2017, doi:10.7554/eLife.28921.
short: M. Lagator, S. Sarikas, H. Acar, J.P. Bollback, C.C. Guet, ELife 6 (2017).
date_created: 2018-12-11T11:47:14Z
date_published: 2017-11-13T00:00:00Z
date_updated: 2021-01-12T08:03:15Z
day: '13'
ddc:
- '576'
department:
- _id: CaGu
- _id: JoBo
- _id: NiBa
doi: 10.7554/eLife.28921
ec_funded: 1
file:
- access_level: open_access
checksum: 273ab17f33305e4eaafd911ff88e7c5b
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:42Z
date_updated: 2020-07-14T12:47:10Z
file_id: '5096'
file_name: IST-2017-918-v1+1_elife-28921-figures-v3.pdf
file_size: 8453470
relation: main_file
- access_level: open_access
checksum: b433f90576c7be597cd43367946f8e7f
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:43Z
date_updated: 2020-07-14T12:47:10Z
file_id: '5097'
file_name: IST-2017-918-v1+2_elife-28921-v3.pdf
file_size: 1953221
relation: main_file
file_date_updated: 2020-07-14T12:47:10Z
has_accepted_license: '1'
intvolume: ' 6'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 2578D616-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '648440'
name: Selective Barriers to Horizontal Gene Transfer
publication: eLife
publication_identifier:
issn:
- 2050084X
publication_status: published
publisher: eLife Sciences Publications
publist_id: '7244'
pubrep_id: '918'
quality_controlled: '1'
scopus_import: 1
status: public
title: Regulatory network structure determines patterns of intermolecular epistasis
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 6
year: '2017'
...
---
_id: '613'
abstract:
- lang: eng
text: 'Bacteria in groups vary individually, and interact with other bacteria and
the environment to produce population-level patterns of gene expression. Investigating
such behavior in detail requires measuring and controlling populations at the
single-cell level alongside precisely specified interactions and environmental
characteristics. Here we present an automated, programmable platform that combines
image-based gene expression and growth measurements with on-line optogenetic expression
control for hundreds of individual Escherichia coli cells over days, in a dynamically
adjustable environment. This integrated platform broadly enables experiments that
bridge individual and population behaviors. We demonstrate: (i) population structuring
by independent closed-loop control of gene expression in many individual cells,
(ii) cell-cell variation control during antibiotic perturbation, (iii) hybrid
bio-digital circuits in single cells, and freely specifiable digital communication
between individual bacteria. These examples showcase the potential for real-time
integration of theoretical models with measurement and control of many individual
cells to investigate and engineer microbial population behavior.'
acknowledgement: We are grateful to M. Lang, H. Janovjak, M. Khammash, A. Milias-Argeitis,
M. Rullan, G. Batt, A. Bosma-Moody, Aryan, S. Leibler, and members of the Guet and
Tkačik groups for helpful discussion, comments, and suggestions. We thank A. Moglich,
T. Mathes, J. Tabor, and S. Schmidl for kind gifts of strains, and R. Hauschild,
B. Knep, M. Lang, T. Asenov, E. Papusheva, T. Menner, T. Adletzberger, and J. Merrin
for technical assistance. The research leading to these results has received funding
from the People Programme (Marie Curie Actions) of the European Union’s Seventh
Framework Programme (FP7/2007–2013) under REA grant agreement no. [291734]. (to
R.C. and J.R.), Austrian Science Fund grant FWF P28844 (to G.T.), and internal IST
Austria Interdisciplinary Project Support. J.R. acknowledges support from the Agence
Nationale de la Recherche (ANR) under Grant Nos. ANR-16-CE33-0018 (MEMIP), ANR-16-CE12-0025
(COGEX) and ANR-10-BINF-06-01 (ICEBERG).
article_number: '1535'
article_processing_charge: Yes (in subscription journal)
author:
- first_name: Remy P
full_name: Chait, Remy P
id: 3464AE84-F248-11E8-B48F-1D18A9856A87
last_name: Chait
orcid: 0000-0003-0876-3187
- first_name: Jakob
full_name: Ruess, Jakob
id: 4A245D00-F248-11E8-B48F-1D18A9856A87
last_name: Ruess
orcid: 0000-0003-1615-3282
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Gasper
full_name: Tkacik, Gasper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkacik
orcid: 0000-0002-6699-1455
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Chait RP, Ruess J, Bergmiller T, Tkačik G, Guet CC. Shaping bacterial population
behavior through computer interfaced control of individual cells. Nature Communications.
2017;8(1). doi:10.1038/s41467-017-01683-1
apa: Chait, R. P., Ruess, J., Bergmiller, T., Tkačik, G., & Guet, C. C. (2017).
Shaping bacterial population behavior through computer interfaced control of individual
cells. Nature Communications. Nature Publishing Group. https://doi.org/10.1038/s41467-017-01683-1
chicago: Chait, Remy P, Jakob Ruess, Tobias Bergmiller, Gašper Tkačik, and Calin
C Guet. “Shaping Bacterial Population Behavior through Computer Interfaced Control
of Individual Cells.” Nature Communications. Nature Publishing Group, 2017.
https://doi.org/10.1038/s41467-017-01683-1.
ieee: R. P. Chait, J. Ruess, T. Bergmiller, G. Tkačik, and C. C. Guet, “Shaping
bacterial population behavior through computer interfaced control of individual
cells,” Nature Communications, vol. 8, no. 1. Nature Publishing Group,
2017.
ista: Chait RP, Ruess J, Bergmiller T, Tkačik G, Guet CC. 2017. Shaping bacterial
population behavior through computer interfaced control of individual cells. Nature
Communications. 8(1), 1535.
mla: Chait, Remy P., et al. “Shaping Bacterial Population Behavior through Computer
Interfaced Control of Individual Cells.” Nature Communications, vol. 8,
no. 1, 1535, Nature Publishing Group, 2017, doi:10.1038/s41467-017-01683-1.
short: R.P. Chait, J. Ruess, T. Bergmiller, G. Tkačik, C.C. Guet, Nature Communications
8 (2017).
date_created: 2018-12-11T11:47:30Z
date_published: 2017-12-01T00:00:00Z
date_updated: 2021-01-12T08:06:15Z
day: '01'
ddc:
- '576'
- '579'
department:
- _id: CaGu
- _id: GaTk
doi: 10.1038/s41467-017-01683-1
ec_funded: 1
file:
- access_level: open_access
checksum: 44bb5d0229926c23a9955d9fe0f9723f
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:16:05Z
date_updated: 2020-07-14T12:47:20Z
file_id: '5190'
file_name: IST-2017-911-v1+1_s41467-017-01683-1.pdf
file_size: 1951699
relation: main_file
file_date_updated: 2020-07-14T12:47:20Z
has_accepted_license: '1'
intvolume: ' 8'
issue: '1'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 254E9036-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P28844-B27
name: Biophysics of information processing in gene regulation
publication: Nature Communications
publication_identifier:
issn:
- '20411723'
publication_status: published
publisher: Nature Publishing Group
publist_id: '7191'
pubrep_id: '911'
quality_controlled: '1'
scopus_import: 1
status: public
title: Shaping bacterial population behavior through computer interfaced control of
individual cells
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 8
year: '2017'
...
---
_id: '624'
abstract:
- lang: eng
text: Bacteria adapt to adverse environmental conditions by altering gene expression
patterns. Recently, a novel stress adaptation mechanism has been described that
allows Escherichia coli to alter gene expression at the post-transcriptional level.
The key player in this regulatory pathway is the endoribonuclease MazF, the toxin
component of the toxin-antitoxin module mazEF that is triggered by various stressful
conditions. In general, MazF degrades the majority of transcripts by cleaving
at ACA sites, which results in the retardation of bacterial growth. Furthermore,
MazF can process a small subset of mRNAs and render them leaderless by removing
their ribosome binding site. MazF concomitantly modifies ribosomes, making them
selective for the translation of leaderless mRNAs. In this study, we employed
fluorescent reporter-systems to investigate mazEF expression during stressful
conditions, and to infer consequences of the mRNA processing mediated by MazF
on gene expression at the single-cell level. Our results suggest that mazEF transcription
is maintained at low levels in single cells encountering adverse conditions, such
as antibiotic stress or amino acid starvation. Moreover, using the grcA mRNA as
a model for MazF-mediated mRNA processing, we found that MazF activation promotes
heterogeneity in the grcA reporter expression, resulting in a subpopulation of
cells with increased levels of GrcA reporter protein.
acknowledgement: 'Austrian Science Fund (FWF): M1697, P22249; Swiss National Science
Foundation (SNF): 145706; European Commission;FWF Special Research Program: RNA-REG
F43'
article_number: '3830'
author:
- first_name: Nela
full_name: Nikolic, Nela
id: 42D9CABC-F248-11E8-B48F-1D18A9856A87
last_name: Nikolic
orcid: 0000-0001-9068-6090
- first_name: Zrinka
full_name: Didara, Zrinka
last_name: Didara
- first_name: Isabella
full_name: Moll, Isabella
last_name: Moll
citation:
ama: Nikolic N, Didara Z, Moll I. MazF activation promotes translational heterogeneity
of the grcA mRNA in Escherichia coli populations. PeerJ. 2017;2017(9).
doi:10.7717/peerj.3830
apa: Nikolic, N., Didara, Z., & Moll, I. (2017). MazF activation promotes translational
heterogeneity of the grcA mRNA in Escherichia coli populations. PeerJ.
PeerJ. https://doi.org/10.7717/peerj.3830
chicago: Nikolic, Nela, Zrinka Didara, and Isabella Moll. “MazF Activation Promotes
Translational Heterogeneity of the GrcA MRNA in Escherichia Coli Populations.”
PeerJ. PeerJ, 2017. https://doi.org/10.7717/peerj.3830.
ieee: N. Nikolic, Z. Didara, and I. Moll, “MazF activation promotes translational
heterogeneity of the grcA mRNA in Escherichia coli populations,” PeerJ,
vol. 2017, no. 9. PeerJ, 2017.
ista: Nikolic N, Didara Z, Moll I. 2017. MazF activation promotes translational
heterogeneity of the grcA mRNA in Escherichia coli populations. PeerJ. 2017(9),
3830.
mla: Nikolic, Nela, et al. “MazF Activation Promotes Translational Heterogeneity
of the GrcA MRNA in Escherichia Coli Populations.” PeerJ, vol. 2017, no.
9, 3830, PeerJ, 2017, doi:10.7717/peerj.3830.
short: N. Nikolic, Z. Didara, I. Moll, PeerJ 2017 (2017).
date_created: 2018-12-11T11:47:33Z
date_published: 2017-09-21T00:00:00Z
date_updated: 2021-01-12T08:06:48Z
day: '21'
ddc:
- '579'
department:
- _id: CaGu
doi: 10.7717/peerj.3830
file:
- access_level: open_access
checksum: 3d79ae6b6eabc90b0eaaed82ff3493b0
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:11:51Z
date_updated: 2020-07-14T12:47:24Z
file_id: '4908'
file_name: IST-2017-909-v1+1_peerj-3830.pdf
file_size: 682064
relation: main_file
file_date_updated: 2020-07-14T12:47:24Z
has_accepted_license: '1'
intvolume: ' 2017'
issue: '9'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
publication: PeerJ
publication_identifier:
issn:
- '21678359'
publication_status: published
publisher: PeerJ
publist_id: '7172'
pubrep_id: '909'
quality_controlled: '1'
scopus_import: 1
status: public
title: MazF activation promotes translational heterogeneity of the grcA mRNA in Escherichia
coli populations
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 2017
year: '2017'
...
---
_id: '655'
abstract:
- lang: eng
text: 'The bacterial flagellum is a self-assembling nanomachine. The external flagellar
filament, several times longer than a bacterial cell body, is made of a few tens
of thousands subunits of a single protein: flagellin. A fundamental problem concerns
the molecular mechanism of how the flagellum grows outside the cell, where no
discernible energy source is available. Here, we monitored the dynamic assembly
of individual flagella using in situ labelling and real-time immunostaining of
elongating flagellar filaments. We report that the rate of flagellum growth, initially
~1,700 amino acids per second, decreases with length and that the previously proposed
chain mechanism does not contribute to the filament elongation dynamics. Inhibition
of the proton motive force-dependent export apparatus revealed a major contribution
of substrate injection in driving filament elongation. The combination of experimental
and mathematical evidence demonstrates that a simple, injection-diffusion mechanism
controls bacterial flagella growth outside the cell.'
article_number: e23136
author:
- first_name: Thibaud
full_name: Renault, Thibaud
last_name: Renault
- first_name: Anthony
full_name: Abraham, Anthony
last_name: Abraham
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Guillaume
full_name: Paradis, Guillaume
last_name: Paradis
- first_name: Simon
full_name: Rainville, Simon
last_name: Rainville
- first_name: Emmanuelle
full_name: Charpentier, Emmanuelle
last_name: Charpentier
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
- first_name: Yuhai
full_name: Tu, Yuhai
last_name: Tu
- first_name: Keiichi
full_name: Namba, Keiichi
last_name: Namba
- first_name: James
full_name: Keener, James
last_name: Keener
- first_name: Tohru
full_name: Minamino, Tohru
last_name: Minamino
- first_name: Marc
full_name: Erhardt, Marc
last_name: Erhardt
citation:
ama: Renault T, Abraham A, Bergmiller T, et al. Bacterial flagella grow through
an injection diffusion mechanism. eLife. 2017;6. doi:10.7554/eLife.23136
apa: Renault, T., Abraham, A., Bergmiller, T., Paradis, G., Rainville, S., Charpentier,
E., … Erhardt, M. (2017). Bacterial flagella grow through an injection diffusion
mechanism. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.23136
chicago: Renault, Thibaud, Anthony Abraham, Tobias Bergmiller, Guillaume Paradis,
Simon Rainville, Emmanuelle Charpentier, Calin C Guet, et al. “Bacterial Flagella
Grow through an Injection Diffusion Mechanism.” ELife. eLife Sciences Publications,
2017. https://doi.org/10.7554/eLife.23136.
ieee: T. Renault et al., “Bacterial flagella grow through an injection diffusion
mechanism,” eLife, vol. 6. eLife Sciences Publications, 2017.
ista: Renault T, Abraham A, Bergmiller T, Paradis G, Rainville S, Charpentier E,
Guet CC, Tu Y, Namba K, Keener J, Minamino T, Erhardt M. 2017. Bacterial flagella
grow through an injection diffusion mechanism. eLife. 6, e23136.
mla: Renault, Thibaud, et al. “Bacterial Flagella Grow through an Injection Diffusion
Mechanism.” ELife, vol. 6, e23136, eLife Sciences Publications, 2017, doi:10.7554/eLife.23136.
short: T. Renault, A. Abraham, T. Bergmiller, G. Paradis, S. Rainville, E. Charpentier,
C.C. Guet, Y. Tu, K. Namba, J. Keener, T. Minamino, M. Erhardt, ELife 6 (2017).
date_created: 2018-12-11T11:47:44Z
date_published: 2017-03-06T00:00:00Z
date_updated: 2021-01-12T08:07:55Z
day: '06'
ddc:
- '579'
department:
- _id: CaGu
doi: 10.7554/eLife.23136
file:
- access_level: open_access
checksum: 39e1c3e82ddac83a30422fa72fa1a383
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:08:53Z
date_updated: 2020-07-14T12:47:33Z
file_id: '4716'
file_name: IST-2017-904-v1+1_elife-23136-v2.pdf
file_size: 5520359
relation: main_file
- access_level: open_access
checksum: a6d542253028f52e00aa29739ddffe8f
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:08:54Z
date_updated: 2020-07-14T12:47:33Z
file_id: '4717'
file_name: IST-2017-904-v1+2_elife-23136-figures-v2.pdf
file_size: 11242920
relation: main_file
file_date_updated: 2020-07-14T12:47:33Z
has_accepted_license: '1'
intvolume: ' 6'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
issn:
- 2050084X
publication_status: published
publisher: eLife Sciences Publications
publist_id: '7082'
pubrep_id: '904'
quality_controlled: '1'
scopus_import: 1
status: public
title: Bacterial flagella grow through an injection diffusion mechanism
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 6
year: '2017'
...
---
_id: '541'
abstract:
- lang: eng
text: 'While we have good understanding of bacterial metabolism at the population
level, we know little about the metabolic behavior of individual cells: do single
cells in clonal populations sometimes specialize on different metabolic pathways?
Such metabolic specialization could be driven by stochastic gene expression and
could provide individual cells with growth benefits of specialization. We measured
the degree of phenotypic specialization in two parallel metabolic pathways, the
assimilation of glucose and arabinose. We grew Escherichia coli in chemostats,
and used isotope-labeled sugars in combination with nanometer-scale secondary
ion mass spectrometry and mathematical modeling to quantify sugar assimilation
at the single-cell level. We found large variation in metabolic activities between
single cells, both in absolute assimilation and in the degree to which individual
cells specialize in the assimilation of different sugars. Analysis of transcriptional
reporters indicated that this variation was at least partially based on cell-to-cell
variation in gene expression. Metabolic differences between cells in clonal populations
could potentially reduce metabolic incompatibilities between different pathways,
and increase the rate at which parallel reactions can be performed.'
article_number: e1007122
author:
- first_name: Nela
full_name: Nikolic, Nela
id: 42D9CABC-F248-11E8-B48F-1D18A9856A87
last_name: Nikolic
orcid: 0000-0001-9068-6090
- first_name: Frank
full_name: Schreiber, Frank
last_name: Schreiber
- first_name: Alma
full_name: Dal Co, Alma
last_name: Dal Co
- first_name: Daniel
full_name: Kiviet, Daniel
last_name: Kiviet
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Sten
full_name: Littmann, Sten
last_name: Littmann
- first_name: Marcel
full_name: Kuypers, Marcel
last_name: Kuypers
- first_name: Martin
full_name: Ackermann, Martin
last_name: Ackermann
citation:
ama: Nikolic N, Schreiber F, Dal Co A, et al. Cell-to-cell variation and specialization
in sugar metabolism in clonal bacterial populations. PLoS Genetics. 2017;13(12).
doi:10.1371/journal.pgen.1007122
apa: Nikolic, N., Schreiber, F., Dal Co, A., Kiviet, D., Bergmiller, T., Littmann,
S., … Ackermann, M. (2017). Cell-to-cell variation and specialization in sugar
metabolism in clonal bacterial populations. PLoS Genetics. Public Library
of Science. https://doi.org/10.1371/journal.pgen.1007122
chicago: Nikolic, Nela, Frank Schreiber, Alma Dal Co, Daniel Kiviet, Tobias Bergmiller,
Sten Littmann, Marcel Kuypers, and Martin Ackermann. “Cell-to-Cell Variation and
Specialization in Sugar Metabolism in Clonal Bacterial Populations.” PLoS Genetics.
Public Library of Science, 2017. https://doi.org/10.1371/journal.pgen.1007122.
ieee: N. Nikolic et al., “Cell-to-cell variation and specialization in sugar
metabolism in clonal bacterial populations,” PLoS Genetics, vol. 13, no.
12. Public Library of Science, 2017.
ista: Nikolic N, Schreiber F, Dal Co A, Kiviet D, Bergmiller T, Littmann S, Kuypers
M, Ackermann M. 2017. Cell-to-cell variation and specialization in sugar metabolism
in clonal bacterial populations. PLoS Genetics. 13(12), e1007122.
mla: Nikolic, Nela, et al. “Cell-to-Cell Variation and Specialization in Sugar Metabolism
in Clonal Bacterial Populations.” PLoS Genetics, vol. 13, no. 12, e1007122,
Public Library of Science, 2017, doi:10.1371/journal.pgen.1007122.
short: N. Nikolic, F. Schreiber, A. Dal Co, D. Kiviet, T. Bergmiller, S. Littmann,
M. Kuypers, M. Ackermann, PLoS Genetics 13 (2017).
date_created: 2018-12-11T11:47:04Z
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title: Cell-to-cell variation and specialization in sugar metabolism in clonal bacterial
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name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
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abstract:
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text: information on culture conditions, phage mutagenesis, verification and lysate
preparation; Raw data
article_processing_charge: No
author:
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full_name: Pleska, Maros
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last_name: Pleska
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ama: Pleska M, Guet CC. Supplementary materials and methods; Full data set from
effects of mutations in phage restriction sites during escape from restriction–modification.
2017. doi:10.6084/m9.figshare.5633917.v1
apa: Pleska, M., & Guet, C. C. (2017). Supplementary materials and methods;
Full data set from effects of mutations in phage restriction sites during escape
from restriction–modification. The Royal Society. https://doi.org/10.6084/m9.figshare.5633917.v1
chicago: Pleska, Maros, and Calin C Guet. “Supplementary Materials and Methods;
Full Data Set from Effects of Mutations in Phage Restriction Sites during Escape
from Restriction–Modification.” The Royal Society, 2017. https://doi.org/10.6084/m9.figshare.5633917.v1.
ieee: M. Pleska and C. C. Guet, “Supplementary materials and methods; Full data
set from effects of mutations in phage restriction sites during escape from restriction–modification.”
The Royal Society, 2017.
ista: Pleska M, Guet CC. 2017. Supplementary materials and methods; Full data set
from effects of mutations in phage restriction sites during escape from restriction–modification,
The Royal Society, 10.6084/m9.figshare.5633917.v1.
mla: Pleska, Maros, and Calin C. Guet. Supplementary Materials and Methods; Full
Data Set from Effects of Mutations in Phage Restriction Sites during Escape from
Restriction–Modification. The Royal Society, 2017, doi:10.6084/m9.figshare.5633917.v1.
short: M. Pleska, C.C. Guet, (2017).
date_created: 2021-08-09T13:54:38Z
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department:
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publisher: The Royal Society
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...
---
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abstract:
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text: "Estimates of 13 C-arabinose and 2 H-glucose uptake from the fractions of
heavy isotopes measured\tin single cells"
article_processing_charge: No
author:
- first_name: Nela
full_name: Nikolic, Nela
id: 42D9CABC-F248-11E8-B48F-1D18A9856A87
last_name: Nikolic
orcid: 0000-0001-9068-6090
- first_name: Frank
full_name: Schreiber, Frank
last_name: Schreiber
- first_name: Alma
full_name: Dal Co, Alma
last_name: Dal Co
- first_name: Daniel
full_name: Kiviet, Daniel
last_name: Kiviet
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Sten
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- first_name: Marcel
full_name: Kuypers, Marcel
last_name: Kuypers
- first_name: Martin
full_name: Ackermann, Martin
last_name: Ackermann
citation:
ama: Nikolic N, Schreiber F, Dal Co A, et al. Mathematical model. 2017. doi:10.1371/journal.pgen.1007122.s017
apa: Nikolic, N., Schreiber, F., Dal Co, A., Kiviet, D., Bergmiller, T., Littmann,
S., … Ackermann, M. (2017). Mathematical model. Public Library of Science. https://doi.org/10.1371/journal.pgen.1007122.s017
chicago: Nikolic, Nela, Frank Schreiber, Alma Dal Co, Daniel Kiviet, Tobias Bergmiller,
Sten Littmann, Marcel Kuypers, and Martin Ackermann. “Mathematical Model.” Public
Library of Science, 2017. https://doi.org/10.1371/journal.pgen.1007122.s017.
ieee: N. Nikolic et al., “Mathematical model.” Public Library of Science,
2017.
ista: Nikolic N, Schreiber F, Dal Co A, Kiviet D, Bergmiller T, Littmann S, Kuypers
M, Ackermann M. 2017. Mathematical model, Public Library of Science, 10.1371/journal.pgen.1007122.s017.
mla: Nikolic, Nela, et al. Mathematical Model. Public Library of Science,
2017, doi:10.1371/journal.pgen.1007122.s017.
short: N. Nikolic, F. Schreiber, A. Dal Co, D. Kiviet, T. Bergmiller, S. Littmann,
M. Kuypers, M. Ackermann, (2017).
date_created: 2021-08-09T13:31:51Z
date_published: 2017-12-18T00:00:00Z
date_updated: 2023-02-23T12:25:04Z
day: '18'
department:
- _id: CaGu
doi: 10.1371/journal.pgen.1007122.s017
month: '12'
oa_version: None
publisher: Public Library of Science
related_material:
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title: Mathematical model
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2017'
...
---
_id: '9849'
abstract:
- lang: eng
text: This text provides additional information about the model, a derivation of
the analytic results in Eq (4), and details about simulations of an additional
parameter set.
article_processing_charge: No
author:
- first_name: Marta
full_name: Lukacisinova, Marta
id: 4342E402-F248-11E8-B48F-1D18A9856A87
last_name: Lukacisinova
orcid: 0000-0002-2519-8004
- first_name: Sebastian
full_name: Novak, Sebastian
id: 461468AE-F248-11E8-B48F-1D18A9856A87
last_name: Novak
- first_name: Tiago
full_name: Paixao, Tiago
id: 2C5658E6-F248-11E8-B48F-1D18A9856A87
last_name: Paixao
orcid: 0000-0003-2361-3953
citation:
ama: Lukacisinova M, Novak S, Paixao T. Modelling and simulation details. 2017.
doi:10.1371/journal.pcbi.1005609.s001
apa: Lukacisinova, M., Novak, S., & Paixao, T. (2017). Modelling and simulation
details. Public Library of Science. https://doi.org/10.1371/journal.pcbi.1005609.s001
chicago: Lukacisinova, Marta, Sebastian Novak, and Tiago Paixao. “Modelling and
Simulation Details.” Public Library of Science, 2017. https://doi.org/10.1371/journal.pcbi.1005609.s001.
ieee: M. Lukacisinova, S. Novak, and T. Paixao, “Modelling and simulation details.”
