---
_id: '7569'
abstract:
- lang: eng
text: 'Genes differ in the frequency at which they are expressed and in the form
of regulation used to control their activity. In particular, positive or negative
regulation can lead to activation of a gene in response to an external signal.
Previous works proposed that the form of regulation of a gene correlates with
its frequency of usage: positive regulation when the gene is frequently expressed
and negative regulation when infrequently expressed. Such network design means
that, in the absence of their regulators, the genes are found in their least required
activity state, hence regulatory intervention is often necessary. Due to the multitude
of genes and regulators, spurious binding and unbinding events, called “crosstalk”,
could occur. To determine how the form of regulation affects the global crosstalk
in the network, we used a mathematical model that includes multiple regulators
and multiple target genes. We found that crosstalk depends non-monotonically on
the availability of regulators. Our analysis showed that excess use of regulation
entailed by the formerly suggested network design caused high crosstalk levels
in a large part of the parameter space. We therefore considered the opposite ‘idle’
design, where the default unregulated state of genes is their frequently required
activity state. We found, that ‘idle’ design minimized the use of regulation and
thus minimized crosstalk. In addition, we estimated global crosstalk of S. cerevisiae
using transcription factors binding data. We demonstrated that even partial network
data could suffice to estimate its global crosstalk, suggesting its applicability
to additional organisms. We found that S. cerevisiae estimated crosstalk is lower
than that of a random network, suggesting that natural selection reduces crosstalk.
In summary, our study highlights a new type of protein production cost which is
typically overlooked: that of regulatory interference caused by the presence of
excess regulators in the cell. It demonstrates the importance of whole-network
descriptions, which could show effects missed by single-gene models.'
article_number: e1007642
article_processing_charge: No
article_type: original
author:
- first_name: Rok
full_name: Grah, Rok
id: 483E70DE-F248-11E8-B48F-1D18A9856A87
last_name: Grah
orcid: 0000-0003-2539-3560
- first_name: Tamar
full_name: Friedlander, Tamar
last_name: Friedlander
citation:
ama: Grah R, Friedlander T. The relation between crosstalk and gene regulation form
revisited. PLOS Computational Biology. 2020;16(2). doi:10.1371/journal.pcbi.1007642
apa: Grah, R., & Friedlander, T. (2020). The relation between crosstalk and
gene regulation form revisited. PLOS Computational Biology. Public Library
of Science. https://doi.org/10.1371/journal.pcbi.1007642
chicago: Grah, Rok, and Tamar Friedlander. “The Relation between Crosstalk and Gene
Regulation Form Revisited.” PLOS Computational Biology. Public Library
of Science, 2020. https://doi.org/10.1371/journal.pcbi.1007642.
ieee: R. Grah and T. Friedlander, “The relation between crosstalk and gene regulation
form revisited,” PLOS Computational Biology, vol. 16, no. 2. Public Library
of Science, 2020.
ista: Grah R, Friedlander T. 2020. The relation between crosstalk and gene regulation
form revisited. PLOS Computational Biology. 16(2), e1007642.
mla: Grah, Rok, and Tamar Friedlander. “The Relation between Crosstalk and Gene
Regulation Form Revisited.” PLOS Computational Biology, vol. 16, no. 2,
e1007642, Public Library of Science, 2020, doi:10.1371/journal.pcbi.1007642.
short: R. Grah, T. Friedlander, PLOS Computational Biology 16 (2020).
date_created: 2020-03-06T07:39:38Z
date_published: 2020-02-25T00:00:00Z
date_updated: 2023-09-12T11:02:24Z
day: '25'
ddc:
- '000'
- '570'
department:
- _id: CaGu
- _id: GaTk
doi: 10.1371/journal.pcbi.1007642
external_id:
isi:
- '000526725200019'
file:
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date_created: 2020-03-09T15:12:21Z
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file_size: 2209325
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month: '02'
oa: 1
oa_version: Published Version
publication: PLOS Computational Biology
publication_identifier:
issn:
- 1553-7358
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
related_material:
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relation: research_data
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relation: research_data
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relation: used_in_publication
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- id: '8155'
relation: dissertation_contains
status: public
- id: '9777'
relation: research_data
status: public
scopus_import: '1'
status: public
title: The relation between crosstalk and gene regulation form revisited
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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 16
year: '2020'
...
