---
_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:
- id: '541'
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:
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- '29237814'
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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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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:
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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
relation: main_file
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has_accepted_license: '1'
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:
- id: '1835'
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
file_date_updated: 2020-07-14T12:44:44Z
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'
file:
- access_level: open_access
checksum: 59cdd4400fb41280122d414fea971546
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:17:49Z
date_updated: 2020-07-14T12:48:16Z
file_id: '5306'
file_name: IST-2017-841-v1+1_elife-25192-v2.pdf
file_size: 2441529
relation: main_file
- access_level: open_access
checksum: b69024880558b858eb8c5d47a92b6377
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:17:50Z
date_updated: 2020-07-14T12:48:16Z
file_id: '5307'
file_name: IST-2017-841-v1+2_elife-25192-figures-v2.pdf
file_size: 3752660
relation: main_file
file_date_updated: 2020-07-14T12:48:16Z
has_accepted_license: '1'
intvolume: ' 6'
isi: 1
language:
- iso: eng
month: '05'
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
- _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:
- access_level: open_access
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:11:29Z
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
file_date_updated: 2018-12-12T10:11:29Z
has_accepted_license: '1'
isi: 1
language:
- iso: eng
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:
- access_level: open_access
checksum: 31a0c01d022721073241a23d192cc37e
content_type: application/zip
creator: system
date_created: 2018-12-12T13:03:18Z
date_updated: 2020-07-14T12:47:03Z
file_id: '5627'
file_name: IST-2017-65-v1+1_D_anc_1.fastq.zip
file_size: 1225959109
relation: main_file
- access_level: open_access
checksum: d8f26f83ce7e7e45436121f9c6cd9b83
content_type: application/zip
creator: system
date_created: 2018-12-12T13:03:30Z
date_updated: 2020-07-14T12:47:03Z
file_id: '5628'
file_name: IST-2017-65-v1+1_D_anc_2.fastq.zip
file_size: 1422656107
relation: main_file
- access_level: open_access
checksum: e07b99bcfe55b5f132ca03b8b48c8cbc
content_type: application/zip
creator: system
date_created: 2018-12-12T13:03:33Z
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status: public
title: Fastq files for "Complex chromosomal neighborhood effects determine the adaptive
potential of a gene under selection"
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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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checksum: d77859af757ac8025c50c7b12b52eaf3
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creator: system
date_created: 2018-12-12T13:02:38Z
date_updated: 2020-07-14T12:47:03Z
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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:
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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:
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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
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intvolume: ' 56'
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language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
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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
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creator: system
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date_updated: 2020-07-14T12:47:48Z
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oa: 1
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publication: eLife
publication_identifier:
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pubrep_id: '890'
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- id: '26'
relation: dissertation_contains
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scopus_import: 1
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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'
...