Public Library of Science, 2017.
ista: Lukacisinova M, Novak S, Paixao T. 2017. Modelling and simulation details,
Public Library of Science, 10.1371/journal.pcbi.1005609.s001.
mla: Lukacisinova, Marta, et al. Modelling and Simulation Details. Public
Library of Science, 2017, doi:10.1371/journal.pcbi.1005609.s001.
short: M. Lukacisinova, S. Novak, T. Paixao, (2017).
date_created: 2021-08-09T14:02:34Z
date_published: 2017-07-18T00:00:00Z
date_updated: 2023-02-23T12:55:39Z
day: '18'
department:
- _id: ToBo
- _id: NiBa
- _id: CaGu
doi: 10.1371/journal.pcbi.1005609.s001
month: '07'
oa_version: Published Version
publisher: Public Library of Science
related_material:
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...
---
_id: '9850'
abstract:
- lang: eng
text: In this text, we discuss how a cost of resistance and the possibility of lethal
mutations impact our model.
article_processing_charge: No
author:
- first_name: Marta
full_name: Lukacisinova, Marta
id: 4342E402-F248-11E8-B48F-1D18A9856A87
last_name: Lukacisinova
orcid: 0000-0002-2519-8004
- first_name: Sebastian
full_name: Novak, Sebastian
id: 461468AE-F248-11E8-B48F-1D18A9856A87
last_name: Novak
- first_name: Tiago
full_name: Paixao, Tiago
id: 2C5658E6-F248-11E8-B48F-1D18A9856A87
last_name: Paixao
orcid: 0000-0003-2361-3953
citation:
ama: Lukacisinova M, Novak S, Paixao T. Extensions of the model. 2017. doi:10.1371/journal.pcbi.1005609.s002
apa: Lukacisinova, M., Novak, S., & Paixao, T. (2017). Extensions of the model.
Public Library of Science. https://doi.org/10.1371/journal.pcbi.1005609.s002
chicago: Lukacisinova, Marta, Sebastian Novak, and Tiago Paixao. “Extensions of
the Model.” Public Library of Science, 2017. https://doi.org/10.1371/journal.pcbi.1005609.s002.
ieee: M. Lukacisinova, S. Novak, and T. Paixao, “Extensions of the model.” Public
Library of Science, 2017.
ista: Lukacisinova M, Novak S, Paixao T. 2017. Extensions of the model, Public Library
of Science, 10.1371/journal.pcbi.1005609.s002.
mla: Lukacisinova, Marta, et al. Extensions of the Model. Public Library
of Science, 2017, doi:10.1371/journal.pcbi.1005609.s002.
short: M. Lukacisinova, S. Novak, T. Paixao, (2017).
date_created: 2021-08-09T14:05:24Z
date_published: 2017-07-18T00:00:00Z
date_updated: 2023-02-23T12:55:39Z
day: '18'
department:
- _id: ToBo
- _id: CaGu
- _id: NiBa
doi: 10.1371/journal.pcbi.1005609.s002
month: '07'
oa_version: Published Version
publisher: Public Library of Science
related_material:
record:
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relation: used_in_publication
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status: public
title: Extensions of the model
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2017'
...
---
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article_processing_charge: No
author:
- first_name: Nela
full_name: Nikolic, Nela
id: 42D9CABC-F248-11E8-B48F-1D18A9856A87
last_name: Nikolic
orcid: 0000-0001-9068-6090
- first_name: Frank
full_name: Schreiber, Frank
last_name: Schreiber
- first_name: Alma
full_name: Dal Co, Alma
last_name: Dal Co
- first_name: Daniel
full_name: Kiviet, Daniel
last_name: Kiviet
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Sten
full_name: Littmann, Sten
last_name: Littmann
- first_name: Marcel
full_name: Kuypers, Marcel
last_name: Kuypers
- first_name: Martin
full_name: Ackermann, Martin
last_name: Ackermann
citation:
ama: Nikolic N, Schreiber F, Dal Co A, et al. Supplementary methods. 2017. doi:10.1371/journal.pgen.1007122.s016
apa: Nikolic, N., Schreiber, F., Dal Co, A., Kiviet, D., Bergmiller, T., Littmann,
S., … Ackermann, M. (2017). Supplementary methods. Public Library of Science.
https://doi.org/10.1371/journal.pgen.1007122.s016
chicago: Nikolic, Nela, Frank Schreiber, Alma Dal Co, Daniel Kiviet, Tobias Bergmiller,
Sten Littmann, Marcel Kuypers, and Martin Ackermann. “Supplementary Methods.”
Public Library of Science, 2017. https://doi.org/10.1371/journal.pgen.1007122.s016.
ieee: N. Nikolic et al., “Supplementary methods.” Public Library of Science,
2017.
ista: Nikolic N, Schreiber F, Dal Co A, Kiviet D, Bergmiller T, Littmann S, Kuypers
M, Ackermann M. 2017. Supplementary methods, Public Library of Science, 10.1371/journal.pgen.1007122.s016.
mla: Nikolic, Nela, et al. Supplementary Methods. Public Library of Science,
2017, doi:10.1371/journal.pgen.1007122.s016.
short: N. Nikolic, F. Schreiber, A. Dal Co, D. Kiviet, T. Bergmiller, S. Littmann,
M. Kuypers, M. Ackermann, (2017).
date_created: 2021-08-09T13:35:17Z
date_published: 2017-12-18T00:00:00Z
date_updated: 2023-02-23T12:25:04Z
day: '18'
department:
- _id: CaGu
doi: 10.1371/journal.pgen.1007122.s016
month: '12'
oa_version: Published Version
publisher: Public Library of Science
related_material:
record:
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relation: used_in_publication
status: public
status: public
title: Supplementary methods
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2017'
...
---
_id: '9851'
abstract:
- lang: eng
text: Based on the intuitive derivation of the dynamics of SIM allele frequency
pM in the main text, we present a heuristic prediction for the long-term SIM allele
frequencies with χ > 1 stresses and compare it to numerical simulations.
article_processing_charge: No
author:
- first_name: Marta
full_name: Lukacisinova, Marta
id: 4342E402-F248-11E8-B48F-1D18A9856A87
last_name: Lukacisinova
orcid: 0000-0002-2519-8004
- first_name: Sebastian
full_name: Novak, Sebastian
id: 461468AE-F248-11E8-B48F-1D18A9856A87
last_name: Novak
- first_name: Tiago
full_name: Paixao, Tiago
id: 2C5658E6-F248-11E8-B48F-1D18A9856A87
last_name: Paixao
orcid: 0000-0003-2361-3953
citation:
ama: Lukacisinova M, Novak S, Paixao T. Heuristic prediction for multiple stresses.
2017. doi:10.1371/journal.pcbi.1005609.s003
apa: Lukacisinova, M., Novak, S., & Paixao, T. (2017). Heuristic prediction
for multiple stresses. Public Library of Science. https://doi.org/10.1371/journal.pcbi.1005609.s003
chicago: Lukacisinova, Marta, Sebastian Novak, and Tiago Paixao. “Heuristic Prediction
for Multiple Stresses.” Public Library of Science, 2017. https://doi.org/10.1371/journal.pcbi.1005609.s003.
ieee: M. Lukacisinova, S. Novak, and T. Paixao, “Heuristic prediction for multiple
stresses.” Public Library of Science, 2017.
ista: Lukacisinova M, Novak S, Paixao T. 2017. Heuristic prediction for multiple
stresses, Public Library of Science, 10.1371/journal.pcbi.1005609.s003.
mla: Lukacisinova, Marta, et al. Heuristic Prediction for Multiple Stresses.
Public Library of Science, 2017, doi:10.1371/journal.pcbi.1005609.s003.
short: M. Lukacisinova, S. Novak, T. Paixao, (2017).
date_created: 2021-08-09T14:08:14Z
date_published: 2017-07-18T00:00:00Z
date_updated: 2023-02-23T12:55:39Z
day: '18'
department:
- _id: ToBo
- _id: CaGu
- _id: NiBa
doi: 10.1371/journal.pcbi.1005609.s003
month: '07'
oa_version: Published Version
publisher: Public Library of Science
related_material:
record:
- id: '696'
relation: used_in_publication
status: public
status: public
title: Heuristic prediction for multiple stresses
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2017'
...
---
_id: '9852'
abstract:
- lang: eng
text: We show how different combination strategies affect the fraction of individuals
that are multi-resistant.
article_processing_charge: No
author:
- first_name: Marta
full_name: Lukacisinova, Marta
id: 4342E402-F248-11E8-B48F-1D18A9856A87
last_name: Lukacisinova
orcid: 0000-0002-2519-8004
- first_name: Sebastian
full_name: Novak, Sebastian
id: 461468AE-F248-11E8-B48F-1D18A9856A87
last_name: Novak
- first_name: Tiago
full_name: Paixao, Tiago
id: 2C5658E6-F248-11E8-B48F-1D18A9856A87
last_name: Paixao
orcid: 0000-0003-2361-3953
citation:
ama: Lukacisinova M, Novak S, Paixao T. Resistance frequencies for different combination
strategies. 2017. doi:10.1371/journal.pcbi.1005609.s004
apa: Lukacisinova, M., Novak, S., & Paixao, T. (2017). Resistance frequencies
for different combination strategies. Public Library of Science. https://doi.org/10.1371/journal.pcbi.1005609.s004
chicago: Lukacisinova, Marta, Sebastian Novak, and Tiago Paixao. “Resistance Frequencies
for Different Combination Strategies.” Public Library of Science, 2017. https://doi.org/10.1371/journal.pcbi.1005609.s004.
ieee: M. Lukacisinova, S. Novak, and T. Paixao, “Resistance frequencies for different
combination strategies.” Public Library of Science, 2017.
ista: Lukacisinova M, Novak S, Paixao T. 2017. Resistance frequencies for different
combination strategies, Public Library of Science, 10.1371/journal.pcbi.1005609.s004.
mla: Lukacisinova, Marta, et al. Resistance Frequencies for Different Combination
Strategies. Public Library of Science, 2017, doi:10.1371/journal.pcbi.1005609.s004.
short: M. Lukacisinova, S. Novak, T. Paixao, (2017).
date_created: 2021-08-09T14:11:40Z
date_published: 2017-07-18T00:00:00Z
date_updated: 2023-02-23T12:55:39Z
day: '18'
department:
- _id: ToBo
- _id: CaGu
- _id: NiBa
doi: 10.1371/journal.pcbi.1005609.s004
month: '07'
oa_version: Published Version
publisher: Public Library of Science
related_material:
record:
- id: '696'
relation: used_in_publication
status: public
status: public
title: Resistance frequencies for different combination strategies
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2017'
...
---
_id: '9844'
article_processing_charge: No
author:
- first_name: Nela
full_name: Nikolic, Nela
id: 42D9CABC-F248-11E8-B48F-1D18A9856A87
last_name: Nikolic
orcid: 0000-0001-9068-6090
- first_name: Frank
full_name: Schreiber, Frank
last_name: Schreiber
- first_name: Alma
full_name: Dal Co, Alma
last_name: Dal Co
- first_name: Daniel
full_name: Kiviet, Daniel
last_name: Kiviet
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Sten
full_name: Littmann, Sten
last_name: Littmann
- first_name: Marcel
full_name: Kuypers, Marcel
last_name: Kuypers
- first_name: Martin
full_name: Ackermann, Martin
last_name: Ackermann
citation:
ama: Nikolic N, Schreiber F, Dal Co A, et al. Source data for figures and tables.
2017. doi:10.1371/journal.pgen.1007122.s018
apa: Nikolic, N., Schreiber, F., Dal Co, A., Kiviet, D., Bergmiller, T., Littmann,
S., … Ackermann, M. (2017). Source data for figures and tables. Public Library
of Science. https://doi.org/10.1371/journal.pgen.1007122.s018
chicago: Nikolic, Nela, Frank Schreiber, Alma Dal Co, Daniel Kiviet, Tobias Bergmiller,
Sten Littmann, Marcel Kuypers, and Martin Ackermann. “Source Data for Figures
and Tables.” Public Library of Science, 2017. https://doi.org/10.1371/journal.pgen.1007122.s018.
ieee: N. Nikolic et al., “Source data for figures and tables.” Public Library
of Science, 2017.
ista: Nikolic N, Schreiber F, Dal Co A, Kiviet D, Bergmiller T, Littmann S, Kuypers
M, Ackermann M. 2017. Source data for figures and tables, Public Library of Science,
10.1371/journal.pgen.1007122.s018.
mla: Nikolic, Nela, et al. Source Data for Figures and Tables. Public Library
of Science, 2017, doi:10.1371/journal.pgen.1007122.s018.
short: N. Nikolic, F. Schreiber, A. Dal Co, D. Kiviet, T. Bergmiller, S. Littmann,
M. Kuypers, M. Ackermann, (2017).
date_created: 2021-08-09T13:27:16Z
date_published: 2017-12-18T00:00:00Z
date_updated: 2023-02-23T12:25:04Z
day: '18'
department:
- _id: CaGu
doi: 10.1371/journal.pgen.1007122.s018
month: '12'
oa_version: Published Version
publisher: Public Library of Science
related_material:
record:
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relation: used_in_publication
status: public
status: public
title: Source data for figures and tables
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2017'
...
---
_id: '561'
abstract:
- lang: eng
text: Restriction–modification systems are widespread genetic elements that protect
bacteria from bacteriophage infections by recognizing and cleaving heterologous
DNA at short, well-defined sequences called restriction sites. Bioinformatic evidence
shows that restriction sites are significantly underrepresented in bacteriophage
genomes, presumably because bacteriophages with fewer restriction sites are more
likely to escape cleavage by restriction–modification systems. However, how mutations
in restriction sites affect the likelihood of bacteriophage escape is unknown.
Using the bacteriophage l and the restriction–modification system EcoRI, we show
that while mutation effects at different restriction sites are unequal, they are
independent. As a result, the probability of bacteriophage escape increases with
each mutated restriction site. Our results experimentally support the role of
restriction site avoidance as a response to selection imposed by restriction–modification
systems and offer an insight into the events underlying the process of bacteriophage
escape.
acknowledgement: This work was funded by an HFSP Young Investigators' grant RGY0079/2011
(C.C.G.). M.P. is a recipient of a DOC Fellowship of the Austrian Academy of Science
at the Institute of Science and Technology Austria.
article_number: '20170646'
article_processing_charge: No
article_type: original
author:
- first_name: Maros
full_name: Pleska, Maros
id: 4569785E-F248-11E8-B48F-1D18A9856A87
last_name: Pleska
orcid: 0000-0001-7460-7479
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Pleska M, Guet CC. Effects of mutations in phage restriction sites during escape
from restriction–modification. Biology Letters. 2017;13(12). doi:10.1098/rsbl.2017.0646
apa: Pleska, M., & Guet, C. C. (2017). Effects of mutations in phage restriction
sites during escape from restriction–modification. Biology Letters. The
Royal Society. https://doi.org/10.1098/rsbl.2017.0646
chicago: Pleska, Maros, and Calin C Guet. “Effects of Mutations in Phage Restriction
Sites during Escape from Restriction–Modification.” Biology Letters. The
Royal Society, 2017. https://doi.org/10.1098/rsbl.2017.0646.
ieee: M. Pleska and C. C. Guet, “Effects of mutations in phage restriction sites
during escape from restriction–modification,” Biology Letters, vol. 13,
no. 12. The Royal Society, 2017.
ista: Pleska M, Guet CC. 2017. Effects of mutations in phage restriction sites during
escape from restriction–modification. Biology Letters. 13(12), 20170646.
mla: Pleska, Maros, and Calin C. Guet. “Effects of Mutations in Phage Restriction
Sites during Escape from Restriction–Modification.” Biology Letters, vol.
13, no. 12, 20170646, The Royal Society, 2017, doi:10.1098/rsbl.2017.0646.
short: M. Pleska, C.C. Guet, Biology Letters 13 (2017).
date_created: 2018-12-11T11:47:11Z
date_published: 2017-12-01T00:00:00Z
date_updated: 2023-09-07T11:59:32Z
day: '01'
department:
- _id: CaGu
doi: 10.1098/rsbl.2017.0646
external_id:
pmid:
- '29237814'
intvolume: ' 13'
issue: '12'
language:
- iso: eng
main_file_link:
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month: '12'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 251BCBEC-B435-11E9-9278-68D0E5697425
grant_number: RGY0079/2011
name: Multi-Level Conflicts in Evolutionary Dynamics of Restriction-Modification
Systems (HFSP Young investigators' grant)
- _id: 251D65D8-B435-11E9-9278-68D0E5697425
grant_number: '24210'
name: Effects of Stochasticity on the Function of Restriction-Modi cation Systems
at the Single-Cell Level (DOC Fellowship)
publication: Biology Letters
publication_identifier:
issn:
- 1744-9561
publication_status: published
publisher: The Royal Society
publist_id: '7253'
quality_controlled: '1'
related_material:
record:
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relation: research_data
status: public
- id: '202'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Effects of mutations in phage restriction sites during escape from restriction–modification
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 13
year: '2017'
...
---
_id: '202'
abstract:
- lang: eng
text: 'Restriction-modification (RM) represents the simplest and possibly the most
widespread mechanism of self/non-self discrimination in nature. In order to provide
bacteria with immunity against bacteriophages and other parasitic genetic elements,
RM systems rely on a balance between two enzymes: the restriction enzyme, which
cleaves non-self DNA at specific restriction sites, and the modification enzyme,
which tags the host’s DNA as self and thus protects it from cleavage. In this
thesis, I use population and single-cell level experiments in combination with
mathematical modeling to study different aspects of the interplay between RM systems,
bacteria and bacteriophages. First, I analyze how mutations in phage restriction
sites affect the probability of phage escape – an inherently stochastic process,
during which phages accidently get modified instead of restricted. Next, I use
single-cell experiments to show that RM systems can, with a low probability, attack
the genome of their bacterial host and that this primitive form of autoimmunity
leads to a tradeoff between the evolutionary cost and benefit of RM systems. Finally,
I investigate the nature of interactions between bacteria, RM systems and temperate
bacteriophages to find that, as a consequence of phage escape and its impact on
population dynamics, RM systems can promote acquisition of symbiotic bacteriophages,
rather than limit it. The results presented here uncover new fundamental biological
properties of RM systems and highlight their importance in the ecology and evolution
of bacteria, bacteriophages and their interactions.'
acknowledgement: "During my PhD studies, I received help from many people, all of
which unfortunately cannot be listed here. I thank them deeply and hope that I never
made them regret their kindness.\r\nI would like to express my deepest gratitude
to Călin Guet, who went far beyond his responsibilities as an advisor and was to
me also a great mentor and a friend. Călin never questioned my potential or lacked
compassion and I cannot thank him enough for cultivating in me an independent scientist.
I was amazed by his ability to recognize the most fascinating scientific problems
in objects of study that others would find mundane. I hope I adopted at least a
fraction of this ability.\r\nI will be forever grateful to Bruce Levin for all his
support and especially for giving me the best possible example of how one can practice
excellent science with humor and style. Working with Bruce was a true privilege.\r\nI
thank Jonathan Bollback and Gašper Tkačik for serving in my PhD committee and the
Austrian Academy of Science for funding my PhD research via the DOC fellowship.\r\nI
thank all our lab members: Tobias Bergmiller for his guidance, especially in the
first years of my research, and for being a good friend throughout; Remy Chait for
staying in the lab at unreasonable hours and for the good laughs at bad jokes we
shared; Anna Staron for supportively listening to my whines whenever I had to run
a gel; Magdalena Steinrück for her pioneering work in the lab; Kathrin Tomasek for
keeping the entropic forces in check and for her FACS virtuosity; Isabella Tomanek
for always being nice to me, no matter how much bench space I took from her.\r\nI
thank all my collaborators: Reiko Okura and Yuichi Wakamoto for performing and analyzing
the microfluidic experiments; Long Qian and Edo Kussell for their bioinformatics
analysis; Dominik Refardt for the λ kan phage; Moritz for his help with the mathematical
modeling. I thank Fabienne Jesse for her tireless editorial work on all our manuscripts.\r\nFinally,
I would like to thank my family and especially my wife Edita, who sacrificed a lot
so that I can pursue my goals and dreams.\r\n"
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Maros
full_name: Pleska, Maros
id: 4569785E-F248-11E8-B48F-1D18A9856A87
last_name: Pleska
orcid: 0000-0001-7460-7479
citation:
ama: Pleska M. Biology of restriction-modification systems at the single-cell and
population level. 2017. doi:10.15479/AT:ISTA:th_916
apa: Pleska, M. (2017). Biology of restriction-modification systems at the single-cell
and population level. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th_916
chicago: Pleska, Maros. “Biology of Restriction-Modification Systems at the Single-Cell
and Population Level.” Institute of Science and Technology Austria, 2017. https://doi.org/10.15479/AT:ISTA:th_916.
ieee: M. Pleska, “Biology of restriction-modification systems at the single-cell
and population level,” Institute of Science and Technology Austria, 2017.
ista: Pleska M. 2017. Biology of restriction-modification systems at the single-cell
and population level. Institute of Science and Technology Austria.
mla: Pleska, Maros. Biology of Restriction-Modification Systems at the Single-Cell
and Population Level. Institute of Science and Technology Austria, 2017, doi:10.15479/AT:ISTA:th_916.
short: M. Pleska, Biology of Restriction-Modification Systems at the Single-Cell
and Population Level, Institute of Science and Technology Austria, 2017.
date_created: 2018-12-11T11:45:10Z
date_published: 2017-10-01T00:00:00Z
date_updated: 2023-09-15T12:04:56Z
day: '01'
ddc:
- '576'
- '579'
degree_awarded: PhD
department:
- _id: CaGu
doi: 10.15479/AT:ISTA:th_916
file:
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file_id: '6204'
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language:
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month: '10'
oa: 1
oa_version: Published Version
page: '126'
project:
- _id: 251D65D8-B435-11E9-9278-68D0E5697425
grant_number: '24210'
name: Effects of Stochasticity on the Function of Restriction-Modi cation Systems
at the Single-Cell Level (DOC Fellowship)
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '7711'
pubrep_id: '916'
related_material:
record:
- id: '1243'
relation: part_of_dissertation
status: public
- id: '561'
relation: part_of_dissertation
status: public
- id: '457'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
title: Biology of restriction-modification systems at the single-cell and population
level
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2017'
...
---
_id: '1351'
abstract:
- lang: eng
text: The behaviour of gene regulatory networks (GRNs) is typically analysed using
simulation-based statistical testing-like methods. In this paper, we demonstrate
that we can replace this approach by a formal verification-like method that gives
higher assurance and scalability. We focus on Wagner’s weighted GRN model with
varying weights, which is used in evolutionary biology. In the model, weight parameters
represent the gene interaction strength that may change due to genetic mutations.
For a property of interest, we synthesise the constraints over the parameter space
that represent the set of GRNs satisfying the property. We experimentally show
that our parameter synthesis procedure computes the mutational robustness of GRNs—an
important problem of interest in evolutionary biology—more efficiently than the
classical simulation method. We specify the property in linear temporal logic.
We employ symbolic bounded model checking and SMT solving to compute the space
of GRNs that satisfy the property, which amounts to synthesizing a set of linear
constraints on the weights.
article_processing_charge: No
author:
- first_name: Mirco
full_name: Giacobbe, Mirco
id: 3444EA5E-F248-11E8-B48F-1D18A9856A87
last_name: Giacobbe
orcid: 0000-0001-8180-0904
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
- first_name: Ashutosh
full_name: Gupta, Ashutosh
id: 335E5684-F248-11E8-B48F-1D18A9856A87
last_name: Gupta
- first_name: Thomas A
full_name: Henzinger, Thomas A
id: 40876CD8-F248-11E8-B48F-1D18A9856A87
last_name: Henzinger
orcid: 0000−0002−2985−7724
- first_name: Tiago
full_name: Paixao, Tiago
id: 2C5658E6-F248-11E8-B48F-1D18A9856A87
last_name: Paixao
orcid: 0000-0003-2361-3953
- first_name: Tatjana
full_name: Petrov, Tatjana
id: 3D5811FC-F248-11E8-B48F-1D18A9856A87
last_name: Petrov
orcid: 0000-0002-9041-0905
citation:
ama: Giacobbe M, Guet CC, Gupta A, Henzinger TA, Paixao T, Petrov T. Model checking
the evolution of gene regulatory networks. Acta Informatica. 2017;54(8):765-787.
doi:10.1007/s00236-016-0278-x
apa: Giacobbe, M., Guet, C. C., Gupta, A., Henzinger, T. A., Paixao, T., & Petrov,
T. (2017). Model checking the evolution of gene regulatory networks. Acta Informatica.
Springer. https://doi.org/10.1007/s00236-016-0278-x
chicago: Giacobbe, Mirco, Calin C Guet, Ashutosh Gupta, Thomas A Henzinger, Tiago
Paixao, and Tatjana Petrov. “Model Checking the Evolution of Gene Regulatory Networks.”