---
_id: '7680'
abstract:
- lang: eng
text: "Proteins and their complex dynamic interactions regulate cellular mechanisms
from sensing and transducing extracellular signals, to mediating genetic responses,
and sustaining or changing cell morphology. To manipulate these protein-protein
interactions (PPIs) that govern the behavior and fate of cells, synthetically
constructed, genetically encoded tools provide the means to precisely target proteins
of interest (POIs), and control their subcellular localization and activity in
vitro and in vivo. Ideal synthetic tools react to an orthogonal cue, i.e. a trigger
that does not activate any other endogenous process, thereby allowing manipulation
of the POI alone.\r\nIn optogenetics, naturally occurring photosensory domain
from plants, algae and bacteria are re-purposed and genetically fused to POIs.
Illumination with light of a specific wavelength triggers a conformational change
that can mediate PPIs, such as dimerization or oligomerization. By using light
as a trigger, these tools can be activated with high spatial and temporal precision,
on subcellular and millisecond scales. Chemogenetic tools consist of protein domains
that recognize and bind small molecules. By genetic fusion to POIs, these domains
can mediate PPIs upon addition of their specific ligands, which are often synthetically
designed to provide highly specific interactions and exhibit good bioavailability.\r\nMost
optogenetic tools to mediate PPIs are based on well-studied photoreceptors responding
to red, blue or near-UV light, leaving a striking gap in the green band of the
visible light spectrum. Among both optogenetic and chemogenetic tools, there is
an abundance of methods to induce PPIs, but tools to disrupt them require UV illumination,
rely on covalent linkage and subsequent enzymatic cleavage or initially result
in protein clustering of unknown stoichiometry.\r\nThis work describes how the
recently structurally and photochemically characterized green-light responsive
cobalamin-binding domains (CBDs) from bacterial transcription factors were re-purposed
to function as a green-light responsive optogenetic tool. In contrast to previously
engineered optogenetic tools, CBDs do not induce PPI, but rather confer a PPI
already upon expression, which can be rapidly disrupted by illumination. This
was employed to mimic inhibition of constitutive activity of a growth factor receptor,
and successfully implement for cell signalling in mammalian cells and in vivo
to rescue development in zebrafish. This work further describes the development
and application of a chemically induced de-dimerizer (CDD) based on a recently
identified and structurally described bacterial oxyreductase. CDD forms a dimer
upon expression in absence of its cofactor, the flavin derivative F420. Safety
and of domain expression and ligand exposure are demonstrated in vitro and in
vivo in zebrafish. The system is further applied to inhibit cell signalling output
from a chimeric receptor upon F420 treatment.\r\nCBDs and CDD expand the repertoire
of synthetic tools by providing novel mechanisms of mediating PPIs, and by recognizing
previously not utilized cues. In the future, they can readily be combined with
existing synthetic tools to functionally manipulate PPIs in vitro and in vivo."
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Stephanie
full_name: Kainrath, Stephanie
id: 32CFBA64-F248-11E8-B48F-1D18A9856A87
last_name: Kainrath
citation:
ama: Kainrath S. Synthetic tools for optogenetic and chemogenetic inhibition of
cellular signals. 2020. doi:10.15479/AT:ISTA:7680
apa: Kainrath, S. (2020). Synthetic tools for optogenetic and chemogenetic inhibition
of cellular signals. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:7680
chicago: Kainrath, Stephanie. “Synthetic Tools for Optogenetic and Chemogenetic
Inhibition of Cellular Signals.” Institute of Science and Technology Austria,
2020. https://doi.org/10.15479/AT:ISTA:7680.
ieee: S. Kainrath, “Synthetic tools for optogenetic and chemogenetic inhibition
of cellular signals,” Institute of Science and Technology Austria, 2020.
ista: Kainrath S. 2020. Synthetic tools for optogenetic and chemogenetic inhibition
of cellular signals. Institute of Science and Technology Austria.
mla: Kainrath, Stephanie. Synthetic Tools for Optogenetic and Chemogenetic Inhibition
of Cellular Signals. Institute of Science and Technology Austria, 2020, doi:10.15479/AT:ISTA:7680.
short: S. Kainrath, Synthetic Tools for Optogenetic and Chemogenetic Inhibition
of Cellular Signals, Institute of Science and Technology Austria, 2020.