Acta Informatica. Springer, 2017. https://doi.org/10.1007/s00236-016-0278-x.
ieee: M. Giacobbe, C. C. Guet, A. Gupta, T. A. Henzinger, T. Paixao, and T. Petrov,
“Model checking the evolution of gene regulatory networks,” Acta Informatica,
vol. 54, no. 8. Springer, pp. 765–787, 2017.
ista: Giacobbe M, Guet CC, Gupta A, Henzinger TA, Paixao T, Petrov T. 2017. Model
checking the evolution of gene regulatory networks. Acta Informatica. 54(8), 765–787.
mla: Giacobbe, Mirco, et al. “Model Checking the Evolution of Gene Regulatory Networks.”
Acta Informatica, vol. 54, no. 8, Springer, 2017, pp. 765–87, doi:10.1007/s00236-016-0278-x.
short: M. Giacobbe, C.C. Guet, A. Gupta, T.A. Henzinger, T. Paixao, T. Petrov, Acta
Informatica 54 (2017) 765–787.
date_created: 2018-12-11T11:51:32Z
date_published: 2017-12-01T00:00:00Z
date_updated: 2023-09-20T11:06:03Z
day: '01'
ddc:
- '006'
- '576'
department:
- _id: ToHe
- _id: CaGu
- _id: NiBa
doi: 10.1007/s00236-016-0278-x
ec_funded: 1
external_id:
isi:
- '000414343200003'
file:
- access_level: open_access
checksum: 4e661d9135d7f8c342e8e258dee76f3e
content_type: application/pdf
creator: dernst
date_created: 2019-01-17T15:57:29Z
date_updated: 2020-07-14T12:44:46Z
file_id: '5841'
file_name: 2017_ActaInformatica_Giacobbe.pdf
file_size: 755241
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intvolume: ' 54'
isi: 1
issue: '8'
language:
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month: '12'
oa: 1
oa_version: Published Version
page: 765 - 787
project:
- _id: 25EE3708-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '267989'
name: Quantitative Reactive Modeling
- _id: 25832EC2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: S 11407_N23
name: Rigorous Systems Engineering
- _id: 25F42A32-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Z211
name: The Wittgenstein Prize
- _id: 25B1EC9E-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618091'
name: Speed of Adaptation in Population Genetics and Evolutionary Computation
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 25B07788-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '250152'
name: Limits to selection in biology and in evolutionary computation
publication: Acta Informatica
publication_identifier:
issn:
- '00015903'
publication_status: published
publisher: Springer
publist_id: '5898'
pubrep_id: '649'
quality_controlled: '1'
related_material:
record:
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relation: earlier_version
status: public
scopus_import: '1'
status: public
title: Model checking the evolution of gene regulatory networks
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 54
year: '2017'
...
---
_id: '1336'
abstract:
- lang: eng
text: Evolutionary algorithms (EAs) form a popular optimisation paradigm inspired
by natural evolution. In recent years the field of evolutionary computation has
developed a rigorous analytical theory to analyse the runtimes of EAs on many
illustrative problems. Here we apply this theory to a simple model of natural
evolution. In the Strong Selection Weak Mutation (SSWM) evolutionary regime the
time between occurrences of new mutations is much longer than the time it takes
for a mutated genotype to take over the population. In this situation, the population
only contains copies of one genotype and evolution can be modelled as a stochastic
process evolving one genotype by means of mutation and selection between the resident
and the mutated genotype. The probability of accepting the mutated genotype then
depends on the change in fitness. We study this process, SSWM, from an algorithmic
perspective, quantifying its expected optimisation time for various parameters
and investigating differences to a similar evolutionary algorithm, the well-known
(1+1) EA. We show that SSWM can have a moderate advantage over the (1+1) EA at
crossing fitness valleys and study an example where SSWM outperforms the (1+1)
EA by taking advantage of information on the fitness gradient.
article_processing_charge: No
author:
- first_name: Tiago
full_name: Paixao, Tiago
id: 2C5658E6-F248-11E8-B48F-1D18A9856A87
last_name: Paixao
orcid: 0000-0003-2361-3953
- first_name: Jorge
full_name: Pérez Heredia, Jorge
last_name: Pérez Heredia
- first_name: Dirk
full_name: Sudholt, Dirk
last_name: Sudholt
- first_name: Barbora
full_name: Trubenova, Barbora
id: 42302D54-F248-11E8-B48F-1D18A9856A87
last_name: Trubenova
orcid: 0000-0002-6873-2967
citation:
ama: Paixao T, Pérez Heredia J, Sudholt D, Trubenova B. Towards a runtime comparison
of natural and artificial evolution. Algorithmica. 2017;78(2):681-713.
doi:10.1007/s00453-016-0212-1
apa: Paixao, T., Pérez Heredia, J., Sudholt, D., & Trubenova, B. (2017). Towards
a runtime comparison of natural and artificial evolution. Algorithmica.
Springer. https://doi.org/10.1007/s00453-016-0212-1
chicago: Paixao, Tiago, Jorge Pérez Heredia, Dirk Sudholt, and Barbora Trubenova.
“Towards a Runtime Comparison of Natural and Artificial Evolution.” Algorithmica.
Springer, 2017. https://doi.org/10.1007/s00453-016-0212-1.
ieee: T. Paixao, J. Pérez Heredia, D. Sudholt, and B. Trubenova, “Towards a runtime
comparison of natural and artificial evolution,” Algorithmica, vol. 78,
no. 2. Springer, pp. 681–713, 2017.
ista: Paixao T, Pérez Heredia J, Sudholt D, Trubenova B. 2017. Towards a runtime
comparison of natural and artificial evolution. Algorithmica. 78(2), 681–713.
mla: Paixao, Tiago, et al. “Towards a Runtime Comparison of Natural and Artificial
Evolution.” Algorithmica, vol. 78, no. 2, Springer, 2017, pp. 681–713,
doi:10.1007/s00453-016-0212-1.
short: T. Paixao, J. Pérez Heredia, D. Sudholt, B. Trubenova, Algorithmica 78 (2017)
681–713.
date_created: 2018-12-11T11:51:27Z
date_published: 2017-06-01T00:00:00Z
date_updated: 2023-09-20T11:14:42Z
day: '01'
ddc:
- '576'
department:
- _id: NiBa
- _id: CaGu
doi: 10.1007/s00453-016-0212-1
ec_funded: 1
external_id:
isi:
- '000400379500013'
file:
- access_level: open_access
checksum: 7873f665a0c598ac747c908f34cb14b9
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:10:19Z
date_updated: 2020-07-14T12:44:44Z
file_id: '4805'
file_name: IST-2016-658-v1+1_s00453-016-0212-1.pdf
file_size: 710206
relation: main_file
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has_accepted_license: '1'
intvolume: ' 78'
isi: 1
issue: '2'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: 681 - 713
project:
- _id: 25B1EC9E-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618091'
name: Speed of Adaptation in Population Genetics and Evolutionary Computation
publication: Algorithmica
publication_identifier:
issn:
- '01784617'
publication_status: published
publisher: Springer
publist_id: '5931'
pubrep_id: '658'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Towards a runtime comparison of natural and artificial evolution
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 78
year: '2017'
...
---
_id: '1084'
abstract:
- lang: eng
text: 'BceRS and PsdRS are paralogous two-component systems in Bacillus subtilis
controlling the response to antimicrobial peptides. In the presence of extracellular
bacitracin and nisin, respectively, the two response regulators (RRs) bind their
target promoters, PbceA or PpsdA, resulting in a strong up-regulation of target
gene expression and ultimately antibiotic resistance. Despite high sequence similarity
between the RRs BceR and PsdR and their known binding sites, no cross-regulation
has been observed between them. We therefore investigated the specificity determinants
of PbceA and PpsdA that ensure the insulation of these two paralogous pathways
at the RR–promoter interface. In vivo and in vitro analyses demonstrate that the
regulatory regions within these two promoters contain three important elements:
in addition to the known (main) binding site, we identified a linker region and
a secondary binding site that are crucial for functionality. Initial binding to
the high-affinity, low-specificity main binding site is a prerequisite for the
subsequent highly specific binding of a second RR dimer to the low-affinity secondary
binding site. In addition to this hierarchical cooperative binding, discrimination
requires a competition of the two RRs for their respective binding site mediated
by only slight differences in binding affinities.'
article_processing_charge: No
author:
- first_name: Chong
full_name: Fang, Chong
last_name: Fang
- first_name: Anna A
full_name: Nagy-Staron, Anna A
id: 3ABC5BA6-F248-11E8-B48F-1D18A9856A87
last_name: Nagy-Staron
orcid: 0000-0002-1391-8377
- first_name: Martin
full_name: Grafe, Martin
last_name: Grafe
- first_name: Ralf
full_name: Heermann, Ralf
last_name: Heermann
- first_name: Kirsten
full_name: Jung, Kirsten
last_name: Jung
- first_name: Susanne
full_name: Gebhard, Susanne
last_name: Gebhard
- first_name: Thorsten
full_name: Mascher, Thorsten
last_name: Mascher
citation:
ama: Fang C, Nagy-Staron AA, Grafe M, et al. Insulation and wiring specificity of
BceR like response regulators and their target promoters in Bacillus subtilis.
Molecular Microbiology. 2017;104(1):16-31. doi:10.1111/mmi.13597
apa: Fang, C., Nagy-Staron, A. A., Grafe, M., Heermann, R., Jung, K., Gebhard, S.,
& Mascher, T. (2017). Insulation and wiring specificity of BceR like response
regulators and their target promoters in Bacillus subtilis. Molecular Microbiology.
Wiley-Blackwell. https://doi.org/10.1111/mmi.13597
chicago: Fang, Chong, Anna A Nagy-Staron, Martin Grafe, Ralf Heermann, Kirsten Jung,
Susanne Gebhard, and Thorsten Mascher. “Insulation and Wiring Specificity of BceR
like Response Regulators and Their Target Promoters in Bacillus Subtilis.” Molecular
Microbiology. Wiley-Blackwell, 2017. https://doi.org/10.1111/mmi.13597.
ieee: C. Fang et al., “Insulation and wiring specificity of BceR like response
regulators and their target promoters in Bacillus subtilis,” Molecular Microbiology,
vol. 104, no. 1. Wiley-Blackwell, pp. 16–31, 2017.
ista: Fang C, Nagy-Staron AA, Grafe M, Heermann R, Jung K, Gebhard S, Mascher T.
2017. Insulation and wiring specificity of BceR like response regulators and their
target promoters in Bacillus subtilis. Molecular Microbiology. 104(1), 16–31.
mla: Fang, Chong, et al. “Insulation and Wiring Specificity of BceR like Response
Regulators and Their Target Promoters in Bacillus Subtilis.” Molecular Microbiology,
vol. 104, no. 1, Wiley-Blackwell, 2017, pp. 16–31, doi:10.1111/mmi.13597.
short: C. Fang, A.A. Nagy-Staron, M. Grafe, R. Heermann, K. Jung, S. Gebhard, T.
Mascher, Molecular Microbiology 104 (2017) 16–31.
date_created: 2018-12-11T11:50:03Z
date_published: 2017-04-01T00:00:00Z
date_updated: 2023-09-20T11:48:43Z
day: '01'
department:
- _id: CaGu
doi: 10.1111/mmi.13597
external_id:
isi:
- '000398059200002'
intvolume: ' 104'
isi: 1
issue: '1'
language:
- iso: eng
month: '04'
oa_version: None
page: 16 - 31
publication: Molecular Microbiology
publication_identifier:
issn:
- ' 0950382X'
publication_status: published
publisher: Wiley-Blackwell
publist_id: '6294'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Insulation and wiring specificity of BceR like response regulators and their
target promoters in Bacillus subtilis
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 104
year: '2017'
...
---
_id: '954'
abstract:
- lang: eng
text: Understanding the relation between genotype and phenotype remains a major
challenge. The difficulty of predicting individual mutation effects, and particularly
the interactions between them, has prevented the development of a comprehensive
theory that links genotypic changes to their phenotypic effects. We show that
a general thermodynamic framework for gene regulation, based on a biophysical
understanding of protein-DNA binding, accurately predicts the sign of epistasis
in a canonical cis-regulatory element consisting of overlapping RNA polymerase
and repressor binding sites. Sign and magnitude of individual mutation effects
are sufficient to predict the sign of epistasis and its environmental dependence.
Thus, the thermodynamic model offers the correct null prediction for epistasis
between mutations across DNA-binding sites. Our results indicate that a predictive
theory for the effects of cis-regulatory mutations is possible from first principles,
as long as the essential molecular mechanisms and the constraints these impose
on a biological system are accounted for.
article_number: e25192
article_processing_charge: Yes
author:
- first_name: Mato
full_name: Lagator, Mato
id: 345D25EC-F248-11E8-B48F-1D18A9856A87
last_name: Lagator
- first_name: Tiago
full_name: Paixao, Tiago
id: 2C5658E6-F248-11E8-B48F-1D18A9856A87
last_name: Paixao
orcid: 0000-0003-2361-3953
- first_name: Nicholas H
full_name: Barton, Nicholas H
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
orcid: 0000-0002-8548-5240
- first_name: Jonathan P
full_name: Bollback, Jonathan P
id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
last_name: Bollback
orcid: 0000-0002-4624-4612
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Lagator M, Paixao T, Barton NH, Bollback JP, Guet CC. On the mechanistic nature
of epistasis in a canonical cis-regulatory element. eLife. 2017;6. doi:10.7554/eLife.25192
apa: Lagator, M., Paixao, T., Barton, N. H., Bollback, J. P., & Guet, C. C.
(2017). On the mechanistic nature of epistasis in a canonical cis-regulatory element.
ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.25192
chicago: Lagator, Mato, Tiago Paixao, Nicholas H Barton, Jonathan P Bollback, and
Calin C Guet. “On the Mechanistic Nature of Epistasis in a Canonical Cis-Regulatory
Element.” ELife. eLife Sciences Publications, 2017. https://doi.org/10.7554/eLife.25192.
ieee: M. Lagator, T. Paixao, N. H. Barton, J. P. Bollback, and C. C. Guet, “On the
mechanistic nature of epistasis in a canonical cis-regulatory element,” eLife,
vol. 6. eLife Sciences Publications, 2017.
ista: Lagator M, Paixao T, Barton NH, Bollback JP, Guet CC. 2017. On the mechanistic
nature of epistasis in a canonical cis-regulatory element. eLife. 6, e25192.
mla: Lagator, Mato, et al. “On the Mechanistic Nature of Epistasis in a Canonical
Cis-Regulatory Element.” ELife, vol. 6, e25192, eLife Sciences Publications,
2017, doi:10.7554/eLife.25192.
short: M. Lagator, T. Paixao, N.H. Barton, J.P. Bollback, C.C. Guet, ELife 6 (2017).
date_created: 2018-12-11T11:49:23Z
date_published: 2017-05-18T00:00:00Z
date_updated: 2023-09-22T10:01:17Z
day: '18'
ddc:
- '576'
department:
- _id: CaGu
- _id: NiBa
- _id: JoBo
doi: 10.7554/eLife.25192
ec_funded: 1
external_id:
isi:
- '000404024800001'
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intvolume: ' 6'
isi: 1
language:
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month: '05'
oa: 1
oa_version: Published Version
project:
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call_identifier: FP7
grant_number: '618091'
name: Speed of Adaptation in Population Genetics and Evolutionary Computation
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 2578D616-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '648440'
name: Selective Barriers to Horizontal Gene Transfer
publication: eLife
publication_identifier:
issn:
- 2050084X
publication_status: published
publisher: eLife Sciences Publications
publist_id: '6460'
pubrep_id: '841'
quality_controlled: '1'
scopus_import: '1'
status: public
title: On the mechanistic nature of epistasis in a canonical cis-regulatory element
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 6
year: '2017'
...
---
_id: '1007'
abstract:
- lang: eng
text: 'A nonlinear system possesses an invariance with respect to a set of transformations
if its output dynamics remain invariant when transforming the input, and adjusting
the initial condition accordingly. Most research has focused on invariances with
respect to time-independent pointwise transformations like translational-invariance
(u(t) -> u(t) + p, p in R) or scale-invariance (u(t) -> pu(t), p in R>0).
In this article, we introduce the concept of s0-invariances with respect to continuous
input transformations exponentially growing/decaying over time. We show that s0-invariant
systems not only encompass linear time-invariant (LTI) systems with transfer functions
having an irreducible zero at s0 in R, but also that the input/output relationship
of nonlinear s0-invariant systems possesses properties well known from their linear
counterparts. Furthermore, we extend the concept of s0-invariances to second-
and higher-order s0-invariances, corresponding to invariances with respect to
transformations of the time-derivatives of the input, and encompassing LTI systems
with zeros of multiplicity two or higher. Finally, we show that nth-order 0-invariant
systems realize – under mild conditions – nth-order nonlinear differential operators:
when excited by an input of a characteristic functional form, the system’s output
converges to a constant value only depending on the nth (nonlinear) derivative
of the input.'
article_processing_charge: Yes (in subscription journal)
author:
- first_name: Moritz
full_name: Lang, Moritz
id: 29E0800A-F248-11E8-B48F-1D18A9856A87
last_name: Lang
- first_name: Eduardo
full_name: Sontag, Eduardo
last_name: Sontag
citation:
ama: Lang M, Sontag E. Zeros of nonlinear systems with input invariances. Automatica.
2017;81C:46-55. doi:10.1016/j.automatica.2017.03.030
apa: Lang, M., & Sontag, E. (2017). Zeros of nonlinear systems with input invariances.
Automatica. International Federation of Automatic Control. https://doi.org/10.1016/j.automatica.2017.03.030
chicago: Lang, Moritz, and Eduardo Sontag. “Zeros of Nonlinear Systems with Input
Invariances.” Automatica. International Federation of Automatic Control,
2017. https://doi.org/10.1016/j.automatica.2017.03.030.
ieee: M. Lang and E. Sontag, “Zeros of nonlinear systems with input invariances,”
Automatica, vol. 81C. International Federation of Automatic Control, pp.
46–55, 2017.
ista: Lang M, Sontag E. 2017. Zeros of nonlinear systems with input invariances.
Automatica. 81C, 46–55.
mla: Lang, Moritz, and Eduardo Sontag. “Zeros of Nonlinear Systems with Input Invariances.”
Automatica, vol. 81C, International Federation of Automatic Control, 2017,
pp. 46–55, doi:10.1016/j.automatica.2017.03.030.
short: M. Lang, E. Sontag, Automatica 81C (2017) 46–55.
date_created: 2018-12-11T11:49:39Z
date_published: 2017-06-01T00:00:00Z
date_updated: 2023-10-17T08:51:18Z
day: '01'
ddc:
- '000'
department:
- _id: CaGu
- _id: GaTk
doi: 10.1016/j.automatica.2017.03.030
ec_funded: 1
external_id:
isi:
- '000403513900006'
file:
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content_type: application/pdf
creator: system
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date_updated: 2018-12-12T10:11:29Z
file_id: '4884'
file_name: IST-2017-813-v1+1_ZerosOfNonlinearSystems.pdf
file_size: 1401954
relation: main_file
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isi: 1
language:
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month: '06'
oa: 1
oa_version: Published Version
page: 46 - 55
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
publication: Automatica
publication_identifier:
issn:
- 0005-1098
publication_status: published
publisher: International Federation of Automatic Control
publist_id: '6391'
pubrep_id: '813'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Zeros of nonlinear systems with input invariances
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 81C
year: '2017'
...
---
_id: '5564'
abstract:
- lang: eng
text: Compressed Fastq files with whole-genome sequencing data of IS-wt strain D
and clones from four evolved populations (A11, C08, C10, D08). Information on
this data collection is available in the Methods Section of the primary publication.
article_processing_charge: No
author:
- first_name: Magdalena
full_name: Steinrück, Magdalena
id: 2C023F40-F248-11E8-B48F-1D18A9856A87
last_name: Steinrück
orcid: 0000-0003-1229-9719
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Steinrück M, Guet CC. Fastq files for “Complex chromosomal neighborhood effects
determine the adaptive potential of a gene under selection.” 2017. doi:10.15479/AT:ISTA:65
apa: Steinrück, M., & Guet, C. C. (2017). Fastq files for “Complex chromosomal
neighborhood effects determine the adaptive potential of a gene under selection.”
Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:65
chicago: Steinrück, Magdalena, and Calin C Guet. “Fastq Files for ‘Complex Chromosomal
Neighborhood Effects Determine the Adaptive Potential of a Gene under Selection.’”
Institute of Science and Technology Austria, 2017. https://doi.org/10.15479/AT:ISTA:65.
ieee: M. Steinrück and C. C. Guet, “Fastq files for ‘Complex chromosomal neighborhood
effects determine the adaptive potential of a gene under selection.’” Institute
of Science and Technology Austria, 2017.
ista: Steinrück M, Guet CC. 2017. Fastq files for ‘Complex chromosomal neighborhood
effects determine the adaptive potential of a gene under selection’, Institute
of Science and Technology Austria, 10.15479/AT:ISTA:65.
mla: Steinrück, Magdalena, and Calin C. Guet. Fastq Files for “Complex Chromosomal
Neighborhood Effects Determine the Adaptive Potential of a Gene under Selection.”
Institute of Science and Technology Austria, 2017, doi:10.15479/AT:ISTA:65.
short: M. Steinrück, C.C. Guet, (2017).
datarep_id: '65'
date_created: 2018-12-12T12:31:33Z
date_published: 2017-04-11T00:00:00Z
date_updated: 2024-02-21T13:47:28Z
day: '11'
ddc:
- '576'
department:
- _id: CaGu
doi: 10.15479/AT:ISTA:65
file:
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creator: system
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date_updated: 2020-07-14T12:47:03Z
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date_updated: 2020-07-14T12:47:03Z
file_id: '5628'
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content_type: application/zip
creator: system
date_created: 2018-12-12T13:03:33Z
date_updated: 2020-07-14T12:47:03Z
file_id: '5629'
file_name: IST-2017-65-v1+2_D_A11_1.fastq.zip
file_size: 565014975
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creator: system
date_created: 2018-12-12T13:03:42Z
date_updated: 2020-07-14T12:47:03Z
file_id: '5630'
file_name: IST-2017-65-v1+3_D_A11_2.fastq.zip
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creator: system
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date_updated: 2020-07-14T12:47:03Z
file_id: '5631'
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file_size: 875430169
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date_updated: 2020-07-14T12:47:03Z
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oa: 1
oa_version: Published Version
publisher: Institute of Science and Technology Austria
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relation: research_paper
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status: public
title: Fastq files for "Complex chromosomal neighborhood effects determine the adaptive
potential of a gene under selection"
tmp:
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legal_code_url: https://creativecommons.org/publicdomain/zero/1.0/legalcode
name: Creative Commons Public Domain Dedication (CC0 1.0)
short: CC0 (1.0)
type: research_data
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year: '2017'
...
---
_id: '5560'
abstract:
- lang: eng
text: "This repository contains the data collected for the manuscript \"Biased partitioning
of the multi-drug efflux pump AcrAB-TolC underlies long-lived phenotypic heterogeneity\".\r\nThe
data is compressed into a single archive. Within the archive, different folders
correspond to figures of the main text and the SI of the related publication.\r\nData
is saved as plain text, with each folder containing a separate readme file describing
the format. Typically, the data is from fluorescence microscopy measurements of
single cells growing in a microfluidic \"mother machine\" device, and consists
of relevant values (primarily arbitrary unit or normalized fluorescence measurements,
and division times / growth rates) after raw microscopy images have been processed,
segmented, and their features extracted, as described in the methods section of
the related publication."
article_processing_charge: No
author:
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Anna M
full_name: Andersson, Anna M
id: 2B8A40DA-F248-11E8-B48F-1D18A9856A87
last_name: Andersson
orcid: 0000-0003-2912-6769
- first_name: Kathrin
full_name: Tomasek, Kathrin
id: 3AEC8556-F248-11E8-B48F-1D18A9856A87
last_name: Tomasek
orcid: 0000-0003-3768-877X
- first_name: Enrique
full_name: Balleza, Enrique
last_name: Balleza
- first_name: Daniel
full_name: Kiviet, Daniel
last_name: Kiviet
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Gasper
full_name: Tkacik, Gasper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkacik
orcid: 0000-0002-6699-1455
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Bergmiller T, Andersson AM, Tomasek K, et al. Biased partitioning of the multi-drug
efflux pump AcrAB-TolC underlies long-lived phenotypic heterogeneity. 2017. doi:10.15479/AT:ISTA:53
apa: Bergmiller, T., Andersson, A. M., Tomasek, K., Balleza, E., Kiviet, D., Hauschild,
R., … Guet, C. C. (2017). Biased partitioning of the multi-drug efflux pump AcrAB-TolC
underlies long-lived phenotypic heterogeneity. Institute of Science and Technology
Austria. https://doi.org/10.15479/AT:ISTA:53
chicago: Bergmiller, Tobias, Anna M Andersson, Kathrin Tomasek, Enrique Balleza,
Daniel Kiviet, Robert Hauschild, Gašper Tkačik, and Calin C Guet. “Biased Partitioning
of the Multi-Drug Efflux Pump AcrAB-TolC Underlies Long-Lived Phenotypic Heterogeneity.”
Institute of Science and Technology Austria, 2017. https://doi.org/10.15479/AT:ISTA:53.
ieee: T. Bergmiller et al., “Biased partitioning of the multi-drug efflux
pump AcrAB-TolC underlies long-lived phenotypic heterogeneity.” Institute of Science
and Technology Austria, 2017.
ista: Bergmiller T, Andersson AM, Tomasek K, Balleza E, Kiviet D, Hauschild R, Tkačik
G, Guet CC. 2017. Biased partitioning of the multi-drug efflux pump AcrAB-TolC
underlies long-lived phenotypic heterogeneity, Institute of Science and Technology
Austria, 10.15479/AT:ISTA:53.
mla: Bergmiller, Tobias, et al. Biased Partitioning of the Multi-Drug Efflux
Pump AcrAB-TolC Underlies Long-Lived Phenotypic Heterogeneity. Institute of
Science and Technology Austria, 2017, doi:10.15479/AT:ISTA:53.
short: T. Bergmiller, A.M. Andersson, K. Tomasek, E. Balleza, D. Kiviet, R. Hauschild,
G. Tkačik, C.C. Guet, (2017).
datarep_id: '53'
date_created: 2018-12-12T12:31:32Z
date_published: 2017-03-10T00:00:00Z
date_updated: 2024-02-21T13:49:00Z
day: '10'
ddc:
- '571'
department:
- _id: CaGu
- _id: GaTk
- _id: Bio
doi: 10.15479/AT:ISTA:53
file:
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creator: system
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date_updated: 2020-07-14T12:47:03Z
file_id: '5603'
file_name: IST-2017-53-v1+1_Data_MDE.zip
file_size: 6773204
relation: main_file
file_date_updated: 2020-07-14T12:47:03Z
has_accepted_license: '1'
keyword:
- single cell microscopy
- mother machine microfluidic device
- AcrAB-TolC pump
- multi-drug efflux
- Escherichia coli
month: '03'
oa: 1
oa_version: Published Version
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '665'
relation: research_paper
status: public
status: public
title: Biased partitioning of the multi-drug efflux pump AcrAB-TolC underlies long-lived
phenotypic heterogeneity
tmp:
image: /images/cc_0.png
legal_code_url: https://creativecommons.org/publicdomain/zero/1.0/legalcode
name: Creative Commons Public Domain Dedication (CC0 1.0)
short: CC0 (1.0)
type: research_data
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2017'
...
---
_id: '665'
abstract:
- lang: eng
text: The molecular mechanisms underlying phenotypic variation in isogenic bacterial
populations remain poorly understood.We report that AcrAB-TolC, the main multidrug
efflux pump of Escherichia coli, exhibits a strong partitioning bias for old cell
poles by a segregation mechanism that is mediated by ternary AcrAB-TolC complex
formation. Mother cells inheriting old poles are phenotypically distinct and display
increased drug efflux activity relative to daughters. Consequently, we find systematic
and long-lived growth differences between mother and daughter cells in the presence
of subinhibitory drug concentrations. A simple model for biased partitioning predicts
a population structure of long-lived and highly heterogeneous phenotypes. This
straightforward mechanism of generating sustained growth rate differences at subinhibitory
antibiotic concentrations has implications for understanding the emergence of
multidrug resistance in bacteria.
article_processing_charge: No
article_type: original
author:
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Anna M
full_name: Andersson, Anna M
id: 2B8A40DA-F248-11E8-B48F-1D18A9856A87
last_name: Andersson
orcid: 0000-0003-2912-6769
- first_name: Kathrin
full_name: Tomasek, Kathrin
id: 3AEC8556-F248-11E8-B48F-1D18A9856A87
last_name: Tomasek
orcid: 0000-0003-3768-877X
- first_name: Enrique
full_name: Balleza, Enrique
last_name: Balleza
- first_name: Daniel
full_name: Kiviet, Daniel
last_name: Kiviet
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Gasper
full_name: Tkacik, Gasper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkacik
orcid: 0000-0002-6699-1455
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Bergmiller T, Andersson AM, Tomasek K, et al. Biased partitioning of the multidrug
efflux pump AcrAB TolC underlies long lived phenotypic heterogeneity. Science.
2017;356(6335):311-315. doi:10.1126/science.aaf4762
apa: Bergmiller, T., Andersson, A. M., Tomasek, K., Balleza, E., Kiviet, D., Hauschild,
R., … Guet, C. C. (2017). Biased partitioning of the multidrug efflux pump AcrAB
TolC underlies long lived phenotypic heterogeneity. Science. American Association
for the Advancement of Science. https://doi.org/10.1126/science.aaf4762
chicago: Bergmiller, Tobias, Anna M Andersson, Kathrin Tomasek, Enrique Balleza,
Daniel Kiviet, Robert Hauschild, Gašper Tkačik, and Calin C Guet. “Biased Partitioning
of the Multidrug Efflux Pump AcrAB TolC Underlies Long Lived Phenotypic Heterogeneity.”
Science. American Association for the Advancement of Science, 2017. https://doi.org/10.1126/science.aaf4762.
ieee: T. Bergmiller et al., “Biased partitioning of the multidrug efflux
pump AcrAB TolC underlies long lived phenotypic heterogeneity,” Science,
vol. 356, no. 6335. American Association for the Advancement of Science, pp. 311–315,
2017.
ista: Bergmiller T, Andersson AM, Tomasek K, Balleza E, Kiviet D, Hauschild R, Tkačik
G, Guet CC. 2017. Biased partitioning of the multidrug efflux pump AcrAB TolC
underlies long lived phenotypic heterogeneity. Science. 356(6335), 311–315.
mla: Bergmiller, Tobias, et al. “Biased Partitioning of the Multidrug Efflux Pump
AcrAB TolC Underlies Long Lived Phenotypic Heterogeneity.” Science, vol.
356, no. 6335, American Association for the Advancement of Science, 2017, pp.
311–15, doi:10.1126/science.aaf4762.
short: T. Bergmiller, A.M. Andersson, K. Tomasek, E. Balleza, D. Kiviet, R. Hauschild,
G. Tkačik, C.C. Guet, Science 356 (2017) 311–315.
date_created: 2018-12-11T11:47:48Z
date_published: 2017-04-21T00:00:00Z
date_updated: 2024-02-21T13:49:00Z
day: '21'
department:
- _id: CaGu
- _id: GaTk
- _id: Bio
doi: 10.1126/science.aaf4762
intvolume: ' 356'
issue: '6335'
language:
- iso: eng
month: '04'
oa_version: None
page: 311 - 315
project:
- _id: 254E9036-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P28844-B27
name: Biophysics of information processing in gene regulation
publication: Science
publication_identifier:
issn:
- '00368075'
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '7064'
quality_controlled: '1'
related_material:
record:
- id: '5560'
relation: popular_science
status: public
scopus_import: 1
status: public
title: Biased partitioning of the multidrug efflux pump AcrAB TolC underlies long
lived phenotypic heterogeneity
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 356
year: '2017'
...
---
_id: '1028'
abstract:
- lang: eng
text: Optogenetics and photopharmacology provide spatiotemporally precise control
over protein interactions and protein function in cells and animals. Optogenetic
methods that are sensitive to green light and can be used to break protein complexes
are not broadly available but would enable multichromatic experiments with previously
inaccessible biological targets. Herein, we repurposed cobalamin (vitamin B12)
binding domains of bacterial CarH transcription factors for green-light-induced
receptor dissociation. In cultured cells, we observed oligomerization-induced
cell signaling for the fibroblast growth factor receptor 1 fused to cobalamin-binding
domains in the dark that was rapidly eliminated upon illumination. In zebrafish
embryos expressing fusion receptors, green light endowed control over aberrant
fibroblast growth factor signaling during development. Green-light-induced domain
dissociation and light-inactivated receptors will critically expand the optogenetic
toolbox for control of biological processes.
acknowledgement: "This work was supported by a grant from the European Union\U0010FC1Ds
Seventh Framework Programme (CIG-303564). E.R. was supported by the graduate program
MolecularDrugTargets (Austrian Science Fund (FWF), W1232) and a FemTech fellowship
(Austrian Research Promotion Agency, 3580812)"
article_processing_charge: No
author:
- first_name: Stephanie
full_name: Kainrath, Stephanie
id: 32CFBA64-F248-11E8-B48F-1D18A9856A87
last_name: Kainrath
- first_name: Manuela
full_name: Stadler, Manuela
last_name: Stadler
- first_name: Eva
full_name: Gschaider-Reichhart, Eva
id: 3FEE232A-F248-11E8-B48F-1D18A9856A87
last_name: Gschaider-Reichhart
orcid: 0000-0002-7218-7738
- first_name: Martin
full_name: Distel, Martin
last_name: Distel
- first_name: Harald L
full_name: Janovjak, Harald L
id: 33BA6C30-F248-11E8-B48F-1D18A9856A87
last_name: Janovjak
orcid: 0000-0002-8023-9315
citation:
ama: Kainrath S, Stadler M, Gschaider-Reichhart E, Distel M, Janovjak HL. Green-light-induced
inactivation of receptor signaling using cobalamin-binding domains. Angewandte
Chemie - International Edition. 2017;56(16):4608-4611. doi:10.1002/anie.201611998
apa: Kainrath, S., Stadler, M., Gschaider-Reichhart, E., Distel, M., & Janovjak,
H. L. (2017). Green-light-induced inactivation of receptor signaling using cobalamin-binding
domains. Angewandte Chemie - International Edition. Wiley-Blackwell. https://doi.org/10.1002/anie.201611998
chicago: Kainrath, Stephanie, Manuela Stadler, Eva Gschaider-Reichhart, Martin Distel,
and Harald L Janovjak. “Green-Light-Induced Inactivation of Receptor Signaling
Using Cobalamin-Binding Domains.” Angewandte Chemie - International Edition.
Wiley-Blackwell, 2017. https://doi.org/10.1002/anie.201611998.
ieee: S. Kainrath, M. Stadler, E. Gschaider-Reichhart, M. Distel, and H. L. Janovjak,
“Green-light-induced inactivation of receptor signaling using cobalamin-binding
domains,” Angewandte Chemie - International Edition, vol. 56, no. 16. Wiley-Blackwell,
pp. 4608–4611, 2017.
ista: Kainrath S, Stadler M, Gschaider-Reichhart E, Distel M, Janovjak HL. 2017.
Green-light-induced inactivation of receptor signaling using cobalamin-binding
domains. Angewandte Chemie - International Edition. 56(16), 4608–4611.
mla: Kainrath, Stephanie, et al. “Green-Light-Induced Inactivation of Receptor Signaling
Using Cobalamin-Binding Domains.” Angewandte Chemie - International Edition,
vol. 56, no. 16, Wiley-Blackwell, 2017, pp. 4608–11, doi:10.1002/anie.201611998.
short: S. Kainrath, M. Stadler, E. Gschaider-Reichhart, M. Distel, H.L. Janovjak,
Angewandte Chemie - International Edition 56 (2017) 4608–4611.
date_created: 2018-12-11T11:49:46Z
date_published: 2017-03-20T00:00:00Z
date_updated: 2024-03-28T23:30:13Z
day: '20'
ddc:
- '540'
department:
- _id: CaGu
- _id: HaJa
doi: 10.1002/anie.201611998
ec_funded: 1
external_id:
isi:
- '000398154000038'
file:
- access_level: open_access
content_type: application/pdf
creator: dernst
date_created: 2019-01-18T09:39:55Z
date_updated: 2019-01-18T09:39:55Z
file_id: '5845'
file_name: 2017_communications_Kainrath.pdf
file_size: 2614942
relation: main_file
success: 1
file_date_updated: 2019-01-18T09:39:55Z
has_accepted_license: '1'
intvolume: ' 56'
isi: 1
issue: '16'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
page: 4608-4611
project:
- _id: 25548C20-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '303564'
name: Microbial Ion Channels for Synthetic Neurobiology
- _id: 26AA4EF2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: W1232-B24
name: Molecular Drug Targets [do not use to be deleted]
publication: Angewandte Chemie - International Edition
publication_identifier:
issn:
- '14337851'
publication_status: published
publisher: Wiley-Blackwell
publist_id: '6362'
quality_controlled: '1'
related_material:
record:
- id: '418'
relation: dissertation_contains
status: public
- id: '7680'
relation: part_of_dissertation
status: public
scopus_import: '1'
status: public
title: Green-light-induced inactivation of receptor signaling using cobalamin-binding
domains
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 56
year: '2017'
...
---
_id: '704'
abstract:
- lang: eng
text: 'How the organization of genes on a chromosome shapes adaptation is essential
for understanding evolutionary paths. Here, we investigate how adaptation to rapidly
increasing levels of antibiotic depends on the chromosomal neighborhood of a drug-resistance
gene inserted at different positions of the Escherichia coli chromosome. Using
a dual-fluorescence reporter that allows us to distinguish gene amplifications
from other up-mutations, we track in real-time adaptive changes in expression
of the drug-resistance gene. We find that the relative contribution of several
mutation types differs systematically between loci due to properties of neighboring
genes: essentiality, expression, orientation, termination, and presence of duplicates.
These properties determine rate and fitness effects of gene amplification, deletions,
and mutations compromising transcriptional termination. Thus, the adaptive potential
of a gene under selection is a system-property with a complex genetic basis that
is specific for each chromosomal locus, and it can be inferred from detailed functional
and genomic data.'
article_number: e25100
author:
- first_name: Magdalena
full_name: Steinrück, Magdalena
id: 2C023F40-F248-11E8-B48F-1D18A9856A87
last_name: Steinrück
orcid: 0000-0003-1229-9719
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Steinrück M, Guet CC. Complex chromosomal neighborhood effects determine the
adaptive potential of a gene under selection. eLife. 2017;6. doi:10.7554/eLife.25100
apa: Steinrück, M., & Guet, C. C. (2017). Complex chromosomal neighborhood effects
determine the adaptive potential of a gene under selection. ELife. eLife
Sciences Publications. https://doi.org/10.7554/eLife.25100
chicago: Steinrück, Magdalena, and Calin C Guet. “Complex Chromosomal Neighborhood
Effects Determine the Adaptive Potential of a Gene under Selection.” ELife.
eLife Sciences Publications, 2017. https://doi.org/10.7554/eLife.25100.
ieee: M. Steinrück and C. C. Guet, “Complex chromosomal neighborhood effects determine
the adaptive potential of a gene under selection,” eLife, vol. 6. eLife
Sciences Publications, 2017.
ista: Steinrück M, Guet CC. 2017. Complex chromosomal neighborhood effects determine
the adaptive potential of a gene under selection. eLife. 6, e25100.
mla: Steinrück, Magdalena, and Calin C. Guet. “Complex Chromosomal Neighborhood
Effects Determine the Adaptive Potential of a Gene under Selection.” ELife,
vol. 6, e25100, eLife Sciences Publications, 2017, doi:10.7554/eLife.25100.
short: M. Steinrück, C.C. Guet, ELife 6 (2017).
date_created: 2018-12-11T11:48:01Z
date_published: 2017-07-25T00:00:00Z
date_updated: 2024-03-28T23:30:28Z
day: '25'
ddc:
- '576'
department:
- _id: CaGu
doi: 10.7554/eLife.25100
file:
- access_level: open_access
checksum: 6b908b5db9f61f6820ebd7f8fa815571
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:12:54Z
date_updated: 2020-07-14T12:47:48Z
file_id: '4975'
file_name: IST-2017-890-v1+1_elife-25100-v1.pdf
file_size: 2092088
relation: main_file
- access_level: open_access
checksum: ca21530389b720243552678125fdba35
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:12:55Z
date_updated: 2020-07-14T12:47:48Z
file_id: '4976'
file_name: IST-2017-890-v1+2_elife-25100-figures-v1.pdf
file_size: 3428681
relation: main_file
file_date_updated: 2020-07-14T12:47:48Z
has_accepted_license: '1'
intvolume: ' 6'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
issn:
- 2050084X
publication_status: published
publisher: eLife Sciences Publications
publist_id: '6990'
pubrep_id: '890'
quality_controlled: '1'
related_material:
record:
- id: '5564'
relation: popular_science
status: public
- id: '26'
relation: dissertation_contains
status: public
scopus_import: 1
status: public
title: Complex chromosomal neighborhood effects determine the adaptive potential of
a gene under selection
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 6
year: '2017'
...
---
_id: '696'
abstract:
- lang: eng
text: Mutator strains are expected to evolve when the availability and effect of
beneficial mutations are high enough to counteract the disadvantage from deleterious
mutations that will inevitably accumulate. As the population becomes more adapted
to its environment, both availability and effect of beneficial mutations necessarily
decrease and mutation rates are predicted to decrease. It has been shown that
certain molecular mechanisms can lead to increased mutation rates when the organism
finds itself in a stressful environment. While this may be a correlated response
to other functions, it could also be an adaptive mechanism, raising mutation rates
only when it is most advantageous. Here, we use a mathematical model to investigate
the plausibility of the adaptive hypothesis. We show that such a mechanism can
be mantained if the population is subjected to diverse stresses. By simulating
various antibiotic treatment schemes, we find that combination treatments can
reduce the effectiveness of second-order selection on stress-induced mutagenesis.
We discuss the implications of our results to strategies of antibiotic therapy.
article_number: e1005609
article_type: original
author:
- first_name: Marta
full_name: Lukacisinova, Marta
id: 4342E402-F248-11E8-B48F-1D18A9856A87
last_name: Lukacisinova
orcid: 0000-0002-2519-8004
- first_name: Sebastian
full_name: Novak, Sebastian
id: 461468AE-F248-11E8-B48F-1D18A9856A87
last_name: Novak
orcid: 0000-0002-2519-824X
- first_name: Tiago
full_name: Paixao, Tiago
id: 2C5658E6-F248-11E8-B48F-1D18A9856A87
last_name: Paixao
orcid: 0000-0003-2361-3953
citation:
ama: 'Lukacisinova M, Novak S, Paixao T. Stress induced mutagenesis: Stress diversity
facilitates the persistence of mutator genes. PLoS Computational Biology.
2017;13(7). doi:10.1371/journal.pcbi.1005609'
apa: 'Lukacisinova, M., Novak, S., & Paixao, T. (2017). Stress induced mutagenesis:
Stress diversity facilitates the persistence of mutator genes. PLoS Computational
Biology. Public Library of Science. https://doi.org/10.1371/journal.pcbi.1005609'
chicago: 'Lukacisinova, Marta, Sebastian Novak, and Tiago Paixao. “Stress Induced
Mutagenesis: Stress Diversity Facilitates the Persistence of Mutator Genes.” PLoS
Computational Biology. Public Library of Science, 2017. https://doi.org/10.1371/journal.pcbi.1005609.'
ieee: 'M. Lukacisinova, S. Novak, and T. Paixao, “Stress induced mutagenesis: Stress
diversity facilitates the persistence of mutator genes,” PLoS Computational
Biology, vol. 13, no. 7. Public Library of Science, 2017.'
ista: 'Lukacisinova M, Novak S, Paixao T. 2017. Stress induced mutagenesis: Stress
diversity facilitates the persistence of mutator genes. PLoS Computational Biology.
13(7), e1005609.'
mla: 'Lukacisinova, Marta, et al. “Stress Induced Mutagenesis: Stress Diversity
Facilitates the Persistence of Mutator Genes.” PLoS Computational Biology,
vol. 13, no. 7, e1005609, Public Library of Science, 2017, doi:10.1371/journal.pcbi.1005609.'
short: M. Lukacisinova, S. Novak, T. Paixao, PLoS Computational Biology 13 (2017).
date_created: 2018-12-11T11:47:58Z
date_published: 2017-07-18T00:00:00Z
date_updated: 2024-03-28T23:30:28Z
day: '18'
ddc:
- '576'
department:
- _id: ToBo
- _id: NiBa
- _id: CaGu
doi: 10.1371/journal.pcbi.1005609
ec_funded: 1
file:
- access_level: open_access
checksum: 9143c290fa6458ed2563bff4b295554a
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:15:01Z
date_updated: 2020-07-14T12:47:46Z
file_id: '5117'
file_name: IST-2017-894-v1+1_journal.pcbi.1005609.pdf
file_size: 3775716
relation: main_file
file_date_updated: 2020-07-14T12:47:46Z
has_accepted_license: '1'
intvolume: ' 13'
issue: '7'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
project:
- _id: 25B1EC9E-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618091'
name: Speed of Adaptation in Population Genetics and Evolutionary Computation
publication: PLoS Computational Biology
publication_identifier:
issn:
- 1553734X
publication_status: published
publisher: Public Library of Science
publist_id: '7004'
pubrep_id: '894'
quality_controlled: '1'
related_material:
record:
- id: '9849'
relation: research_data
status: public
- id: '9850'
relation: research_data
status: public
- id: '9851'
relation: research_data
status: public
- id: '9852'
relation: research_data
status: public
- id: '6263'
relation: dissertation_contains
status: public
scopus_import: 1
status: public
title: 'Stress induced mutagenesis: Stress diversity facilitates the persistence of
mutator genes'
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 13
year: '2017'
...
---
_id: '735'
abstract:
- lang: eng
text: Cell-cell contact formation constitutes an essential step in evolution, leading
to the differentiation of specialized cell types. However, remarkably little is
known about whether and how the interplay between contact formation and fate specification
affects development. Here, we identify a positive feedback loop between cell-cell
contact duration, morphogen signaling, and mesendoderm cell-fate specification
during zebrafish gastrulation. We show that long-lasting cell-cell contacts enhance
the competence of prechordal plate (ppl) progenitor cells to respond to Nodal
signaling, required for ppl cell-fate specification. We further show that Nodal
signaling promotes ppl cell-cell contact duration, generating a positive feedback
loop between ppl cell-cell contact duration and cell-fate specification. Finally,
by combining mathematical modeling and experimentation, we show that this feedback
determines whether anterior axial mesendoderm cells become ppl or, instead, turn
into endoderm. Thus, the interdependent activities of cell-cell signaling and
contact formation control fate diversification within the developing embryo.
article_processing_charge: No
author:
- first_name: Vanessa
full_name: Barone, Vanessa
id: 419EECCC-F248-11E8-B48F-1D18A9856A87
last_name: Barone
orcid: 0000-0003-2676-3367
- first_name: Moritz
full_name: Lang, Moritz
id: 29E0800A-F248-11E8-B48F-1D18A9856A87
last_name: Lang
- first_name: Gabriel
full_name: Krens, Gabriel
id: 2B819732-F248-11E8-B48F-1D18A9856A87
last_name: Krens
orcid: 0000-0003-4761-5996
- first_name: Saurabh
full_name: Pradhan, Saurabh
last_name: Pradhan
- first_name: Shayan
full_name: Shamipour, Shayan
id: 40B34FE2-F248-11E8-B48F-1D18A9856A87
last_name: Shamipour
- first_name: Keisuke
full_name: Sako, Keisuke
id: 3BED66BE-F248-11E8-B48F-1D18A9856A87
last_name: Sako
orcid: 0000-0002-6453-8075
- first_name: Mateusz K
full_name: Sikora, Mateusz K
id: 2F74BCDE-F248-11E8-B48F-1D18A9856A87
last_name: Sikora
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
citation:
ama: Barone V, Lang M, Krens G, et al. An effective feedback loop between cell-cell
contact duration and morphogen signaling determines cell fate. Developmental
Cell. 2017;43(2):198-211. doi:10.1016/j.devcel.2017.09.014
apa: Barone, V., Lang, M., Krens, G., Pradhan, S., Shamipour, S., Sako, K., … Heisenberg,
C.-P. J. (2017). An effective feedback loop between cell-cell contact duration
and morphogen signaling determines cell fate. Developmental Cell. Cell
Press. https://doi.org/10.1016/j.devcel.2017.09.014
chicago: Barone, Vanessa, Moritz Lang, Gabriel Krens, Saurabh Pradhan, Shayan Shamipour,
Keisuke Sako, Mateusz K Sikora, Calin C Guet, and Carl-Philipp J Heisenberg. “An
Effective Feedback Loop between Cell-Cell Contact Duration and Morphogen Signaling
Determines Cell Fate.” Developmental Cell. Cell Press, 2017. https://doi.org/10.1016/j.devcel.2017.09.014.
ieee: V. Barone et al., “An effective feedback loop between cell-cell contact
duration and morphogen signaling determines cell fate,” Developmental Cell,
vol. 43, no. 2. Cell Press, pp. 198–211, 2017.
ista: Barone V, Lang M, Krens G, Pradhan S, Shamipour S, Sako K, Sikora MK, Guet
CC, Heisenberg C-PJ. 2017. An effective feedback loop between cell-cell contact
duration and morphogen signaling determines cell fate. Developmental Cell. 43(2),
198–211.
mla: Barone, Vanessa, et al. “An Effective Feedback Loop between Cell-Cell Contact
Duration and Morphogen Signaling Determines Cell Fate.” Developmental Cell,
vol. 43, no. 2, Cell Press, 2017, pp. 198–211, doi:10.1016/j.devcel.2017.09.014.
short: V. Barone, M. Lang, G. Krens, S. Pradhan, S. Shamipour, K. Sako, M.K. Sikora,
C.C. Guet, C.-P.J. Heisenberg, Developmental Cell 43 (2017) 198–211.
date_created: 2018-12-11T11:48:13Z
date_published: 2017-10-23T00:00:00Z
date_updated: 2024-03-28T23:30:39Z
day: '23'
department:
- _id: CaHe
- _id: CaGu
- _id: GaTk
doi: 10.1016/j.devcel.2017.09.014
ec_funded: 1
external_id:
isi:
- '000413443700011'
intvolume: ' 43'
isi: 1
issue: '2'
language:
- iso: eng
month: '10'
oa_version: None
page: 198 - 211
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 252DD2A6-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: I2058
name: 'Cell segregation in gastrulation: the role of cell fate specification'
publication: Developmental Cell
publication_identifier:
issn:
- '15345807'
publication_status: published
publisher: Cell Press
publist_id: '6934'
quality_controlled: '1'
related_material:
record:
- id: '961'
relation: dissertation_contains
status: public
- id: '8350'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: An effective feedback loop between cell-cell contact duration and morphogen
signaling determines cell fate
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 43
year: '2017'
...