date_created: 2020-04-24T16:00:51Z
date_published: 2020-04-24T00:00:00Z
date_updated: 2023-09-22T09:20:10Z
day: '24'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: CaGu
doi: 10.15479/AT:ISTA:7680
file:
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checksum: fb9a4468eb27be92690728e35c823796
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date_created: 2020-04-28T11:19:21Z
date_updated: 2021-10-31T23:30:05Z
embargo: 2021-10-30
file_id: '7692'
file_name: Thesis_without-signatures_PDFA.pdf
file_size: 3268017
relation: main_file
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checksum: f6c80ca97104a631a328cb79a2c53493
content_type: application/octet-stream
creator: stgingl
date_created: 2020-04-28T11:19:24Z
date_updated: 2021-10-31T23:30:05Z
embargo_to: open_access
file_id: '7693'
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file_size: 5167703
relation: source_file
file_date_updated: 2021-10-31T23:30:05Z
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language:
- iso: eng
month: '04'
oa: 1
oa_version: None
page: '98'
publication_identifier:
eissn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '1028'
relation: dissertation_contains
status: public
status: public
supervisor:
- first_name: Harald L
full_name: Janovjak, Harald L
id: 33BA6C30-F248-11E8-B48F-1D18A9856A87
last_name: Janovjak
orcid: 0000-0002-8023-9315
title: Synthetic tools for optogenetic and chemogenetic inhibition of cellular signals
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2020'
...
---
_id: '7652'
abstract:
- lang: eng
text: Organisms cope with change by taking advantage of transcriptional regulators.
However, when faced with rare environments, the evolution of transcriptional regulators
and their promoters may be too slow. Here, we investigate whether the intrinsic
instability of gene duplication and amplification provides a generic alternative
to canonical gene regulation. Using real-time monitoring of gene-copy-number mutations
in Escherichia coli, we show that gene duplications and amplifications enable
adaptation to fluctuating environments by rapidly generating copy-number and,
therefore, expression-level polymorphisms. This amplification-mediated gene expression
tuning (AMGET) occurs on timescales that are similar to canonical gene regulation
and can respond to rapid environmental changes. Mathematical modelling shows that
amplifications also tune gene expression in stochastic environments in which transcription-factor-based
schemes are hard to evolve or maintain. The fleeting nature of gene amplifications
gives rise to a generic population-level mechanism that relies on genetic heterogeneity
to rapidly tune the expression of any gene, without leaving any genomic signature.
acknowledgement: We thank L. Hurst, N. Barton, M. Pleska, M. Steinrück, B. Kavcic
and A. Staron for input on the manuscript, and To. Bergmiller and R. Chait for help
with microfluidics experiments. I.T. is a recipient the OMV fellowship. R.G. is
a recipient of a DOC (Doctoral Fellowship Programme of the Austrian Academy of Sciences)
Fellowship of the Austrian Academy of Sciences.
article_processing_charge: No
article_type: original
author:
- first_name: Isabella
full_name: Tomanek, Isabella
id: 3981F020-F248-11E8-B48F-1D18A9856A87
last_name: Tomanek
orcid: 0000-0001-6197-363X
- first_name: Rok
full_name: Grah, Rok
id: 483E70DE-F248-11E8-B48F-1D18A9856A87
last_name: Grah
orcid: 0000-0003-2539-3560
- first_name: M.
full_name: Lagator, M.
last_name: Lagator
- first_name: A. M. C.
full_name: Andersson, A. M. C.
last_name: Andersson
- 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: Gašper
full_name: Tkačik, Gašper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkačik
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: Tomanek I, Grah R, Lagator M, et al. Gene amplification as a form of population-level
gene expression regulation. Nature Ecology & Evolution. 2020;4(4):612-625.
doi:10.1038/s41559-020-1132-7
apa: Tomanek, I., Grah, R., Lagator, M., Andersson, A. M. C., Bollback, J. P., Tkačik,
G., & Guet, C. C. (2020). Gene amplification as a form of population-level
gene expression regulation. Nature Ecology & Evolution. Springer Nature.
https://doi.org/10.1038/s41559-020-1132-7
chicago: Tomanek, Isabella, Rok Grah, M. Lagator, A. M. C. Andersson, Jonathan P
Bollback, Gašper Tkačik, and Calin C Guet. “Gene Amplification as a Form of Population-Level
Gene Expression Regulation.” Nature Ecology & Evolution. Springer Nature,
2020. https://doi.org/10.1038/s41559-020-1132-7.
ieee: I. Tomanek et al., “Gene amplification as a form of population-level
gene expression regulation,” Nature Ecology & Evolution, vol. 4, no.
4. Springer Nature, pp. 612–625, 2020.
ista: Tomanek I, Grah R, Lagator M, Andersson AMC, Bollback JP, Tkačik G, Guet CC.