---
_id: '1008'
abstract:
- lang: eng
text: Feedback loops in biological networks, among others, enable differentiation
and cell cycle progression, and increase robustness in signal transduction. In
natural networks, feedback loops are often complex and intertwined, making it
challenging to identify which loops are mainly responsible for an observed behavior.
However, minimal synthetic replicas could allow for such identification. Here,
we engineered a synthetic permease-inducer-repressor system in Saccharomyces cerevisiae
to analyze if a transport-mediated positive feedback loop could be a core mechanism
for the switch-like behavior in the regulation of metabolic gene networks such
as the S. cerevisiae GAL system or the Escherichia coli lac operon. We characterized
the synthetic circuit using deterministic and stochastic mathematical models.
Similar to its natural counterparts, our synthetic system shows bistable and hysteretic
behavior, and the inducer concentration range for bistability as well as the switching
rates between the two stable states depend on the repressor concentration. Our
results indicate that a generic permease–inducer–repressor circuit with a single
feedback loop is sufficient to explain the experimentally observed bistable behavior
of the natural systems. We anticipate that the approach of reimplementing natural
systems with orthogonal parts to identify crucial network components is applicable
to other natural systems such as signaling pathways.
acknowledgement: We thank Julio Polaina (Instituto de Agroqu ı ́ mica y Tecnolog ı
́ a de Alimentos, C.S.I.C., Paterna, Spain) for the gift of plasmid pMR4, Gregor
W. Schmidt for provision of and support with the micro fl uidic device, Markus Du
̈ rr for the cell tracking R script, and Lukas Widmer for the script for MEIGO using
“ parfor ” in MATLAB. We acknowledge the members of the Stelling group for discussions,
comments, and support.
author:
- first_name: Robert
full_name: Gnügge, Robert
last_name: Gnügge
- first_name: Lekshmi
full_name: Dharmarajan, Lekshmi
last_name: Dharmarajan
- first_name: Moritz
full_name: Lang, Moritz
id: 29E0800A-F248-11E8-B48F-1D18A9856A87
last_name: Lang
- first_name: Jörg
full_name: Stelling, Jörg
last_name: Stelling
citation:
ama: Gnügge R, Dharmarajan L, Lang M, Stelling J. An orthogonal permease–inducer–repressor
feedback loop shows bistability. ACS Synthetic Biology. 2016;5(10):1098-1107.
doi:10.1021/acssynbio.6b00013
apa: Gnügge, R., Dharmarajan, L., Lang, M., & Stelling, J. (2016). An orthogonal
permease–inducer–repressor feedback loop shows bistability. ACS Synthetic Biology.
American Chemical Society. https://doi.org/10.1021/acssynbio.6b00013
chicago: Gnügge, Robert, Lekshmi Dharmarajan, Moritz Lang, and Jörg Stelling. “An
Orthogonal Permease–Inducer–Repressor Feedback Loop Shows Bistability.” ACS
Synthetic Biology. American Chemical Society, 2016. https://doi.org/10.1021/acssynbio.6b00013.
ieee: R. Gnügge, L. Dharmarajan, M. Lang, and J. Stelling, “An orthogonal permease–inducer–repressor
feedback loop shows bistability,” ACS Synthetic Biology, vol. 5, no. 10.
American Chemical Society, pp. 1098–1107, 2016.
ista: Gnügge R, Dharmarajan L, Lang M, Stelling J. 2016. An orthogonal permease–inducer–repressor
feedback loop shows bistability. ACS Synthetic Biology. 5(10), 1098–1107.
mla: Gnügge, Robert, et al. “An Orthogonal Permease–Inducer–Repressor Feedback Loop
Shows Bistability.” ACS Synthetic Biology, vol. 5, no. 10, American Chemical
Society, 2016, pp. 1098–107, doi:10.1021/acssynbio.6b00013.
short: R. Gnügge, L. Dharmarajan, M. Lang, J. Stelling, ACS Synthetic Biology 5
(2016) 1098–1107.
date_created: 2018-12-11T11:49:40Z
date_published: 2016-05-05T00:00:00Z
date_updated: 2021-01-12T06:47:37Z
day: '05'
department:
- _id: CaGu
doi: 10.1021/acssynbio.6b00013
intvolume: ' 5'
issue: '10'
language:
- iso: eng
month: '05'
oa_version: None
page: 1098 - 1107
publication: ACS Synthetic Biology
publication_status: published
publisher: American Chemical Society
publist_id: '6390'
quality_controlled: '1'
status: public
title: An orthogonal permease–inducer–repressor feedback loop shows bistability
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 5
year: '2016'
...
---
_id: '1170'
abstract:
- lang: eng
text: The increasing complexity of dynamic models in systems and synthetic biology
poses computational challenges especially for the identification of model parameters.
While modularization of the corresponding optimization problems could help reduce
the “curse of dimensionality,” abundant feedback and crosstalk mechanisms prohibit
a simple decomposition of most biomolecular networks into subnetworks, or modules.
Drawing on ideas from network modularization and multiple-shooting optimization,
we present here a modular parameter identification approach that explicitly allows
for such interdependencies. Interfaces between our modules are given by the experimentally
measured molecular species. This definition allows deriving good (initial) estimates
for the inter-module communication directly from the experimental data. Given
these estimates, the states and parameter sensitivities of different modules can
be integrated independently. To achieve consistency between modules, we iteratively
adjust the estimates for inter-module communication while optimizing the parameters.
After convergence to an optimal parameter set---but not during earlier iterations---the
intermodule communication as well as the individual modules\' state dynamics agree
with the dynamics of the nonmodularized network. Our modular parameter identification
approach allows for easy parallelization; it can reduce the computational complexity
for larger networks and decrease the probability to converge to suboptimal local
minima. We demonstrate the algorithm\'s performance in parameter estimation for
two biomolecular networks, a synthetic genetic oscillator and a mammalian signaling
pathway.
author:
- first_name: Moritz
full_name: Lang, Moritz
id: 29E0800A-F248-11E8-B48F-1D18A9856A87
last_name: Lang
- first_name: Jörg
full_name: Stelling, Jörg
last_name: Stelling
citation:
ama: Lang M, Stelling J. Modular parameter identification of biomolecular networks.
SIAM Journal on Scientific Computing. 2016;38(6):B988-B1008. doi:10.1137/15M103306X
apa: Lang, M., & Stelling, J. (2016). Modular parameter identification of biomolecular
networks. SIAM Journal on Scientific Computing. Society for Industrial
and Applied Mathematics . https://doi.org/10.1137/15M103306X
chicago: Lang, Moritz, and Jörg Stelling. “Modular Parameter Identification of Biomolecular
Networks.” SIAM Journal on Scientific Computing. Society for Industrial
and Applied Mathematics , 2016. https://doi.org/10.1137/15M103306X.
ieee: M. Lang and J. Stelling, “Modular parameter identification of biomolecular
networks,” SIAM Journal on Scientific Computing, vol. 38, no. 6. Society
for Industrial and Applied Mathematics , pp. B988–B1008, 2016.
ista: Lang M, Stelling J. 2016. Modular parameter identification of biomolecular
networks. SIAM Journal on Scientific Computing. 38(6), B988–B1008.
mla: Lang, Moritz, and Jörg Stelling. “Modular Parameter Identification of Biomolecular
Networks.” SIAM Journal on Scientific Computing, vol. 38, no. 6, Society
for Industrial and Applied Mathematics , 2016, pp. B988–1008, doi:10.1137/15M103306X.
short: M. Lang, J. Stelling, SIAM Journal on Scientific Computing 38 (2016) B988–B1008.
date_created: 2018-12-11T11:50:31Z
date_published: 2016-11-15T00:00:00Z
date_updated: 2021-01-12T06:48:49Z
day: '15'
ddc:
- '003'
- '518'
- '570'
- '621'
department:
- _id: CaGu
- _id: GaTk
doi: 10.1137/15M103306X
file:
- access_level: local
checksum: 781bc3ffd30b2dd65b7727c5a285fc78
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:41Z
date_updated: 2020-07-14T12:44:37Z
file_id: '5095'
file_name: IST-2017-811-v1+1_modular_parameter_identification.pdf
file_size: 871964
relation: main_file
file_date_updated: 2020-07-14T12:44:37Z
has_accepted_license: '1'
intvolume: ' 38'
issue: '6'
language:
- iso: eng
month: '11'
oa_version: Submitted Version
page: B988 - B1008
publication: SIAM Journal on Scientific Computing
publication_status: published
publisher: 'Society for Industrial and Applied Mathematics '
publist_id: '6186'
pubrep_id: '811'
quality_controlled: '1'
scopus_import: 1
status: public
title: Modular parameter identification of biomolecular networks
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 38
year: '2016'
...
---
_id: '1220'
abstract:
- lang: eng
text: Theoretical and numerical aspects of aerodynamic efficiency of propulsion
systems coupled to the boundary layer of a fuselage are studied. We discuss the
effects of local flow fields, which are affected both by conservative flow acceleration
as well as total pressure losses, on the efficiency of boundary layer immersed
propulsion devices. We introduce the concept of a boundary layer retardation turbine
that helps reduce skin friction over the fuselage. We numerically investigate
efficiency gains offered by boundary layer and wake interacting devices. We discuss
the results in terms of a total energy consumption framework and show that efficiency
gains of any device depend on all the other elements of the propulsion system.
author:
- first_name: Gregor
full_name: Mikić, Gregor
last_name: Mikić
- first_name: Alex
full_name: Stoll, Alex
last_name: Stoll
- first_name: Joe
full_name: Bevirt, Joe
last_name: Bevirt
- first_name: Rok
full_name: Grah, Rok
id: 483E70DE-F248-11E8-B48F-1D18A9856A87
last_name: Grah
orcid: 0000-0003-2539-3560
- first_name: Mark
full_name: Moore, Mark
last_name: Moore
citation:
ama: 'Mikić G, Stoll A, Bevirt J, Grah R, Moore M. Fuselage boundary layer ingestion
propulsion applied to a thin haul commuter aircraft for optimal efficiency. In:
AIAA; 2016:1-19. doi:10.2514/6.2016-3764'
apa: 'Mikić, G., Stoll, A., Bevirt, J., Grah, R., & Moore, M. (2016). Fuselage
boundary layer ingestion propulsion applied to a thin haul commuter aircraft for
optimal efficiency (pp. 1–19). Presented at the AIAA: Aviation Technology, Integration,
and Operations Conference, Washington, D.C., USA: AIAA. https://doi.org/10.2514/6.2016-3764'
chicago: Mikić, Gregor, Alex Stoll, Joe Bevirt, Rok Grah, and Mark Moore. “Fuselage
Boundary Layer Ingestion Propulsion Applied to a Thin Haul Commuter Aircraft for
Optimal Efficiency,” 1–19. AIAA, 2016. https://doi.org/10.2514/6.2016-3764.
ieee: 'G. Mikić, A. Stoll, J. Bevirt, R. Grah, and M. Moore, “Fuselage boundary
layer ingestion propulsion applied to a thin haul commuter aircraft for optimal
efficiency,” presented at the AIAA: Aviation Technology, Integration, and Operations
Conference, Washington, D.C., USA, 2016, pp. 1–19.'
ista: 'Mikić G, Stoll A, Bevirt J, Grah R, Moore M. 2016. Fuselage boundary layer
ingestion propulsion applied to a thin haul commuter aircraft for optimal efficiency.
AIAA: Aviation Technology, Integration, and Operations Conference, 1–19.'
mla: Mikić, Gregor, et al. Fuselage Boundary Layer Ingestion Propulsion Applied
to a Thin Haul Commuter Aircraft for Optimal Efficiency. AIAA, 2016, pp. 1–19,
doi:10.2514/6.2016-3764.
short: G. Mikić, A. Stoll, J. Bevirt, R. Grah, M. Moore, in:, AIAA, 2016, pp. 1–19.
conference:
end_date: 2016-06-17
location: Washington, D.C., USA
name: 'AIAA: Aviation Technology, Integration, and Operations Conference'
start_date: 2016-06-13
date_created: 2018-12-11T11:50:47Z
date_published: 2016-06-01T00:00:00Z
date_updated: 2023-02-21T10:17:50Z
day: '01'
department:
- _id: CaGu
- _id: GaTk
doi: 10.2514/6.2016-3764
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://ntrs.nasa.gov/search.jsp?R=20160010167&hterms=Fuselage+boundary+layer+ingestion+propulsion+applied+thin+haul+commuter+aircraft+optimal+efficiency&qs=N%3D0%26Ntk%3DAll%26Ntt%3DFuselage%2520boundary%2520layer%2520ingestion%2520propulsion%2520applied%2520to%2520a%2520thin%2520haul%2520commuter%2520aircraft%2520for%2520optimal%2520efficiency%26Ntx%3Dmode%2520matchallpartial%26Nm%3D123%7CCollection%7CNASA%2520STI%7C%7C17%7CCollection%7CNACA
month: '06'
oa: 1
oa_version: Preprint
page: 1 - 19
publication_status: published
publisher: AIAA
publist_id: '6114'
quality_controlled: '1'
scopus_import: 1
status: public
title: Fuselage boundary layer ingestion propulsion applied to a thin haul commuter
aircraft for optimal efficiency
type: conference
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
year: '2016'
...
---
_id: '1290'
abstract:
- lang: eng
text: We developed a competition-based screening strategy to identify compounds
that invert the selective advantage of antibiotic resistance. Using our assay,
we screened over 19,000 compounds for the ability to select against the TetA tetracycline-resistance
efflux pump in Escherichia coli and identified two hits, β-thujaplicin and disulfiram.
Treating a tetracycline-resistant population with β-thujaplicin selects for loss
of the resistance gene, enabling an effective second-phase treatment with doxycycline.
acknowledgement: "This work was supported in part by National Institute of Allergy
and Infectious Diseases grant U54 AI057159, US National Institutes of Health grants
R01 GM081617 (to R.K.) and GM086258 (to J.C.), European Research Council FP7 ERC
grant 281891 (to R.K.) and a National Science Foundation Graduate Fellowship (to
L.K.S.).\r\n"
author:
- first_name: Laura
full_name: Stone, Laura
last_name: Stone
- first_name: Michael
full_name: Baym, Michael
last_name: Baym
- first_name: Tami
full_name: Lieberman, Tami
last_name: Lieberman
- first_name: Remy P
full_name: Chait, Remy P
id: 3464AE84-F248-11E8-B48F-1D18A9856A87
last_name: Chait
orcid: 0000-0003-0876-3187
- first_name: Jon
full_name: Clardy, Jon
last_name: Clardy
- first_name: Roy
full_name: Kishony, Roy
last_name: Kishony
citation:
ama: Stone L, Baym M, Lieberman T, Chait RP, Clardy J, Kishony R. Compounds that
select against the tetracycline-resistance efflux pump. Nature Chemical Biology.
2016;12(11):902-904. doi:10.1038/nchembio.2176
apa: Stone, L., Baym, M., Lieberman, T., Chait, R. P., Clardy, J., & Kishony,
R. (2016). Compounds that select against the tetracycline-resistance efflux pump.
Nature Chemical Biology. Nature Publishing Group. https://doi.org/10.1038/nchembio.2176
chicago: Stone, Laura, Michael Baym, Tami Lieberman, Remy P Chait, Jon Clardy, and
Roy Kishony. “Compounds That Select against the Tetracycline-Resistance Efflux
Pump.” Nature Chemical Biology. Nature Publishing Group, 2016. https://doi.org/10.1038/nchembio.2176.
ieee: L. Stone, M. Baym, T. Lieberman, R. P. Chait, J. Clardy, and R. Kishony, “Compounds
that select against the tetracycline-resistance efflux pump,” Nature Chemical
Biology, vol. 12, no. 11. Nature Publishing Group, pp. 902–904, 2016.
ista: Stone L, Baym M, Lieberman T, Chait RP, Clardy J, Kishony R. 2016. Compounds
that select against the tetracycline-resistance efflux pump. Nature Chemical Biology.
12(11), 902–904.
mla: Stone, Laura, et al. “Compounds That Select against the Tetracycline-Resistance
Efflux Pump.” Nature Chemical Biology, vol. 12, no. 11, Nature Publishing
Group, 2016, pp. 902–04, doi:10.1038/nchembio.2176.
short: L. Stone, M. Baym, T. Lieberman, R.P. Chait, J. Clardy, R. Kishony, Nature
Chemical Biology 12 (2016) 902–904.
date_created: 2018-12-11T11:51:10Z
date_published: 2016-11-01T00:00:00Z
date_updated: 2021-01-12T06:49:39Z
day: '01'
department:
- _id: CaGu
- _id: GaTk
doi: 10.1038/nchembio.2176
intvolume: ' 12'
issue: '11'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5069154/
month: '11'
oa: 1
oa_version: Preprint
page: 902 - 904
publication: Nature Chemical Biology
publication_status: published
publisher: Nature Publishing Group
publist_id: '6026'
quality_controlled: '1'
scopus_import: 1
status: public
title: Compounds that select against the tetracycline-resistance efflux pump
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 12
year: '2016'
...
---
_id: '1320'
abstract:
- lang: eng
text: 'In recent years, several biomolecular systems have been shown to be scale-invariant
(SI), i.e. to show the same output dynamics when exposed to geometrically scaled
input signals (u → pu, p > 0) after pre-adaptation to accordingly scaled constant
inputs. In this article, we show that SI systems-as well as systems invariant
with respect to other input transformations-can realize nonlinear differential
operators: when excited by inputs obeying functional forms characteristic for
a given class of invariant systems, the systems'' outputs converge to constant
values directly quantifying the speed of the input.'
acknowledgement: The research leading to these results has received funding from the
People Programme (Marie Curie Actions) of the European Union's Seventh Framework
Programme (FP7/2007-2013) under REA grant agreement n° [291734]. Work supported
in part by grants AFOSR FA9550-14-1-0060 and NIH 1R01GM100473.
article_number: '7526722'
author:
- first_name: Moritz
full_name: Lang, Moritz
id: 29E0800A-F248-11E8-B48F-1D18A9856A87
last_name: Lang
- first_name: Eduardo
full_name: Sontag, Eduardo
last_name: Sontag
citation:
ama: 'Lang M, Sontag E. Scale-invariant systems realize nonlinear differential operators.
In: Vol 2016-July. IEEE; 2016. doi:10.1109/ACC.2016.7526722'
apa: 'Lang, M., & Sontag, E. (2016). Scale-invariant systems realize nonlinear
differential operators (Vol. 2016–July). Presented at the ACC: American Control
Conference, Boston, MA, USA: IEEE. https://doi.org/10.1109/ACC.2016.7526722'
chicago: Lang, Moritz, and Eduardo Sontag. “Scale-Invariant Systems Realize Nonlinear
Differential Operators,” Vol. 2016–July. IEEE, 2016. https://doi.org/10.1109/ACC.2016.7526722.
ieee: 'M. Lang and E. Sontag, “Scale-invariant systems realize nonlinear differential
operators,” presented at the ACC: American Control Conference, Boston, MA, USA,
2016, vol. 2016–July.'
ista: 'Lang M, Sontag E. 2016. Scale-invariant systems realize nonlinear differential
operators. ACC: American Control Conference vol. 2016–July, 7526722.'
mla: Lang, Moritz, and Eduardo Sontag. Scale-Invariant Systems Realize Nonlinear
Differential Operators. Vol. 2016–July, 7526722, IEEE, 2016, doi:10.1109/ACC.2016.7526722.
short: M. Lang, E. Sontag, in:, IEEE, 2016.
conference:
end_date: 2016-07-08
location: Boston, MA, USA
name: 'ACC: American Control Conference'
start_date: 2016-07-06
date_created: 2018-12-11T11:51:21Z
date_published: 2016-07-28T00:00:00Z
date_updated: 2021-01-12T06:49:51Z
day: '28'
ddc:
- '003'
- '621'
department:
- _id: CaGu
- _id: GaTk
doi: 10.1109/ACC.2016.7526722
ec_funded: 1
file:
- access_level: local
checksum: 7219432b43defc62a0d45f48d4ce6a19
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:16:17Z
date_updated: 2020-07-14T12:44:43Z
file_id: '5203'
file_name: IST-2017-810-v1+1_root.pdf
file_size: 539166
relation: main_file
file_date_updated: 2020-07-14T12:44:43Z
has_accepted_license: '1'
language:
- iso: eng
month: '07'
oa_version: Preprint
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
publication_status: published
publisher: IEEE
publist_id: '5950'
pubrep_id: '810'
quality_controlled: '1'
scopus_import: 1
status: public
title: Scale-invariant systems realize nonlinear differential operators
type: conference
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 2016-July
year: '2016'
...
---
_id: '1332'
abstract:
- lang: eng
text: Antibiotic-sensitive and -resistant bacteria coexist in natural environments
with low, if detectable, antibiotic concentrations. Except possibly around localized
antibiotic sources, where resistance can provide a strong advantage, bacterial
fitness is dominated by stresses unaffected by resistance to the antibiotic. How
do such mixed and heterogeneous conditions influence the selective advantage or
disadvantage of antibiotic resistance? Here we find that sub-inhibitory levels
of tetracyclines potentiate selection for or against tetracycline resistance around
localized sources of almost any toxin or stress. Furthermore, certain stresses
generate alternating rings of selection for and against resistance around a localized
source of the antibiotic. In these conditions, localized antibiotic sources, even
at high strengths, can actually produce a net selection against resistance to
the antibiotic. Our results show that interactions between the effects of an antibiotic
and other stresses in inhomogeneous environments can generate pervasive, complex
patterns of selection both for and against antibiotic resistance.
acknowledgement: This work was partially supported by US National Institutes of Health
grant R01-GM081617, Israeli Centers of Research Excellence I-CORE Program ISF Grant
No. 152/11, and the European Research Council FP7 ERC Grant 281891.
article_number: '10333'
author:
- first_name: Remy P
full_name: Chait, Remy P
id: 3464AE84-F248-11E8-B48F-1D18A9856A87
last_name: Chait
orcid: 0000-0003-0876-3187
- first_name: Adam
full_name: Palmer, Adam
last_name: Palmer
- first_name: Idan
full_name: Yelin, Idan
last_name: Yelin
- first_name: Roy
full_name: Kishony, Roy
last_name: Kishony
citation:
ama: Chait RP, Palmer A, Yelin I, Kishony R. Pervasive selection for and against
antibiotic resistance in inhomogeneous multistress environments. Nature Communications.
2016;7. doi:10.1038/ncomms10333
apa: Chait, R. P., Palmer, A., Yelin, I., & Kishony, R. (2016). Pervasive selection
for and against antibiotic resistance in inhomogeneous multistress environments.
Nature Communications. Nature Publishing Group. https://doi.org/10.1038/ncomms10333
chicago: Chait, Remy P, Adam Palmer, Idan Yelin, and Roy Kishony. “Pervasive Selection
for and against Antibiotic Resistance in Inhomogeneous Multistress Environments.”
Nature Communications. Nature Publishing Group, 2016. https://doi.org/10.1038/ncomms10333.
ieee: R. P. Chait, A. Palmer, I. Yelin, and R. Kishony, “Pervasive selection for
and against antibiotic resistance in inhomogeneous multistress environments,”
Nature Communications, vol. 7. Nature Publishing Group, 2016.
ista: Chait RP, Palmer A, Yelin I, Kishony R. 2016. Pervasive selection for and
against antibiotic resistance in inhomogeneous multistress environments. Nature
Communications. 7, 10333.
mla: Chait, Remy P., et al. “Pervasive Selection for and against Antibiotic Resistance
in Inhomogeneous Multistress Environments.” Nature Communications, vol.
7, 10333, Nature Publishing Group, 2016, doi:10.1038/ncomms10333.
short: R.P. Chait, A. Palmer, I. Yelin, R. Kishony, Nature Communications 7 (2016).
date_created: 2018-12-11T11:51:25Z
date_published: 2016-01-20T00:00:00Z
date_updated: 2021-01-12T06:49:57Z
day: '20'
ddc:
- '570'
- '579'
department:
- _id: CaGu
- _id: GaTk
doi: 10.1038/ncomms10333
file:
- access_level: open_access
checksum: ef147bcbb8bd37e9079cf3ce06f5815d
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:13:52Z
date_updated: 2020-07-14T12:44:44Z
file_id: '5039'
file_name: IST-2016-662-v1+1_ncomms10333.pdf
file_size: 1844107
relation: main_file
file_date_updated: 2020-07-14T12:44:44Z
has_accepted_license: '1'
intvolume: ' 7'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_status: published
publisher: Nature Publishing Group
publist_id: '5936'
pubrep_id: '662'
quality_controlled: '1'
scopus_import: 1
status: public
title: Pervasive selection for and against antibiotic resistance in inhomogeneous
multistress environments
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 7
year: '2016'
...