2020. Gene amplification as a form of population-level gene expression regulation.
Nature Ecology & Evolution. 4(4), 612–625.
mla: Tomanek, Isabella, et al. “Gene Amplification as a Form of Population-Level
Gene Expression Regulation.” Nature Ecology & Evolution, vol. 4, no.
4, Springer Nature, 2020, pp. 612–25, doi:10.1038/s41559-020-1132-7.
short: I. Tomanek, R. Grah, M. Lagator, A.M.C. Andersson, J.P. Bollback, G. Tkačik,
C.C. Guet, Nature Ecology & Evolution 4 (2020) 612–625.
date_created: 2020-04-08T15:20:53Z
date_published: 2020-04-01T00:00:00Z
date_updated: 2024-03-28T23:30:37Z
day: '01'
ddc:
- '570'
department:
- _id: GaTk
- _id: CaGu
doi: 10.1038/s41559-020-1132-7
external_id:
isi:
- '000519008300005'
file:
- access_level: open_access
checksum: ef3bbf42023e30b2c24a6278025d2040
content_type: application/pdf
creator: dernst
date_created: 2020-10-09T09:56:01Z
date_updated: 2020-10-09T09:56:01Z
file_id: '8640'
file_name: 2020_NatureEcolEvo_Tomanek.pdf
file_size: 745242
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file_date_updated: 2020-10-09T09:56:01Z
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isi: 1
issue: '4'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Submitted Version
page: 612-625
project:
- _id: 267C84F4-B435-11E9-9278-68D0E5697425
name: Biophysically realistic genotype-phenotype maps for regulatory networks
publication: Nature Ecology & Evolution
publication_identifier:
issn:
- 2397-334X
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/how-to-thrive-without-gene-regulation/
record:
- id: '8155'
relation: dissertation_contains
status: public
- id: '7383'
relation: research_data
status: public
- id: '7016'
relation: research_data
status: public
- id: '8653'
relation: used_in_publication
status: public
scopus_import: '1'
status: public
title: Gene amplification as a form of population-level gene expression regulation
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 4
year: '2020'
...
---
_id: '8653'
abstract:
- lang: eng
text: "Mutations are the raw material of evolution and come in many different flavors.
Point mutations change a single letter in the DNA sequence, while copy number
mutations like duplications or deletions add or remove many letters of the DNA
sequence simultaneously. Each type of mutation exhibits specific properties like
its rate of formation and reversal. \r\nGene expression is a fundamental phenotype
that can be altered by both, point and copy number mutations. The following thesis
is concerned with the dynamics of gene expression evolution and how it is affected
by the properties exhibited by point and copy number mutations. Specifically,
we are considering i) copy number mutations during adaptation to fluctuating environments
and ii) the interaction of copy number and point mutations during adaptation to
constant environments. "
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Isabella
full_name: Tomanek, Isabella
id: 3981F020-F248-11E8-B48F-1D18A9856A87
last_name: Tomanek
orcid: 0000-0001-6197-363X
citation:
ama: Tomanek I. The evolution of gene expression by copy number and point mutations.
2020. doi:10.15479/AT:ISTA:8653
apa: Tomanek, I. (2020). The evolution of gene expression by copy number and
point mutations. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:8653
chicago: Tomanek, Isabella. “The Evolution of Gene Expression by Copy Number and
Point Mutations.” Institute of Science and Technology Austria, 2020. https://doi.org/10.15479/AT:ISTA:8653.
ieee: I. Tomanek, “The evolution of gene expression by copy number and point mutations,”
Institute of Science and Technology Austria, 2020.
ista: Tomanek I. 2020. The evolution of gene expression by copy number and point
mutations. Institute of Science and Technology Austria.
mla: Tomanek, Isabella. The Evolution of Gene Expression by Copy Number and Point
Mutations. Institute of Science and Technology Austria, 2020, doi:10.15479/AT:ISTA:8653.
short: I. Tomanek, The Evolution of Gene Expression by Copy Number and Point Mutations,
Institute of Science and Technology Austria, 2020.
date_created: 2020-10-13T13:02:33Z
date_published: 2020-10-13T00:00:00Z
date_updated: 2023-09-07T13:22:42Z
day: '13'
ddc:
- '576'
degree_awarded: PhD
department:
- _id: CaGu
doi: 10.15479/AT:ISTA:8653
file:
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checksum: c01d9f59794b4b70528f37637c17ad02
content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
creator: itomanek
date_created: 2020-10-16T12:14:21Z
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content_type: application/pdf
creator: itomanek
date_created: 2020-10-16T12:14:21Z
date_updated: 2021-10-20T22:30:03Z
embargo: 2021-10-19
file_id: '8667'
file_name: Thesis_ITomanek_final_201016.pdf
file_size: 15405675
relation: main_file
file_date_updated: 2021-10-20T22:30:03Z
has_accepted_license: '1'
keyword:
- duplication
- amplification
- promoter
- CNV
- AMGET
- experimental evolution
- Escherichia coli
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
page: '117'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '7652'
relation: research_data
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: The evolution of gene expression by copy number and point mutations
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2020'
...
---
_id: '6465'
abstract:
- lang: eng
text: Tight control over protein degradation is a fundamental requirement for cells
to respond rapidly to various stimuli and adapt to a fluctuating environment.
Here we develop a versatile, easy-to-handle library of destabilizing tags (degrons)
for the precise regulation of protein expression profiles in mammalian cells by
modulating target protein half-lives in a predictable manner. Using the well-established
tetracycline gene-regulation system as a model, we show that the dynamics of protein
expression can be tuned by fusing appropriate degron tags to gene regulators.
Next, we apply this degron library to tune a synthetic pulse-generating circuit
in mammalian cells. With this toolbox we establish a set of pulse generators with
tailored pulse lengths and magnitudes of protein expression. This methodology
will prove useful in the functional roles of essential proteins, fine-tuning of
gene-expression systems, and enabling a higher complexity in the design of synthetic
biological systems in mammalian cells.
article_number: '2013'
article_processing_charge: No
author:
- first_name: Hélène
full_name: Chassin, Hélène
last_name: Chassin
- first_name: Marius
full_name: Müller, Marius
last_name: Müller
- first_name: Marcel
full_name: Tigges, Marcel
last_name: Tigges
- first_name: Leo
full_name: Scheller, Leo
last_name: Scheller
- first_name: Moritz
full_name: Lang, Moritz
id: 29E0800A-F248-11E8-B48F-1D18A9856A87
last_name: Lang
- first_name: Martin
full_name: Fussenegger, Martin
last_name: Fussenegger
citation:
ama: Chassin H, Müller M, Tigges M, Scheller L, Lang M, Fussenegger M. A modular
degron library for synthetic circuits in mammalian cells. Nature Communications.
2019;10(1). doi:10.1038/s41467-019-09974-5
apa: Chassin, H., Müller, M., Tigges, M., Scheller, L., Lang, M., & Fussenegger,
M. (2019). A modular degron library for synthetic circuits in mammalian cells.
Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-019-09974-5
chicago: Chassin, Hélène, Marius Müller, Marcel Tigges, Leo Scheller, Moritz Lang,
and Martin Fussenegger. “A Modular Degron Library for Synthetic Circuits in Mammalian
Cells.” Nature Communications. Springer Nature, 2019. https://doi.org/10.1038/s41467-019-09974-5.
ieee: H. Chassin, M. Müller, M. Tigges, L. Scheller, M. Lang, and M. Fussenegger,
“A modular degron library for synthetic circuits in mammalian cells,” Nature
Communications, vol. 10, no. 1. Springer Nature, 2019.
ista: Chassin H, Müller M, Tigges M, Scheller L, Lang M, Fussenegger M. 2019. A
modular degron library for synthetic circuits in mammalian cells. Nature Communications.
10(1), 2013.
mla: Chassin, Hélène, et al. “A Modular Degron Library for Synthetic Circuits in
Mammalian Cells.” Nature Communications, vol. 10, no. 1, 2013, Springer
Nature, 2019, doi:10.1038/s41467-019-09974-5.
short: H. Chassin, M. Müller, M. Tigges, L. Scheller, M. Lang, M. Fussenegger, Nature
Communications 10 (2019).
date_created: 2019-05-19T21:59:14Z
date_published: 2019-05-01T00:00:00Z
date_updated: 2023-08-25T10:33:51Z
day: '01'
ddc:
- '570'
department:
- _id: CaGu
doi: 10.1038/s41467-019-09974-5
external_id:
isi:
- '000466338600006'
file:
- access_level: open_access
checksum: e214d3e4f8c81e35981583c4569b51b8
content_type: application/pdf
creator: dernst
date_created: 2019-05-20T07:33:54Z
date_updated: 2020-07-14T12:47:31Z
file_id: '6471'
file_name: 2019_NatureComm_Chassin.pdf
file_size: 1191827
relation: main_file
file_date_updated: 2020-07-14T12:47:31Z
has_accepted_license: '1'
intvolume: ' 10'
isi: 1
issue: '1'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
eissn:
- '20411723'
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- relation: erratum
url: https://doi.org/10.1038/s41467-023-36111-0
scopus_import: '1'
status: public
title: A modular degron library for synthetic circuits in mammalian 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 10
year: '2019'
...