---
_id: '1342'
abstract:
- lang: eng
text: A key aspect of bacterial survival is the ability to evolve while migrating
across spatially varying environmental challenges. Laboratory experiments, however,
often study evolution in well-mixed systems. Here, we introduce an experimental
device, the microbial evolution and growth arena (MEGA)-plate, in which bacteria
spread and evolved on a large antibiotic landscape (120 × 60 centimeters) that
allowed visual observation of mutation and selection in a migrating bacterial
front.While resistance increased consistently, multiple coexisting lineages diversified
both phenotypically and genotypically. Analyzing mutants at and behind the propagating
front,we found that evolution is not always led by the most resistant mutants;
highly resistant mutants may be trapped behindmore sensitive lineages.TheMEGA-plate
provides a versatile platformfor studying microbial adaption and directly visualizing
evolutionary dynamics.
author:
- first_name: Michael
full_name: Baym, Michael
last_name: Baym
- first_name: Tami
full_name: Lieberman, Tami
last_name: Lieberman
- first_name: Eric
full_name: Kelsic, Eric
last_name: Kelsic
- first_name: Remy P
full_name: Chait, Remy P
id: 3464AE84-F248-11E8-B48F-1D18A9856A87
last_name: Chait
orcid: 0000-0003-0876-3187
- first_name: Rotem
full_name: Gross, Rotem
last_name: Gross
- first_name: Idan
full_name: Yelin, Idan
last_name: Yelin
- first_name: Roy
full_name: Kishony, Roy
last_name: Kishony
citation:
ama: Baym M, Lieberman T, Kelsic E, et al. Spatiotemporal microbial evolution on
antibiotic landscapes. Science. 2016;353(6304):1147-1151. doi:10.1126/science.aag0822
apa: Baym, M., Lieberman, T., Kelsic, E., Chait, R. P., Gross, R., Yelin, I., &
Kishony, R. (2016). Spatiotemporal microbial evolution on antibiotic landscapes.
Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.aag0822
chicago: Baym, Michael, Tami Lieberman, Eric Kelsic, Remy P Chait, Rotem Gross,
Idan Yelin, and Roy Kishony. “Spatiotemporal Microbial Evolution on Antibiotic
Landscapes.” Science. American Association for the Advancement of Science,
2016. https://doi.org/10.1126/science.aag0822.
ieee: M. Baym et al., “Spatiotemporal microbial evolution on antibiotic landscapes,”
Science, vol. 353, no. 6304. American Association for the Advancement of
Science, pp. 1147–1151, 2016.
ista: Baym M, Lieberman T, Kelsic E, Chait RP, Gross R, Yelin I, Kishony R. 2016.
Spatiotemporal microbial evolution on antibiotic landscapes. Science. 353(6304),
1147–1151.
mla: Baym, Michael, et al. “Spatiotemporal Microbial Evolution on Antibiotic Landscapes.”
Science, vol. 353, no. 6304, American Association for the Advancement of
Science, 2016, pp. 1147–51, doi:10.1126/science.aag0822.
short: M. Baym, T. Lieberman, E. Kelsic, R.P. Chait, R. Gross, I. Yelin, R. Kishony,
Science 353 (2016) 1147–1151.
date_created: 2018-12-11T11:51:29Z
date_published: 2016-09-09T00:00:00Z
date_updated: 2021-01-12T06:50:01Z
day: '09'
department:
- _id: CaGu
- _id: GaTk
doi: 10.1126/science.aag0822
intvolume: ' 353'
issue: '6304'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5534434/
month: '09'
oa: 1
oa_version: Preprint
page: 1147 - 1151
publication: Science
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '5911'
quality_controlled: '1'
scopus_import: 1
status: public
title: Spatiotemporal microbial evolution on antibiotic landscapes
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 353
year: '2016'
...
---
_id: '1349'
abstract:
- lang: eng
text: Crossing fitness valleys is one of the major obstacles to function optimization.
In this paper we investigate how the structure of the fitness valley, namely its
depth d and length ℓ, influence the runtime of different strategies for crossing
these valleys. We present a runtime comparison between the (1+1) EA and two non-elitist
nature-inspired algorithms, Strong Selection Weak Mutation (SSWM) and the Metropolis
algorithm. While the (1+1) EA has to jump across the valley to a point of higher
fitness because it does not accept decreasing moves, the non-elitist algorithms
may cross the valley by accepting worsening moves. We show that while the runtime
of the (1+1) EA algorithm depends critically on the length of the valley, the
runtimes of the non-elitist algorithms depend crucially only on the depth of the
valley. In particular, the expected runtime of both SSWM and Metropolis is polynomial
in ℓ and exponential in d while the (1+1) EA is efficient only for valleys of
small length. Moreover, we show that both SSWM and Metropolis can also efficiently
optimize a rugged function consisting of consecutive valleys.
author:
- first_name: Pietro
full_name: Oliveto, Pietro
last_name: Oliveto
- first_name: Tiago
full_name: Paixao, Tiago
id: 2C5658E6-F248-11E8-B48F-1D18A9856A87
last_name: Paixao
orcid: 0000-0003-2361-3953
- first_name: Jorge
full_name: Heredia, Jorge
last_name: Heredia
- first_name: Dirk
full_name: Sudholt, Dirk
last_name: Sudholt
- first_name: Barbora
full_name: Trubenova, Barbora
id: 42302D54-F248-11E8-B48F-1D18A9856A87
last_name: Trubenova
orcid: 0000-0002-6873-2967
citation:
ama: 'Oliveto P, Paixao T, Heredia J, Sudholt D, Trubenova B. When non-elitism outperforms
elitism for crossing fitness valleys. In: Proceedings of the Genetic and Evolutionary
Computation Conference 2016 . ACM; 2016:1163-1170. doi:10.1145/2908812.2908909'
apa: 'Oliveto, P., Paixao, T., Heredia, J., Sudholt, D., & Trubenova, B. (2016).
When non-elitism outperforms elitism for crossing fitness valleys. In Proceedings
of the Genetic and Evolutionary Computation Conference 2016 (pp. 1163–1170).
Denver, CO, USA: ACM. https://doi.org/10.1145/2908812.2908909'
chicago: Oliveto, Pietro, Tiago Paixao, Jorge Heredia, Dirk Sudholt, and Barbora
Trubenova. “When Non-Elitism Outperforms Elitism for Crossing Fitness Valleys.”
In Proceedings of the Genetic and Evolutionary Computation Conference 2016
, 1163–70. ACM, 2016. https://doi.org/10.1145/2908812.2908909.
ieee: P. Oliveto, T. Paixao, J. Heredia, D. Sudholt, and B. Trubenova, “When non-elitism
outperforms elitism for crossing fitness valleys,” in Proceedings of the Genetic
and Evolutionary Computation Conference 2016 , Denver, CO, USA, 2016, pp.
1163–1170.
ista: 'Oliveto P, Paixao T, Heredia J, Sudholt D, Trubenova B. 2016. When non-elitism
outperforms elitism for crossing fitness valleys. Proceedings of the Genetic and
Evolutionary Computation Conference 2016 . GECCO: Genetic and evolutionary computation
conference, 1163–1170.'
mla: Oliveto, Pietro, et al. “When Non-Elitism Outperforms Elitism for Crossing
Fitness Valleys.” Proceedings of the Genetic and Evolutionary Computation Conference
2016 , ACM, 2016, pp. 1163–70, doi:10.1145/2908812.2908909.
short: P. Oliveto, T. Paixao, J. Heredia, D. Sudholt, B. Trubenova, in:, Proceedings
of the Genetic and Evolutionary Computation Conference 2016 , ACM, 2016, pp. 1163–1170.
conference:
end_date: 2016-07-24
location: Denver, CO, USA
name: 'GECCO: Genetic and evolutionary computation conference'
start_date: 2016-07-20
date_created: 2018-12-11T11:51:31Z
date_published: 2016-07-20T00:00:00Z
date_updated: 2021-01-12T06:50:03Z
day: '20'
ddc:
- '576'
department:
- _id: NiBa
- _id: CaGu
doi: 10.1145/2908812.2908909
ec_funded: 1
file:
- access_level: open_access
checksum: a1896e39e4113f2711e46b435d5f3e69
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:16:27Z
date_updated: 2020-07-14T12:44:45Z
file_id: '5214'
file_name: IST-2016-650-v1+1_p1163-oliveto.pdf
file_size: 979026
relation: main_file
file_date_updated: 2020-07-14T12:44:45Z
has_accepted_license: '1'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
page: 1163 - 1170
project:
- _id: 25B1EC9E-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618091'
name: Speed of Adaptation in Population Genetics and Evolutionary Computation
publication: 'Proceedings of the Genetic and Evolutionary Computation Conference 2016 '
publication_status: published
publisher: ACM
publist_id: '5900'
pubrep_id: '650'
quality_controlled: '1'
scopus_import: 1
status: public
title: When non-elitism outperforms elitism for crossing fitness valleys
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: conference
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
year: '2016'
...
---
_id: '1359'
abstract:
- lang: eng
text: "The role of gene interactions in the evolutionary process has long\r\nbeen
controversial. Although some argue that they are not of\r\nimportance, because
most variation is additive, others claim that\r\ntheir effect in the long term
can be substantial. Here, we focus on\r\nthe long-term effects of genetic interactions
under directional\r\nselection assuming no mutation or dominance, and that epistasis
is\r\nsymmetrical overall. We ask by how much the mean of a complex\r\ntrait can
be increased by selection and analyze two extreme\r\nregimes, in which either
drift or selection dominate the dynamics\r\nof allele frequencies. In both scenarios,
epistatic interactions affect\r\nthe long-term response to selection by modulating
the additive\r\ngenetic variance. When drift dominates, we extend Robertson\r\n’\r\ns\r\n[Robertson
A (1960)\r\nProc R Soc Lond B Biol Sci\r\n153(951):234\r\n−\r\n249]\r\nargument
to show that, for any form of epistasis, the total response\r\nof a haploid population
is proportional to the initial total genotypic\r\nvariance. In contrast, the total
response of a diploid population is\r\nincreased by epistasis, for a given initial
genotypic variance. When\r\nselection dominates, we show that the total selection
response can\r\nonly be increased by epistasis when s\r\nome initially deleterious
alleles\r\nbecome favored as the genetic background changes. We find a sim-\r\nple
approximation for this effect and show that, in this regime, it is\r\nthe structure
of the genotype - phenotype map that matters and not\r\nthe variance components
of the population."
article_processing_charge: No
article_type: original
author:
- first_name: Tiago
full_name: Paixao, Tiago
id: 2C5658E6-F248-11E8-B48F-1D18A9856A87
last_name: Paixao
orcid: 0000-0003-2361-3953
- first_name: Nicholas H
full_name: Barton, Nicholas H
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
orcid: 0000-0002-8548-5240
citation:
ama: Paixao T, Barton NH. The effect of gene interactions on the long-term response
to selection. PNAS. 2016;113(16):4422-4427. doi:10.1073/pnas.1518830113
apa: Paixao, T., & Barton, N. H. (2016). The effect of gene interactions on
the long-term response to selection. PNAS. National Academy of Sciences.
https://doi.org/10.1073/pnas.1518830113
chicago: Paixao, Tiago, and Nicholas H Barton. “The Effect of Gene Interactions
on the Long-Term Response to Selection.” PNAS. National Academy of Sciences,
2016. https://doi.org/10.1073/pnas.1518830113.
ieee: T. Paixao and N. H. Barton, “The effect of gene interactions on the long-term
response to selection,” PNAS, vol. 113, no. 16. National Academy of Sciences,
pp. 4422–4427, 2016.
ista: Paixao T, Barton NH. 2016. The effect of gene interactions on the long-term
response to selection. PNAS. 113(16), 4422–4427.
mla: Paixao, Tiago, and Nicholas H. Barton. “The Effect of Gene Interactions on
the Long-Term Response to Selection.” PNAS, vol. 113, no. 16, National
Academy of Sciences, 2016, pp. 4422–27, doi:10.1073/pnas.1518830113.
short: T. Paixao, N.H. Barton, PNAS 113 (2016) 4422–4427.
date_created: 2018-12-11T11:51:34Z
date_published: 2016-04-19T00:00:00Z
date_updated: 2021-01-12T06:50:08Z
day: '19'
department:
- _id: NiBa
- _id: CaGu
doi: 10.1073/pnas.1518830113
ec_funded: 1
external_id:
pmid:
- '27044080'
intvolume: ' 113'
issue: '16'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4843425/
month: '04'
oa: 1
oa_version: Published Version
page: 4422 - 4427
pmid: 1
project:
- _id: 25B07788-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '250152'
name: Limits to selection in biology and in evolutionary computation
- _id: 25B1EC9E-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618091'
name: Speed of Adaptation in Population Genetics and Evolutionary Computation
publication: PNAS
publication_status: published
publisher: National Academy of Sciences
publist_id: '5886'
quality_controlled: '1'
scopus_import: 1
status: public
title: The effect of gene interactions on the long-term response to selection
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 113
year: '2016'
...
---
_id: '1427'
abstract:
- lang: eng
text: Changes in gene expression are an important mode of evolution; however, the
proximate mechanism of these changes is poorly understood. In particular, little
is known about the effects of mutations within cis binding sites for transcription
factors, or the nature of epistatic interactions between these mutations. Here,
we tested the effects of single and double mutants in two cis binding sites involved
in the transcriptional regulation of the Escherichia coli araBAD operon, a component
of arabinose metabolism, using a synthetic system. This system decouples transcriptional
control from any posttranslational effects on fitness, allowing a precise estimate
of the effect of single and double mutations, and hence epistasis, on gene expression.
We found that epistatic interactions between mutations in the araBAD cis-regulatory
element are common, and that the predominant form of epistasis is negative. The
magnitude of the interactions depended on whether the mutations are located in
the same or in different operator sites. Importantly, these epistatic interactions
were dependent on the presence of arabinose, a native inducer of the araBAD operon
in vivo, with some interactions changing in sign (e.g., from negative to positive)
in its presence. This study thus reveals that mutations in even relatively simple
cis-regulatory elements interact in complex ways such that selection on the level
of gene expression in one environment might perturb regulation in the other environment
in an unpredictable and uncorrelated manner.
author:
- first_name: Mato
full_name: Lagator, Mato
id: 345D25EC-F248-11E8-B48F-1D18A9856A87
last_name: Lagator
- first_name: Claudia
full_name: Igler, Claudia
id: 46613666-F248-11E8-B48F-1D18A9856A87
last_name: Igler
- first_name: Anaisa
full_name: Moreno, Anaisa
last_name: Moreno
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
- first_name: Jonathan P
full_name: Bollback, Jonathan P
id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
last_name: Bollback
orcid: 0000-0002-4624-4612
citation:
ama: Lagator M, Igler C, Moreno A, Guet CC, Bollback JP. Epistatic interactions
in the arabinose cis-regulatory element. Molecular Biology and Evolution.
2016;33(3):761-769. doi:10.1093/molbev/msv269
apa: Lagator, M., Igler, C., Moreno, A., Guet, C. C., & Bollback, J. P. (2016).
Epistatic interactions in the arabinose cis-regulatory element. Molecular Biology
and Evolution. Oxford University Press. https://doi.org/10.1093/molbev/msv269
chicago: Lagator, Mato, Claudia Igler, Anaisa Moreno, Calin C Guet, and Jonathan
P Bollback. “Epistatic Interactions in the Arabinose Cis-Regulatory Element.”
Molecular Biology and Evolution. Oxford University Press, 2016. https://doi.org/10.1093/molbev/msv269.
ieee: M. Lagator, C. Igler, A. Moreno, C. C. Guet, and J. P. Bollback, “Epistatic
interactions in the arabinose cis-regulatory element,” Molecular Biology and
Evolution, vol. 33, no. 3. Oxford University Press, pp. 761–769, 2016.
ista: Lagator M, Igler C, Moreno A, Guet CC, Bollback JP. 2016. Epistatic interactions
in the arabinose cis-regulatory element. Molecular Biology and Evolution. 33(3),
761–769.
mla: Lagator, Mato, et al. “Epistatic Interactions in the Arabinose Cis-Regulatory
Element.” Molecular Biology and Evolution, vol. 33, no. 3, Oxford University
Press, 2016, pp. 761–69, doi:10.1093/molbev/msv269.
short: M. Lagator, C. Igler, A. Moreno, C.C. Guet, J.P. Bollback, Molecular Biology
and Evolution 33 (2016) 761–769.
date_created: 2018-12-11T11:51:57Z
date_published: 2016-03-01T00:00:00Z
date_updated: 2021-01-12T06:50:39Z
day: '01'
ddc:
- '570'
- '576'
department:
- _id: CaGu
- _id: JoBo
doi: 10.1093/molbev/msv269
ec_funded: 1
file:
- access_level: open_access
checksum: 1f456ce1d2aa2f67176a1709f9702ecf
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:09:27Z
date_updated: 2020-07-14T12:44:53Z
file_id: '4751'
file_name: IST-2016-588-v1+1_Mol_Biol_Evol-2016-Lagator-761-9.pdf
file_size: 648115
relation: main_file
file_date_updated: 2020-07-14T12:44:53Z
has_accepted_license: '1'
intvolume: ' 33'
issue: '3'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
page: 761 - 769
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
publication: Molecular Biology and Evolution
publication_status: published
publisher: Oxford University Press
publist_id: '5772'
pubrep_id: '588'
quality_controlled: '1'
scopus_import: 1
status: public
title: Epistatic interactions in the arabinose cis-regulatory element
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 33
year: '2016'
...
---
_id: '1524'
abstract:
- lang: eng
text: "When designing genetic circuits, the typical primitives used in major existing
modelling formalisms are gene interaction graphs, where edges between genes denote
either an activation or inhibition relation. However, when designing experiments,
it is important to be precise about the low-level mechanistic details as to how
each such relation is implemented. The rule-based modelling language Kappa allows
to unambiguously specify mechanistic details such as DNA binding sites, dimerisation
of transcription factors, or co-operative interactions. Such a detailed description
comes with complexity and computationally costly executions. We propose a general
method for automatically transforming a rule-based program, by eliminating intermediate
species and adjusting the rate constants accordingly. To the best of our knowledge,
we show the first automated reduction of rule-based models based on equilibrium
approximations.\r\nOur algorithm is an adaptation of an existing algorithm, which
was designed for reducing reaction-based programs; our version of the algorithm
scans the rule-based Kappa model in search for those interaction patterns known
to be amenable to equilibrium approximations (e.g. Michaelis-Menten scheme). Additional
checks are then performed in order to verify if the reduction is meaningful in
the context of the full model. The reduced model is efficiently obtained by static
inspection over the rule-set. The tool is tested on a detailed rule-based model
of a λ-phage switch, which lists 92 rules and 13 agents. The reduced model has
11 rules and 5 agents, and provides a dramatic reduction in simulation time of
several orders of magnitude."
acknowledgement: This research was supported by the People Programme (Marie Curie
Actions) of the European Union’s Seventh Framework Programme (FP7/2007-2013) under
REA grant agreement no. 291734, and the SNSF Early Postdoc.Mobility Fellowship,
the grant number P2EZP2_148797.
alternative_title:
- LNCS
author:
- first_name: Andreea
full_name: Beica, Andreea
last_name: Beica
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
- first_name: Tatjana
full_name: Petrov, Tatjana
id: 3D5811FC-F248-11E8-B48F-1D18A9856A87
last_name: Petrov
orcid: 0000-0002-9041-0905
citation:
ama: 'Beica A, Guet CC, Petrov T. Efficient reduction of kappa models by static
inspection of the rule-set. In: Vol 9271. Springer; 2016:173-191. doi:10.1007/978-3-319-26916-0_10'
apa: 'Beica, A., Guet, C. C., & Petrov, T. (2016). Efficient reduction of kappa
models by static inspection of the rule-set (Vol. 9271, pp. 173–191). Presented
at the HSB: Hybrid Systems Biology, Madrid, Spain: Springer. https://doi.org/10.1007/978-3-319-26916-0_10'
chicago: Beica, Andreea, Calin C Guet, and Tatjana Petrov. “Efficient Reduction
of Kappa Models by Static Inspection of the Rule-Set,” 9271:173–91. Springer,
2016. https://doi.org/10.1007/978-3-319-26916-0_10.
ieee: 'A. Beica, C. C. Guet, and T. Petrov, “Efficient reduction of kappa models
by static inspection of the rule-set,” presented at the HSB: Hybrid Systems Biology,
Madrid, Spain, 2016, vol. 9271, pp. 173–191.'
ista: 'Beica A, Guet CC, Petrov T. 2016. Efficient reduction of kappa models by
static inspection of the rule-set. HSB: Hybrid Systems Biology, LNCS, vol. 9271,
173–191.'
mla: Beica, Andreea, et al. Efficient Reduction of Kappa Models by Static Inspection
of the Rule-Set. Vol. 9271, Springer, 2016, pp. 173–91, doi:10.1007/978-3-319-26916-0_10.
short: A. Beica, C.C. Guet, T. Petrov, in:, Springer, 2016, pp. 173–191.
conference:
end_date: 2015-09-05
location: Madrid, Spain
name: 'HSB: Hybrid Systems Biology'
start_date: 2015-09-04
date_created: 2018-12-11T11:52:31Z
date_published: 2016-01-10T00:00:00Z
date_updated: 2021-01-12T06:51:22Z
day: '10'
department:
- _id: CaGu
- _id: ToHe
doi: 10.1007/978-3-319-26916-0_10
ec_funded: 1
intvolume: ' 9271'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://arxiv.org/abs/1501.00440
month: '01'
oa: 1
oa_version: Preprint
page: 173 - 191
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
publication_status: published
publisher: Springer
publist_id: '5649'
quality_controlled: '1'
scopus_import: 1
status: public
title: Efficient reduction of kappa models by static inspection of the rule-set
type: conference
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 9271
year: '2016'
...
---
_id: '1250'
abstract:
- lang: eng
text: In bacteria, replicative aging manifests as a difference in growth or survival
between the two cells emerging from division. One cell can be regarded as an aging
mother with a decreased potential for future survival and division, the other
as a rejuvenated daughter. Here, we aimed at investigating some of the processes
involved in aging in the bacterium Escherichia coli, where the two types of cells
can be distinguished by the age of their cell poles. We found that certain changes
in the regulation of the carbohydrate metabolism can affect aging. A mutation
in the carbon storage regulator gene, csrA, leads to a dramatically shorter replicative
lifespan; csrA mutants stop dividing once their pole exceeds an age of about five
divisions. These old-pole cells accumulate glycogen at their old cell poles; after
their last division, they do not contain a chromosome, presumably because of spatial
exclusion by the glycogen aggregates. The new-pole daughters produced by these
aging mothers are born young; they only express the deleterious phenotype once
their pole is old. These results demonstrate how manipulations of nutrient allocation
can lead to the exclusion of the chromosome and limit replicative lifespan in
E. coli, and illustrate how mutations can have phenotypic effects that are specific
for cells with old poles. This raises the question how bacteria can avoid the
accumulation of such mutations in their genomes over evolutionary times, and how
they can achieve the long replicative lifespans that have recently been reported.
acknowledgement: This manuscript is dedicated to the memory of Alex Böhm, who was
a great friend and a passionate biologist. Alex passed away after the initial submission
of this manuscript. We thank Vesna Olivera and Ursula Sauder from the Zentrum für
Mikroskopie Uni Basel for excellent service, and Olin Silander, Nikki Freed, and
Nela Nikolic for helpful discussions. This work was supported by the Swiss National
Science Foundation grants to M. Ackermann and Urs Jenal (supporting AB).
article_number: e1005974
author:
- first_name: Alex
full_name: Boehm, Alex
last_name: Boehm
- first_name: Markus
full_name: Arnoldini, Markus
last_name: Arnoldini
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Thomas
full_name: Röösli, Thomas
last_name: Röösli
- first_name: Colette
full_name: Bigosch, Colette
last_name: Bigosch
- first_name: Martin
full_name: Ackermann, Martin
last_name: Ackermann
citation:
ama: Boehm A, Arnoldini M, Bergmiller T, Röösli T, Bigosch C, Ackermann M. Genetic
manipulation of glycogen allocation affects replicative lifespan in E coli. PLoS
Genetics. 2016;12(4). doi:10.1371/journal.pgen.1005974
apa: Boehm, A., Arnoldini, M., Bergmiller, T., Röösli, T., Bigosch, C., & Ackermann,
M. (2016). Genetic manipulation of glycogen allocation affects replicative lifespan
in E coli. PLoS Genetics. Public Library of Science. https://doi.org/10.1371/journal.pgen.1005974
chicago: Boehm, Alex, Markus Arnoldini, Tobias Bergmiller, Thomas Röösli, Colette
Bigosch, and Martin Ackermann. “Genetic Manipulation of Glycogen Allocation Affects
Replicative Lifespan in E Coli.” PLoS Genetics. Public Library of Science,
2016. https://doi.org/10.1371/journal.pgen.1005974.
ieee: A. Boehm, M. Arnoldini, T. Bergmiller, T. Röösli, C. Bigosch, and M. Ackermann,
“Genetic manipulation of glycogen allocation affects replicative lifespan in E
coli,” PLoS Genetics, vol. 12, no. 4. Public Library of Science, 2016.
ista: Boehm A, Arnoldini M, Bergmiller T, Röösli T, Bigosch C, Ackermann M. 2016.
Genetic manipulation of glycogen allocation affects replicative lifespan in E
coli. PLoS Genetics. 12(4), e1005974.
mla: Boehm, Alex, et al. “Genetic Manipulation of Glycogen Allocation Affects Replicative
Lifespan in E Coli.” PLoS Genetics, vol. 12, no. 4, e1005974, Public Library
of Science, 2016, doi:10.1371/journal.pgen.1005974.
short: A. Boehm, M. Arnoldini, T. Bergmiller, T. Röösli, C. Bigosch, M. Ackermann,
PLoS Genetics 12 (2016).
date_created: 2018-12-11T11:50:56Z
date_published: 2016-04-19T00:00:00Z
date_updated: 2023-02-23T14:11:39Z
day: '19'
ddc:
- '576'
- '579'
department:
- _id: CaGu
doi: 10.1371/journal.pgen.1005974
file:
- access_level: open_access
checksum: 53d22b2b39e5adc243d34f18b2615a85
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:17Z
date_updated: 2020-07-14T12:44:41Z
file_id: '5067'
file_name: IST-2016-705-v1+1_journal.pgen.1005974.PDF
file_size: 6273249
relation: main_file
file_date_updated: 2020-07-14T12:44:41Z
has_accepted_license: '1'
intvolume: ' 12'
issue: '4'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
publication: PLoS Genetics
publication_status: published
publisher: Public Library of Science
publist_id: '6077'
pubrep_id: '705'
quality_controlled: '1'
related_material:
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relation: research_data
status: public
scopus_import: 1
status: public
title: Genetic manipulation of glycogen allocation affects replicative lifespan in
E coli
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 12
year: '2016'
...
---
_id: '9873'
article_processing_charge: No
author:
- first_name: Alex
full_name: Boehm, Alex
last_name: Boehm
- first_name: Markus
full_name: Arnoldini, Markus
last_name: Arnoldini
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Thomas
full_name: Röösli, Thomas
last_name: Röösli
- first_name: Colette
full_name: Bigosch, Colette
last_name: Bigosch
- first_name: Martin
full_name: Ackermann, Martin
last_name: Ackermann
citation:
ama: Boehm A, Arnoldini M, Bergmiller T, Röösli T, Bigosch C, Ackermann M. Quantification
of the growth rate reduction as a consequence of age-specific mortality. 2016.
doi:10.1371/journal.pgen.1005974.s015
apa: Boehm, A., Arnoldini, M., Bergmiller, T., Röösli, T., Bigosch, C., & Ackermann,
M. (2016). Quantification of the growth rate reduction as a consequence of age-specific
mortality. Public Library of Science. https://doi.org/10.1371/journal.pgen.1005974.s015
chicago: Boehm, Alex, Markus Arnoldini, Tobias Bergmiller, Thomas Röösli, Colette
Bigosch, and Martin Ackermann. “Quantification of the Growth Rate Reduction as
a Consequence of Age-Specific Mortality.” Public Library of Science, 2016. https://doi.org/10.1371/journal.pgen.1005974.s015.
ieee: A. Boehm, M. Arnoldini, T. Bergmiller, T. Röösli, C. Bigosch, and M. Ackermann,
“Quantification of the growth rate reduction as a consequence of age-specific
mortality.” Public Library of Science, 2016.
ista: Boehm A, Arnoldini M, Bergmiller T, Röösli T, Bigosch C, Ackermann M. 2016.
Quantification of the growth rate reduction as a consequence of age-specific mortality,
Public Library of Science, 10.1371/journal.pgen.1005974.s015.
mla: Boehm, Alex, et al. Quantification of the Growth Rate Reduction as a Consequence
of Age-Specific Mortality. Public Library of Science, 2016, doi:10.1371/journal.pgen.1005974.s015.
short: A. Boehm, M. Arnoldini, T. Bergmiller, T. Röösli, C. Bigosch, M. Ackermann,
(2016).
date_created: 2021-08-10T09:42:34Z
date_updated: 2023-02-21T16:50:13Z
day: '19'
department:
- _id: CaGu
doi: 10.1371/journal.pgen.1005974.s015
month: '04'
oa_version: Published Version
publisher: Public Library of Science
related_material:
record:
- id: '1250'
relation: used_in_publication
status: public
status: public
title: Quantification of the growth rate reduction as a consequence of age-specific
mortality
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2016'
...
---
_id: '5749'
abstract:
- lang: eng
text: Parasitism creates selection for resistance mechanisms in host populations
and is hypothesized to promote increased host evolvability. However, the influence
of these traits on host evolution when parasites are no longer present is unclear.
We used experimental evolution and whole-genome sequencing of Escherichia coli
to determine the effects of past and present exposure to parasitic viruses (phages)
on the spread of mutator alleles, resistance, and bacterial competitive fitness.
We found that mutator alleles spread rapidly during adaptation to any of four
different phage species, and this pattern was even more pronounced with multiple
phages present simultaneously. However, hypermutability did not detectably accelerate
adaptation in the absence of phages and recovery of fitness costs associated with
resistance. Several lineages evolved phage resistance through elevated mucoidy,
and during subsequent evolution in phage-free conditions they rapidly reverted
to nonmucoid, phage-susceptible phenotypes. Genome sequencing revealed that this
phenotypic reversion was achieved by additional genetic changes rather than by
genotypic reversion of the initial resistance mutations. Insertion sequence (IS)
elements played a key role in both the acquisition of resistance and adaptation
in the absence of parasites; unlike single nucleotide polymorphisms, IS insertions
were not more frequent in mutator lineages. Our results provide a genetic explanation
for rapid reversion of mucoidy, a phenotype observed in other bacterial species
including human pathogens. Moreover, this demonstrates that the types of genetic
change underlying adaptation to fitness costs, and consequently the impact of
evolvability mechanisms such as increased point-mutation rates, depend critically
on the mechanism of resistance.
acknowledgement: The authors thank three anonymous reviewers and the editor for helpful
comments on the manuscript, as well as Dominique Schneider for feedback on an earlier
draft, Jenna Gallie for lytic λ and Julien Capelle for T5 and T6. This work was
supported by the Swiss National Science Foundation (PZ00P3_148255 to A.H.) and an
EU Marie Curie PEOPLE Postdoctoral Fellowship for Career Development (FP7-PEOPLE-2012-IEF-331824
to S.W.).
article_processing_charge: No
author:
- first_name: Sébastien
full_name: Wielgoss, Sébastien
last_name: Wielgoss
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Anna M.
full_name: Bischofberger, Anna M.
last_name: Bischofberger
- first_name: Alex R.
full_name: Hall, Alex R.
last_name: Hall
citation:
ama: Wielgoss S, Bergmiller T, Bischofberger AM, Hall AR. Adaptation to parasites
and costs of parasite resistance in mutator and nonmutator bacteria. Molecular
Biology and Evolution. 2016;33(3):770-782. doi:10.1093/molbev/msv270
apa: Wielgoss, S., Bergmiller, T., Bischofberger, A. M., & Hall, A. R. (2016).
Adaptation to parasites and costs of parasite resistance in mutator and nonmutator
bacteria. Molecular Biology and Evolution. Oxford University Press. https://doi.org/10.1093/molbev/msv270
chicago: Wielgoss, Sébastien, Tobias Bergmiller, Anna M. Bischofberger, and Alex
R. Hall. “Adaptation to Parasites and Costs of Parasite Resistance in Mutator
and Nonmutator Bacteria.” Molecular Biology and Evolution. Oxford University
Press, 2016. https://doi.org/10.1093/molbev/msv270.
ieee: S. Wielgoss, T. Bergmiller, A. M. Bischofberger, and A. R. Hall, “Adaptation
to parasites and costs of parasite resistance in mutator and nonmutator bacteria,”
Molecular Biology and Evolution, vol. 33, no. 3. Oxford University Press,
pp. 770–782, 2016.
ista: Wielgoss S, Bergmiller T, Bischofberger AM, Hall AR. 2016. Adaptation to parasites
and costs of parasite resistance in mutator and nonmutator bacteria. Molecular
Biology and Evolution. 33(3), 770–782.
mla: Wielgoss, Sébastien, et al. “Adaptation to Parasites and Costs of Parasite
Resistance in Mutator and Nonmutator Bacteria.” Molecular Biology and Evolution,
vol. 33, no. 3, Oxford University Press, 2016, pp. 770–82, doi:10.1093/molbev/msv270.
short: S. Wielgoss, T. Bergmiller, A.M. Bischofberger, A.R. Hall, Molecular Biology
and Evolution 33 (2016) 770–782.
date_created: 2018-12-18T13:18:10Z
date_published: 2016-03-01T00:00:00Z
date_updated: 2023-09-05T13:46:05Z
day: '01'
ddc:
- '576'
department:
- _id: CaGu
doi: 10.1093/molbev/msv270
external_id:
pmid:
- '26609077'
file:
- access_level: open_access
checksum: 47d9010690b6c5c17f2ac830cc63ac5c
content_type: application/pdf
creator: dernst
date_created: 2018-12-18T13:21:45Z
date_updated: 2020-07-14T12:47:10Z
file_id: '5750'
file_name: 2016_MolBiolEvol_Wielgoss.pdf
file_size: 634037
relation: main_file
file_date_updated: 2020-07-14T12:47:10Z
has_accepted_license: '1'
intvolume: ' 33'
issue: '3'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
page: 770-782
pmid: 1
publication: Molecular Biology and Evolution
publication_identifier:
eissn:
- 1537-1719
issn:
- 0737-4038
publication_status: published
publisher: Oxford University Press
pubrep_id: '587'
quality_controlled: '1'
related_material:
record:
- id: '9719'
relation: research_data
status: public
scopus_import: '1'
status: public
title: Adaptation to parasites and costs of parasite resistance in mutator and nonmutator
bacteria
tmp:
image: /images/cc_by_nc.png
legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode
name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
short: CC BY-NC (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 33
year: '2016'
...
---
_id: '1093'
abstract:
- lang: eng
text: 'We introduce a general class of distances (metrics) between Markov chains,
which are based on linear behaviour. This class encompasses distances given topologically
(such as the total variation distance or trace distance) as well as by temporal
logics or automata. We investigate which of the distances can be approximated
by observing the systems, i.e. by black-box testing or simulation, and we provide
both negative and positive results. '
acknowledgement: "This research was funded in part by the European Research Council
(ERC) under grant agreement 267989\r\n(QUAREM), the Austrian Science Fund (FWF)
under grants project S11402-N23 (RiSE and SHiNE)\r\nand Z211-N23 (Wittgenstein Award),
by the Czech Science Foundation Grant No. P202/12/G061, and\r\nby the SNSF Advanced
Postdoc. Mobility Fellowship – grant number P300P2_161067."
alternative_title:
- LIPIcs
article_number: '20'
author:
- first_name: Przemyslaw
full_name: Daca, Przemyslaw
id: 49351290-F248-11E8-B48F-1D18A9856A87
last_name: Daca
- first_name: Thomas A
full_name: Henzinger, Thomas A
id: 40876CD8-F248-11E8-B48F-1D18A9856A87
last_name: Henzinger
orcid: 0000−0002−2985−7724
- first_name: Jan
full_name: Kretinsky, Jan
id: 44CEF464-F248-11E8-B48F-1D18A9856A87
last_name: Kretinsky
orcid: 0000-0002-8122-2881
- first_name: Tatjana
full_name: Petrov, Tatjana
id: 3D5811FC-F248-11E8-B48F-1D18A9856A87
last_name: Petrov
orcid: 0000-0002-9041-0905
citation:
ama: 'Daca P, Henzinger TA, Kretinsky J, Petrov T. Linear distances between Markov
chains. In: Vol 59. Schloss Dagstuhl - Leibniz-Zentrum für Informatik; 2016. doi:10.4230/LIPIcs.CONCUR.2016.20'
apa: 'Daca, P., Henzinger, T. A., Kretinsky, J., & Petrov, T. (2016). Linear
distances between Markov chains (Vol. 59). Presented at the CONCUR: Concurrency
Theory, Quebec City; Canada: Schloss Dagstuhl - Leibniz-Zentrum für Informatik.
https://doi.org/10.4230/LIPIcs.CONCUR.2016.20'
chicago: Daca, Przemyslaw, Thomas A Henzinger, Jan Kretinsky, and Tatjana Petrov.
“Linear Distances between Markov Chains,” Vol. 59. Schloss Dagstuhl - Leibniz-Zentrum
für Informatik, 2016. https://doi.org/10.4230/LIPIcs.CONCUR.2016.20.
ieee: 'P. Daca, T. A. Henzinger, J. Kretinsky, and T. Petrov, “Linear distances
between Markov chains,” presented at the CONCUR: Concurrency Theory, Quebec City;
Canada, 2016, vol. 59.'
ista: 'Daca P, Henzinger TA, Kretinsky J, Petrov T. 2016. Linear distances between
Markov chains. CONCUR: Concurrency Theory, LIPIcs, vol. 59, 20.'
mla: Daca, Przemyslaw, et al. Linear Distances between Markov Chains. Vol.
59, 20, Schloss Dagstuhl - Leibniz-Zentrum für Informatik, 2016, doi:10.4230/LIPIcs.CONCUR.2016.20.
short: P. Daca, T.A. Henzinger, J. Kretinsky, T. Petrov, in:, Schloss Dagstuhl -
Leibniz-Zentrum für Informatik, 2016.
conference:
end_date: 2016-08-26
location: Quebec City; Canada
name: 'CONCUR: Concurrency Theory'
start_date: 2016-08-23
date_created: 2018-12-11T11:50:06Z
date_published: 2016-08-01T00:00:00Z
date_updated: 2023-09-07T11:58:33Z
day: '01'
ddc:
- '004'
department:
- _id: ToHe
- _id: KrCh
- _id: CaGu
doi: 10.4230/LIPIcs.CONCUR.2016.20
ec_funded: 1
file:
- access_level: open_access
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:11:39Z
date_updated: 2018-12-12T10:11:39Z
file_id: '4895'
file_name: IST-2017-794-v1+1_LIPIcs-CONCUR-2016-20.pdf
file_size: 501827
relation: main_file
file_date_updated: 2018-12-12T10:11:39Z
has_accepted_license: '1'
intvolume: ' 59'
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
project:
- _id: 25EE3708-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '267989'
name: Quantitative Reactive Modeling
- _id: 25832EC2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: S 11407_N23
name: Rigorous Systems Engineering
- _id: 25F42A32-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Z211
name: The Wittgenstein Prize
publication_status: published
publisher: Schloss Dagstuhl - Leibniz-Zentrum für Informatik
publist_id: '6283'
pubrep_id: '794'
quality_controlled: '1'
related_material:
record:
- id: '1155'
relation: dissertation_contains
status: public
scopus_import: 1
status: public
title: Linear distances between Markov chains
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: conference
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 59
year: '2016'
...
---
_id: '1234'
abstract:
- lang: eng
text: We present a new algorithm for the statistical model checking of Markov chains
with respect to unbounded temporal properties, including full linear temporal
logic. The main idea is that we monitor each simulation run on the fly, in order
to detect quickly if a bottom strongly connected component is entered with high
probability, in which case the simulation run can be terminated early. As a result,
our simulation runs are often much shorter than required by termination bounds
that are computed a priori for a desired level of confidence on a large state
space. In comparison to previous algorithms for statistical model checking our
method is not only faster in many cases but also requires less information about
the system, namely, only the minimum transition probability that occurs in the
Markov chain. In addition, our method can be generalised to unbounded quantitative
properties such as mean-payoff bounds.
acknowledgement: "This research was funded in part by the European Research Council
(ERC) under\r\ngrant agreement 267989 (QUAREM), the Austrian Science Fund
\ (FWF) under\r\ngrants project S11402-N23 (RiSE) and Z211-N23 (Wittgenstein Award),
the Peo-\r\nple Programme (Marie Curie Actions) of the European Union’s Seventh
Framework\r\nProgramme (FP7/2007-2013) REA Grant No 291734, the SNSF Advanced Postdoc.\r\nMobility
Fellowship – grant number P300P2\r\n161067, and the Czech Science Foun-\r\ndation
under grant agreement P202/12/G061."
alternative_title:
- LNCS
author:
- first_name: Przemyslaw
full_name: Daca, Przemyslaw
id: 49351290-F248-11E8-B48F-1D18A9856A87
last_name: Daca
- first_name: Thomas A
full_name: Henzinger, Thomas A
id: 40876CD8-F248-11E8-B48F-1D18A9856A87
last_name: Henzinger
orcid: 0000−0002−2985−7724
- first_name: Jan
full_name: Kretinsky, Jan
id: 44CEF464-F248-11E8-B48F-1D18A9856A87
last_name: Kretinsky
orcid: 0000-0002-8122-2881
- first_name: Tatjana
full_name: Petrov, Tatjana
id: 3D5811FC-F248-11E8-B48F-1D18A9856A87
last_name: Petrov
orcid: 0000-0002-9041-0905
citation:
ama: 'Daca P, Henzinger TA, Kretinsky J, Petrov T. Faster statistical model checking
for unbounded temporal properties. In: Vol 9636. Springer; 2016:112-129. doi:10.1007/978-3-662-49674-9_7'
apa: 'Daca, P., Henzinger, T. A., Kretinsky, J., & Petrov, T. (2016). Faster
statistical model checking for unbounded temporal properties (Vol. 9636, pp. 112–129).
Presented at the TACAS: Tools and Algorithms for the Construction and Analysis
of Systems, Eindhoven, The Netherlands: Springer. https://doi.org/10.1007/978-3-662-49674-9_7'
chicago: Daca, Przemyslaw, Thomas A Henzinger, Jan Kretinsky, and Tatjana Petrov.
“Faster Statistical Model Checking for Unbounded Temporal Properties,” 9636:112–29.
Springer, 2016. https://doi.org/10.1007/978-3-662-49674-9_7.
ieee: 'P. Daca, T. A. Henzinger, J. Kretinsky, and T. Petrov, “Faster statistical
model checking for unbounded temporal properties,” presented at the TACAS: Tools
and Algorithms for the Construction and Analysis of Systems, Eindhoven, The Netherlands,
2016, vol. 9636, pp. 112–129.'
ista: 'Daca P, Henzinger TA, Kretinsky J, Petrov T. 2016. Faster statistical model
checking for unbounded temporal properties. TACAS: Tools and Algorithms for the
Construction and Analysis of Systems, LNCS, vol. 9636, 112–129.'
mla: Daca, Przemyslaw, et al. Faster Statistical Model Checking for Unbounded
Temporal Properties. Vol. 9636, Springer, 2016, pp. 112–29, doi:10.1007/978-3-662-49674-9_7.
short: P. Daca, T.A. Henzinger, J. Kretinsky, T. Petrov, in:, Springer, 2016, pp.
112–129.
conference:
end_date: 2016-04-08
location: Eindhoven, The Netherlands
name: 'TACAS: Tools and Algorithms for the Construction and Analysis of Systems'
start_date: 2016-04-02
date_created: 2018-12-11T11:50:51Z
date_published: 2016-01-01T00:00:00Z
date_updated: 2023-09-07T11:58:33Z
day: '01'
department:
- _id: ToHe
- _id: CaGu
doi: 10.1007/978-3-662-49674-9_7
ec_funded: 1
intvolume: ' 9636'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://arxiv.org/abs/1504.05739
month: '01'
oa: 1
oa_version: Preprint
page: 112 - 129
project:
- _id: 25EE3708-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '267989'
name: Quantitative Reactive Modeling
- _id: 25832EC2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: S 11407_N23
name: Rigorous Systems Engineering
- _id: 25F42A32-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Z211
name: The Wittgenstein Prize
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
publication_status: published
publisher: Springer
publist_id: '6099'
quality_controlled: '1'
related_material:
record:
- id: '471'
relation: later_version
status: public
- id: '1155'
relation: dissertation_contains
status: public
scopus_import: 1
status: public
title: Faster statistical model checking for unbounded temporal properties
type: conference
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 9636
year: '2016'
...
---
_id: '1243'
abstract:
- lang: eng
text: Restriction-modification (RM) systems represent a minimal and ubiquitous biological
system of self/non-self discrimination in prokaryotes [1], which protects hosts
from exogenous DNA [2]. The mechanism is based on the balance between methyltransferase
(M) and cognate restriction endonuclease (R). M tags endogenous DNA as self by
methylating short specific DNA sequences called restriction sites, whereas R recognizes
unmethylated restriction sites as non-self and introduces a double-stranded DNA
break [3]. Restriction sites are significantly underrepresented in prokaryotic
genomes [4-7], suggesting that the discrimination mechanism is imperfect and occasionally
leads to autoimmunity due to self-DNA cleavage (self-restriction) [8]. Furthermore,
RM systems can promote DNA recombination [9] and contribute to genetic variation
in microbial populations, thus facilitating adaptive evolution [10]. However,
cleavage of self-DNA by RM systems as elements shaping prokaryotic genomes has
not been directly detected, and its cause, frequency, and outcome are unknown.
We quantify self-restriction caused by two RM systems of Escherichia coli and
find that, in agreement with levels of restriction site avoidance, EcoRI, but
not EcoRV, cleaves self-DNA at a measurable rate. Self-restriction is a stochastic
process, which temporarily induces the SOS response, and is followed by DNA repair,
maintaining cell viability. We find that RM systems with higher restriction efficiency
against bacteriophage infections exhibit a higher rate of self-restriction, and
that this rate can be further increased by stochastic imbalance between R and
M. Our results identify molecular noise in RM systems as a factor shaping prokaryotic
genomes.
acknowledgement: This work was funded by an HFSP Young Investigators’ grant. M.P.
is a recipient of a DOC Fellowship of the Austrian Academy of Science at the Institute
of Science and Technology Austria. R.O. and Y.W. were supported by the Platform
for Dynamic Approaches to Living System from MEXT, Japan. We wish to thank I. Kobayashi
for providing us with the EcoRI and EcoRV plasmids, and A. Campbell for providing
us with the λ vir phage. We thank D. Siekhaus and C. Uhler and members of the C.C.G.
and J.P. Bollback laboratories for in-depth discussions. We thank B. Stern for comments
on an earlier version of the manuscript. We especially thank B.R. Levin for advice
and comments, and the anonymous reviewers for significantly improving the manuscript.
author:
- first_name: Maros
full_name: Pleska, Maros
id: 4569785E-F248-11E8-B48F-1D18A9856A87
last_name: Pleska
orcid: 0000-0001-7460-7479
- first_name: Long
full_name: Qian, Long
last_name: Qian
- first_name: Reiko
full_name: Okura, Reiko
last_name: Okura
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Yuichi
full_name: Wakamoto, Yuichi
last_name: Wakamoto
- first_name: Edo
full_name: Kussell, Edo
last_name: Kussell
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Pleska M, Qian L, Okura R, et al. Bacterial autoimmunity due to a restriction-modification
system. Current Biology. 2016;26(3):404-409. doi:10.1016/j.cub.2015.12.041
apa: Pleska, M., Qian, L., Okura, R., Bergmiller, T., Wakamoto, Y., Kussell, E.,
& Guet, C. C. (2016). Bacterial autoimmunity due to a restriction-modification
system. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2015.12.041
chicago: Pleska, Maros, Long Qian, Reiko Okura, Tobias Bergmiller, Yuichi Wakamoto,
Edo Kussell, and Calin C Guet. “Bacterial Autoimmunity Due to a Restriction-Modification
System.” Current Biology. Cell Press, 2016. https://doi.org/10.1016/j.cub.2015.12.041.
ieee: M. Pleska et al., “Bacterial autoimmunity due to a restriction-modification
system,” Current Biology, vol. 26, no. 3. Cell Press, pp. 404–409, 2016.
ista: Pleska M, Qian L, Okura R, Bergmiller T, Wakamoto Y, Kussell E, Guet CC. 2016.
Bacterial autoimmunity due to a restriction-modification system. Current Biology.
26(3), 404–409.
mla: Pleska, Maros, et al. “Bacterial Autoimmunity Due to a Restriction-Modification
System.” Current Biology, vol. 26, no. 3, Cell Press, 2016, pp. 404–09,
doi:10.1016/j.cub.2015.12.041.
short: M. Pleska, L. Qian, R. Okura, T. Bergmiller, Y. Wakamoto, E. Kussell, C.C.
Guet, Current Biology 26 (2016) 404–409.
date_created: 2018-12-11T11:50:54Z
date_published: 2016-02-08T00:00:00Z
date_updated: 2023-09-07T11:59:32Z
day: '08'
department:
- _id: CaGu
doi: 10.1016/j.cub.2015.12.041
intvolume: ' 26'
issue: '3'
language:
- iso: eng
month: '02'
oa_version: None
page: 404 - 409
project:
- _id: 251D65D8-B435-11E9-9278-68D0E5697425
grant_number: '24210'
name: Effects of Stochasticity on the Function of Restriction-Modi cation Systems
at the Single-Cell Level (DOC Fellowship)
publication: Current Biology
publication_status: published
publisher: Cell Press
publist_id: '6087'
quality_controlled: '1'
related_material:
record:
- id: '202'
relation: dissertation_contains
status: public
scopus_import: 1
status: public
title: Bacterial autoimmunity due to a restriction-modification system
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 26
year: '2016'
...
---
_id: '1358'
abstract:
- lang: eng
text: 'Gene regulation relies on the specificity of transcription factor (TF)–DNA
interactions. Limited specificity may lead to crosstalk: a regulatory state in
which a gene is either incorrectly activated due to noncognate TF–DNA interactions
or remains erroneously inactive. As each TF can have numerous interactions with
noncognate cis-regulatory elements, crosstalk is inherently a global problem,
yet has previously not been studied as such. We construct a theoretical framework
to analyse the effects of global crosstalk on gene regulation. We find that crosstalk
presents a significant challenge for organisms with low-specificity TFs, such
as metazoans. Crosstalk is not easily mitigated by known regulatory schemes acting
at equilibrium, including variants of cooperativity and combinatorial regulation.
Our results suggest that crosstalk imposes a previously unexplored global constraint
on the functioning and evolution of regulatory networks, which is qualitatively
distinct from the known constraints that act at the level of individual gene regulatory
elements.'
article_number: '12307'
author:
- first_name: Tamar
full_name: Friedlander, Tamar
id: 36A5845C-F248-11E8-B48F-1D18A9856A87
last_name: Friedlander
- first_name: Roshan
full_name: Prizak, Roshan
id: 4456104E-F248-11E8-B48F-1D18A9856A87
last_name: Prizak
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
- first_name: Nicholas H
full_name: Barton, Nicholas H
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
orcid: 0000-0002-8548-5240
- first_name: Gasper
full_name: Tkacik, Gasper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkacik
orcid: 0000-0002-6699-1455
citation:
ama: Friedlander T, Prizak R, Guet CC, Barton NH, Tkačik G. Intrinsic limits to
gene regulation by global crosstalk. Nature Communications. 2016;7. doi:10.1038/ncomms12307
apa: Friedlander, T., Prizak, R., Guet, C. C., Barton, N. H., & Tkačik, G. (2016).
Intrinsic limits to gene regulation by global crosstalk. Nature Communications.
Nature Publishing Group. https://doi.org/10.1038/ncomms12307
chicago: Friedlander, Tamar, Roshan Prizak, Calin C Guet, Nicholas H Barton, and
Gašper Tkačik. “Intrinsic Limits to Gene Regulation by Global Crosstalk.” Nature
Communications. Nature Publishing Group, 2016. https://doi.org/10.1038/ncomms12307.
ieee: T. Friedlander, R. Prizak, C. C. Guet, N. H. Barton, and G. Tkačik, “Intrinsic
limits to gene regulation by global crosstalk,” Nature Communications,
vol. 7. Nature Publishing Group, 2016.
ista: Friedlander T, Prizak R, Guet CC, Barton NH, Tkačik G. 2016. Intrinsic limits
to gene regulation by global crosstalk. Nature Communications. 7, 12307.
mla: Friedlander, Tamar, et al. “Intrinsic Limits to Gene Regulation by Global Crosstalk.”
Nature Communications, vol. 7, 12307, Nature Publishing Group, 2016, doi:10.1038/ncomms12307.
short: T. Friedlander, R. Prizak, C.C. Guet, N.H. Barton, G. Tkačik, Nature Communications
7 (2016).
date_created: 2018-12-11T11:51:34Z
date_published: 2016-08-04T00:00:00Z
date_updated: 2023-09-07T12:53:49Z
day: '04'
ddc:
- '576'
department:
- _id: GaTk
- _id: NiBa
- _id: CaGu
doi: 10.1038/ncomms12307
ec_funded: 1
file:
- access_level: open_access
checksum: fe3f3a1526d180b29fe691ab11435b78
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:12:01Z
date_updated: 2020-07-14T12:44:46Z
file_id: '4919'
file_name: IST-2016-627-v1+1_ncomms12307.pdf
file_size: 861805
relation: main_file
- access_level: open_access
checksum: 164864a1a675f3ad80e9917c27aba07f
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:12:02Z
date_updated: 2020-07-14T12:44:46Z
file_id: '4920'
file_name: IST-2016-627-v1+2_ncomms12307-s1.pdf
file_size: 1084703
relation: main_file
file_date_updated: 2020-07-14T12:44:46Z
has_accepted_license: '1'
intvolume: ' 7'
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 25B07788-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '250152'
name: Limits to selection in biology and in evolutionary computation
- _id: 254E9036-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P28844-B27
name: Biophysics of information processing in gene regulation
publication: Nature Communications
publication_status: published
publisher: Nature Publishing Group
publist_id: '5887'
pubrep_id: '627'
quality_controlled: '1'
related_material:
record:
- id: '6071'
relation: dissertation_contains
status: public
scopus_import: 1
status: public
title: Intrinsic limits to gene regulation by global crosstalk
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 7
year: '2016'
...
---
_id: '1430'
abstract:
- lang: eng
text: Evolutionary algorithms (EAs) form a popular optimisation paradigm inspired
by natural evolution. In recent years the field of evolutionary computation has
developed a rigorous analytical theory to analyse their runtime on many illustrative
problems. Here we apply this theory to a simple model of natural evolution. In
the Strong Selection Weak Mutation (SSWM) evolutionary regime the time between
occurrence of new mutations is much longer than the time it takes for a new beneficial
mutation to take over the population. In this situation, the population only contains
copies of one genotype and evolution can be modelled as a (1+1)-type process where
the probability of accepting a new genotype (improvements or worsenings) depends
on the change in fitness. We present an initial runtime analysis of SSWM, quantifying
its performance for various parameters and investigating differences to the (1+1)
EA. We show that SSWM can have a moderate advantage over the (1+1) EA at crossing
fitness valleys and study an example where SSWM outperforms the (1+1) EA by taking
advantage of information on the fitness gradient.
author:
- first_name: Tiago
full_name: Paixao, Tiago
id: 2C5658E6-F248-11E8-B48F-1D18A9856A87
last_name: Paixao
orcid: 0000-0003-2361-3953
- first_name: Dirk
full_name: Sudholt, Dirk
last_name: Sudholt
- first_name: Jorge
full_name: Heredia, Jorge
last_name: Heredia
- first_name: Barbora
full_name: Trubenova, Barbora
id: 42302D54-F248-11E8-B48F-1D18A9856A87
last_name: Trubenova
orcid: 0000-0002-6873-2967
citation:
ama: 'Paixao T, Sudholt D, Heredia J, Trubenova B. First steps towards a runtime
comparison of natural and artificial evolution. In: Proceedings of the 2015
Annual Conference on Genetic and Evolutionary Computation. ACM; 2015:1455-1462.
doi:10.1145/2739480.2754758'
apa: 'Paixao, T., Sudholt, D., Heredia, J., & Trubenova, B. (2015). First steps
towards a runtime comparison of natural and artificial evolution. In Proceedings
of the 2015 Annual Conference on Genetic and Evolutionary Computation (pp.
1455–1462). Madrid, Spain: ACM. https://doi.org/10.1145/2739480.2754758'
chicago: Paixao, Tiago, Dirk Sudholt, Jorge Heredia, and Barbora Trubenova. “First
Steps towards a Runtime Comparison of Natural and Artificial Evolution.” In Proceedings
of the 2015 Annual Conference on Genetic and Evolutionary Computation, 1455–62.
ACM, 2015. https://doi.org/10.1145/2739480.2754758.
ieee: T. Paixao, D. Sudholt, J. Heredia, and B. Trubenova, “First steps towards
a runtime comparison of natural and artificial evolution,” in Proceedings of
the 2015 Annual Conference on Genetic and Evolutionary Computation, Madrid,
Spain, 2015, pp. 1455–1462.
ista: 'Paixao T, Sudholt D, Heredia J, Trubenova B. 2015. First steps towards a
runtime comparison of natural and artificial evolution. Proceedings of the 2015
Annual Conference on Genetic and Evolutionary Computation. GECCO: Genetic and
evolutionary computation conference, 1455–1462.'
mla: Paixao, Tiago, et al. “First Steps towards a Runtime Comparison of Natural
and Artificial Evolution.” Proceedings of the 2015 Annual Conference on Genetic
and Evolutionary Computation, ACM, 2015, pp. 1455–62, doi:10.1145/2739480.2754758.
short: T. Paixao, D. Sudholt, J. Heredia, B. Trubenova, in:, Proceedings of the
2015 Annual Conference on Genetic and Evolutionary Computation, ACM, 2015, pp.
1455–1462.
conference:
end_date: 2015-07-15
location: Madrid, Spain
name: 'GECCO: Genetic and evolutionary computation conference'
start_date: 2015-07-11
date_created: 2018-12-11T11:51:58Z
date_published: 2015-07-11T00:00:00Z
date_updated: 2021-01-12T06:50:41Z
day: '11'
department:
- _id: NiBa
- _id: CaGu
doi: 10.1145/2739480.2754758
ec_funded: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://arxiv.org/abs/1504.06260
month: '07'
oa: 1
oa_version: Preprint
page: 1455 - 1462
project:
- _id: 25B1EC9E-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618091'
name: Speed of Adaptation in Population Genetics and Evolutionary Computation
publication: Proceedings of the 2015 Annual Conference on Genetic and Evolutionary
Computation
publication_status: published
publisher: ACM
publist_id: '5768'
quality_controlled: '1'
scopus_import: 1
status: public
title: First steps towards a runtime comparison of natural and artificial evolution
type: conference
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2015'
...
---
_id: '1542'
abstract:
- lang: eng
text: 'The theory of population genetics and evolutionary computation have been
evolving separately for nearly 30 years. Many results have been independently
obtained in both fields and many others are unique to its respective field. We
aim to bridge this gap by developing a unifying framework for evolutionary processes
that allows both evolutionary algorithms and population genetics models to be
cast in the same formal framework. The framework we present here decomposes the
evolutionary process into its several components in order to facilitate the identification
of similarities between different models. In particular, we propose a classification
of evolutionary operators based on the defining properties of the different components.
We cast several commonly used operators from both fields into this common framework.
Using this, we map different evolutionary and genetic algorithms to different
evolutionary regimes and identify candidates with the most potential for the translation
of results between the fields. This provides a unified description of evolutionary
processes and represents a stepping stone towards new tools and results to both
fields. '
author:
- first_name: Tiago
full_name: Paixao, Tiago
id: 2C5658E6-F248-11E8-B48F-1D18A9856A87
last_name: Paixao
orcid: 0000-0003-2361-3953
- first_name: Golnaz
full_name: Badkobeh, Golnaz
last_name: Badkobeh
- first_name: Nicholas H
full_name: Barton, Nicholas H
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
orcid: 0000-0002-8548-5240
- first_name: Doğan
full_name: Çörüş, Doğan
last_name: Çörüş
- first_name: Duccuong
full_name: Dang, Duccuong
last_name: Dang
- first_name: Tobias
full_name: Friedrich, Tobias
last_name: Friedrich
- first_name: Per
full_name: Lehre, Per
last_name: Lehre
- first_name: Dirk
full_name: Sudholt, Dirk
last_name: Sudholt
- first_name: Andrew
full_name: Sutton, Andrew
last_name: Sutton
- first_name: Barbora
full_name: Trubenova, Barbora
id: 42302D54-F248-11E8-B48F-1D18A9856A87
last_name: Trubenova
orcid: 0000-0002-6873-2967
citation:
ama: Paixao T, Badkobeh G, Barton NH, et al. Toward a unifying framework for evolutionary
processes. Journal of Theoretical Biology. 2015;383:28-43. doi:10.1016/j.jtbi.2015.07.011
apa: Paixao, T., Badkobeh, G., Barton, N. H., Çörüş, D., Dang, D., Friedrich, T.,
… Trubenova, B. (2015). Toward a unifying framework for evolutionary processes.
Journal of Theoretical Biology. Elsevier. https://doi.org/10.1016/j.jtbi.2015.07.011
chicago: Paixao, Tiago, Golnaz Badkobeh, Nicholas H Barton, Doğan Çörüş, Duccuong
Dang, Tobias Friedrich, Per Lehre, Dirk Sudholt, Andrew Sutton, and Barbora Trubenova.
“Toward a Unifying Framework for Evolutionary Processes.” Journal of Theoretical
Biology. Elsevier, 2015. https://doi.org/10.1016/j.jtbi.2015.07.011.
ieee: T. Paixao et al., “Toward a unifying framework for evolutionary processes,”
Journal of Theoretical Biology, vol. 383. Elsevier, pp. 28–43, 2015.
ista: Paixao T, Badkobeh G, Barton NH, Çörüş D, Dang D, Friedrich T, Lehre P, Sudholt
D, Sutton A, Trubenova B. 2015. Toward a unifying framework for evolutionary processes. Journal
of Theoretical Biology. 383, 28–43.
mla: Paixao, Tiago, et al. “Toward a Unifying Framework for Evolutionary Processes.”
Journal of Theoretical Biology, vol. 383, Elsevier, 2015, pp. 28–43, doi:10.1016/j.jtbi.2015.07.011.
short: T. Paixao, G. Badkobeh, N.H. Barton, D. Çörüş, D. Dang, T. Friedrich, P.
Lehre, D. Sudholt, A. Sutton, B. Trubenova, Journal of Theoretical Biology 383
(2015) 28–43.
date_created: 2018-12-11T11:52:37Z
date_published: 2015-10-21T00:00:00Z
date_updated: 2021-01-12T06:51:29Z
day: '21'
ddc:
- '570'
department:
- _id: NiBa
- _id: CaGu
doi: 10.1016/j.jtbi.2015.07.011
ec_funded: 1
file:
- access_level: open_access
checksum: 33b60ecfea60764756a9ee9df5eb65ca
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:16:53Z
date_updated: 2020-07-14T12:45:01Z
file_id: '5244'
file_name: IST-2016-483-v1+1_1-s2.0-S0022519315003409-main.pdf
file_size: 595307
relation: main_file
file_date_updated: 2020-07-14T12:45:01Z
has_accepted_license: '1'
intvolume: ' 383'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
page: 28 - 43
project:
- _id: 25B1EC9E-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618091'
name: Speed of Adaptation in Population Genetics and Evolutionary Computation
- _id: 25B07788-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '250152'
name: Limits to selection in biology and in evolutionary computation
publication: ' Journal of Theoretical Biology'
publication_status: published
publisher: Elsevier
publist_id: '5629'
pubrep_id: '483'
quality_controlled: '1'
scopus_import: 1
status: public
title: Toward a unifying framework for evolutionary processes
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 383
year: '2015'
...
---
_id: '1840'
abstract:
- lang: eng
text: In this paper, we present a method for reducing a regular, discrete-time Markov
chain (DTMC) to another DTMC with a given, typically much smaller number of states.
The cost of reduction is defined as the Kullback-Leibler divergence rate between
a projection of the original process through a partition function and a DTMC on
the correspondingly partitioned state space. Finding the reduced model with minimal
cost is computationally expensive, as it requires an exhaustive search among all
state space partitions, and an exact evaluation of the reduction cost for each
candidate partition. Our approach deals with the latter problem by minimizing
an upper bound on the reduction cost instead of minimizing the exact cost. The
proposed upper bound is easy to compute and it is tight if the original chain
is lumpable with respect to the partition. Then, we express the problem in the
form of information bottleneck optimization, and propose using the agglomerative
information bottleneck algorithm for searching a suboptimal partition greedily,
rather than exhaustively. The theory is illustrated with examples and one application
scenario in the context of modeling bio-molecular interactions.
acknowledgement: "This work was supported by the Austrian Research Association under
Project 06/12684, by the Swiss National Science Foundation (SNSF) under Grant PP00P2
128503/1, by the SystemsX.ch (the Swiss Inititative for Systems Biology), and by
a SNSF Early Postdoc.Mobility Fellowship grant P2EZP2_148797.\r\n"
author:
- first_name: Bernhard
full_name: Geiger, Bernhard
last_name: Geiger
- first_name: Tatjana
full_name: Petrov, Tatjana
id: 3D5811FC-F248-11E8-B48F-1D18A9856A87
last_name: Petrov
orcid: 0000-0002-9041-0905
- first_name: Gernot
full_name: Kubin, Gernot
last_name: Kubin
- first_name: Heinz
full_name: Koeppl, Heinz
last_name: Koeppl
citation:
ama: Geiger B, Petrov T, Kubin G, Koeppl H. Optimal Kullback-Leibler aggregation
via information bottleneck. IEEE Transactions on Automatic Control. 2015;60(4):1010-1022.
doi:10.1109/TAC.2014.2364971
apa: Geiger, B., Petrov, T., Kubin, G., & Koeppl, H. (2015). Optimal Kullback-Leibler
aggregation via information bottleneck. IEEE Transactions on Automatic Control.
IEEE. https://doi.org/10.1109/TAC.2014.2364971
chicago: Geiger, Bernhard, Tatjana Petrov, Gernot Kubin, and Heinz Koeppl. “Optimal
Kullback-Leibler Aggregation via Information Bottleneck.” IEEE Transactions
on Automatic Control. IEEE, 2015. https://doi.org/10.1109/TAC.2014.2364971.
ieee: B. Geiger, T. Petrov, G. Kubin, and H. Koeppl, “Optimal Kullback-Leibler aggregation
via information bottleneck,” IEEE Transactions on Automatic Control, vol.
60, no. 4. IEEE, pp. 1010–1022, 2015.
ista: Geiger B, Petrov T, Kubin G, Koeppl H. 2015. Optimal Kullback-Leibler aggregation
via information bottleneck. IEEE Transactions on Automatic Control. 60(4), 1010–1022.
mla: Geiger, Bernhard, et al. “Optimal Kullback-Leibler Aggregation via Information
Bottleneck.” IEEE Transactions on Automatic Control, vol. 60, no. 4, IEEE,
2015, pp. 1010–22, doi:10.1109/TAC.2014.2364971.
short: B. Geiger, T. Petrov, G. Kubin, H. Koeppl, IEEE Transactions on Automatic
Control 60 (2015) 1010–1022.
date_created: 2018-12-11T11:54:18Z
date_published: 2015-04-01T00:00:00Z
date_updated: 2021-01-12T06:53:33Z
day: '01'
department:
- _id: CaGu
- _id: ToHe
doi: 10.1109/TAC.2014.2364971
intvolume: ' 60'
issue: '4'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://arxiv.org/abs/1304.6603
month: '04'
oa: 1
oa_version: Preprint
page: 1010 - 1022
publication: IEEE Transactions on Automatic Control
publication_identifier:
issn:
- 0018-9286
publication_status: published
publisher: IEEE
publist_id: '5262'
quality_controlled: '1'
scopus_import: 1
status: public
title: Optimal Kullback-Leibler aggregation via information bottleneck
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 60
year: '2015'
...
---
_id: '9712'
article_processing_charge: No
author:
- first_name: Murat
full_name: Tugrul, Murat
id: 37C323C6-F248-11E8-B48F-1D18A9856A87
last_name: Tugrul
orcid: 0000-0002-8523-0758
- first_name: Tiago
full_name: Paixao, Tiago
id: 2C5658E6-F248-11E8-B48F-1D18A9856A87
last_name: Paixao
orcid: 0000-0003-2361-3953
- first_name: Nicholas H
full_name: Barton, Nicholas H
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
orcid: 0000-0002-8548-5240
- first_name: Gašper
full_name: Tkačik, Gašper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkačik
orcid: 0000-0002-6699-1455
citation:
ama: Tugrul M, Paixao T, Barton NH, Tkačik G. Other fitness models for comparison
& for interacting TFBSs. 2015. doi:10.1371/journal.pgen.1005639.s001
apa: Tugrul, M., Paixao, T., Barton, N. H., & Tkačik, G. (2015). Other fitness
models for comparison & for interacting TFBSs. Public Library of Science.
https://doi.org/10.1371/journal.pgen.1005639.s001
chicago: Tugrul, Murat, Tiago Paixao, Nicholas H Barton, and Gašper Tkačik. “Other
Fitness Models for Comparison & for Interacting TFBSs.” Public Library of
Science, 2015. https://doi.org/10.1371/journal.pgen.1005639.s001.
ieee: M. Tugrul, T. Paixao, N. H. Barton, and G. Tkačik, “Other fitness models for
comparison & for interacting TFBSs.” Public Library of Science, 2015.
ista: Tugrul M, Paixao T, Barton NH, Tkačik G. 2015. Other fitness models for comparison
& for interacting TFBSs, Public Library of Science, 10.1371/journal.pgen.1005639.s001.
mla: Tugrul, Murat, et al. Other Fitness Models for Comparison & for Interacting
TFBSs. Public Library of Science, 2015, doi:10.1371/journal.pgen.1005639.s001.
short: M. Tugrul, T. Paixao, N.H. Barton, G. Tkačik, (2015).
date_created: 2021-07-23T12:00:37Z
date_published: 2015-11-06T00:00:00Z
date_updated: 2023-02-23T10:09:08Z
day: '06'
department:
- _id: NiBa
- _id: CaGu
- _id: GaTk
doi: 10.1371/journal.pgen.1005639.s001
month: '11'
oa_version: Published Version
publisher: Public Library of Science
related_material:
record:
- id: '1666'
relation: used_in_publication
status: public
status: public
title: Other fitness models for comparison & for interacting TFBSs
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2015'
...
---
_id: '9719'
abstract:
- lang: eng
text: Parasitism creates selection for resistance mechanisms in host populations
and is hypothesized to promote increased host evolvability. However, the influence
of these traits on host evolution when parasites are no longer present is unclear.
We used experimental evolution and whole-genome sequencing of Escherichia coli
to determine the effects of past and present exposure to parasitic viruses (phages)
on the spread of mutator alleles, resistance, and bacterial competitive fitness.
We found that mutator alleles spread rapidly during adaptation to any of four
different phage species, and this pattern was even more pronounced with multiple
phages present simultaneously. However, hypermutability did not detectably accelerate
adaptation in the absence of phages and recovery of fitness costs associated with
resistance. Several lineages evolved phage resistance through elevated mucoidy,
and during subsequent evolution in phage-free conditions they rapidly reverted
to nonmucoid, phage-susceptible phenotypes. Genome sequencing revealed that this
phenotypic reversion was achieved by additional genetic changes rather than by
genotypic reversion of the initial resistance mutations. Insertion sequence (IS)
elements played a key role in both the acquisition of resistance and adaptation
in the absence of parasites; unlike single nucleotide polymorphisms, IS insertions
were not more frequent in mutator lineages. Our results provide a genetic explanation
for rapid reversion of mucoidy, a phenotype observed in other bacterial species
including human pathogens. Moreover, this demonstrates that the types of genetic
change underlying adaptation to fitness costs, and consequently the impact of
evolvability mechanisms such as increased point-mutation rates, depend critically
on the mechanism of resistance.
article_processing_charge: No
author:
- first_name: Sébastien
full_name: Wielgoss, Sébastien
last_name: Wielgoss
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Anna M.
full_name: Bischofberger, Anna M.
last_name: Bischofberger
- first_name: Alex R.
full_name: Hall, Alex R.
last_name: Hall
citation:
ama: 'Wielgoss S, Bergmiller T, Bischofberger AM, Hall AR. Data from: Adaptation
to parasites and costs of parasite resistance in mutator and non-mutator bacteria.
2015. doi:10.5061/dryad.cj910'
apa: 'Wielgoss, S., Bergmiller, T., Bischofberger, A. M., & Hall, A. R. (2015).
Data from: Adaptation to parasites and costs of parasite resistance in mutator
and non-mutator bacteria. Dryad. https://doi.org/10.5061/dryad.cj910'
chicago: 'Wielgoss, Sébastien, Tobias Bergmiller, Anna M. Bischofberger, and Alex
R. Hall. “Data from: Adaptation to Parasites and Costs of Parasite Resistance
in Mutator and Non-Mutator Bacteria.” Dryad, 2015. https://doi.org/10.5061/dryad.cj910.'
ieee: 'S. Wielgoss, T. Bergmiller, A. M. Bischofberger, and A. R. Hall, “Data from:
Adaptation to parasites and costs of parasite resistance in mutator and non-mutator
bacteria.” Dryad, 2015.'
ista: 'Wielgoss S, Bergmiller T, Bischofberger AM, Hall AR. 2015. Data from: Adaptation
to parasites and costs of parasite resistance in mutator and non-mutator bacteria,
Dryad, 10.5061/dryad.cj910.'
mla: 'Wielgoss, Sébastien, et al. Data from: Adaptation to Parasites and Costs
of Parasite Resistance in Mutator and Non-Mutator Bacteria. Dryad, 2015, doi:10.5061/dryad.cj910.'
short: S. Wielgoss, T. Bergmiller, A.M. Bischofberger, A.R. Hall, (2015).
date_created: 2021-07-26T08:44:04Z
date_published: 2015-12-21T00:00:00Z
date_updated: 2023-09-05T13:46:04Z
day: '21'
department:
- _id: CaGu
doi: 10.5061/dryad.cj910
main_file_link:
- open_access: '1'
url: https://doi.org/10.5061/dryad.cj910
month: '12'
oa: 1
oa_version: Published Version
publisher: Dryad
related_material:
record:
- id: '5749'
relation: used_in_publication
status: public
status: public
title: 'Data from: Adaptation to parasites and costs of parasite resistance in mutator
and non-mutator bacteria'
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2015'
...