---
_id: '6717'
abstract:
- lang: eng
text: With the recent publication by Silpe and Bassler (2019), considering phage
detection of a bacterial quorum-sensing (QS) autoinducer, we now have as many
as five examples of phage-associated intercellular communication (Table 1). Each
potentially involves ecological inferences by phages as to concentrations of surrounding
phage-infected or uninfected bacteria. While the utility of phage detection of
bacterial QS molecules may at first glance appear to be straightforward, we suggest
in this commentary that the underlying ecological explanation is unlikely to be
simple.
article_number: '1171'
article_processing_charge: Yes (via OA deal)
author:
- first_name: Claudia
full_name: Igler, Claudia
id: 46613666-F248-11E8-B48F-1D18A9856A87
last_name: Igler
- first_name: Stephen T.
full_name: Abedon, Stephen T.
last_name: Abedon
citation:
ama: 'Igler C, Abedon ST. Commentary: A host-produced quorum-sensing autoinducer
controls a phage lysis-lysogeny decision. Frontiers in Microbiology. 2019;10.
doi:10.3389/fmicb.2019.01171'
apa: 'Igler, C., & Abedon, S. T. (2019). Commentary: A host-produced quorum-sensing
autoinducer controls a phage lysis-lysogeny decision. Frontiers in Microbiology.
Frontiers. https://doi.org/10.3389/fmicb.2019.01171'
chicago: 'Igler, Claudia, and Stephen T. Abedon. “Commentary: A Host-Produced Quorum-Sensing
Autoinducer Controls a Phage Lysis-Lysogeny Decision.” Frontiers in Microbiology.
Frontiers, 2019. https://doi.org/10.3389/fmicb.2019.01171.'
ieee: 'C. Igler and S. T. Abedon, “Commentary: A host-produced quorum-sensing autoinducer
controls a phage lysis-lysogeny decision,” Frontiers in Microbiology, vol.
10. Frontiers, 2019.'
ista: 'Igler C, Abedon ST. 2019. Commentary: A host-produced quorum-sensing autoinducer
controls a phage lysis-lysogeny decision. Frontiers in Microbiology. 10, 1171.'
mla: 'Igler, Claudia, and Stephen T. Abedon. “Commentary: A Host-Produced Quorum-Sensing
Autoinducer Controls a Phage Lysis-Lysogeny Decision.” Frontiers in Microbiology,
vol. 10, 1171, Frontiers, 2019, doi:10.3389/fmicb.2019.01171.'
short: C. Igler, S.T. Abedon, Frontiers in Microbiology 10 (2019).
date_created: 2019-07-28T21:59:18Z
date_published: 2019-06-03T00:00:00Z
date_updated: 2023-08-29T06:41:20Z
day: '03'
ddc:
- '570'
department:
- _id: CaGu
doi: 10.3389/fmicb.2019.01171
external_id:
isi:
- '000470131200001'
file:
- access_level: open_access
checksum: 317a06067e9a8e717bb55f23e0d77ba7
content_type: application/pdf
creator: apreinsp
date_created: 2019-07-29T07:51:54Z
date_updated: 2020-07-14T12:47:38Z
file_id: '6722'
file_name: 2019_Frontiers_Igler.pdf
file_size: 246151
relation: main_file
file_date_updated: 2020-07-14T12:47:38Z
has_accepted_license: '1'
intvolume: ' 10'
isi: 1
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
project:
- _id: 251EE76E-B435-11E9-9278-68D0E5697425
grant_number: '24573'
name: Design principles underlying genetic switch architecture (DOC Fellowship)
publication: Frontiers in Microbiology
publication_status: published
publisher: Frontiers
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Commentary: A host-produced quorum-sensing autoinducer controls a phage lysis-lysogeny
decision'
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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 10
year: '2019'
...
---
_id: '6784'
abstract:
- lang: eng
text: Mathematical models have been used successfully at diverse scales of biological
organization, ranging from ecology and population dynamics to stochastic reaction
events occurring between individual molecules in single cells. Generally, many
biological processes unfold across multiple scales, with mutations being the best
studied example of how stochasticity at the molecular scale can influence outcomes
at the population scale. In many other contexts, however, an analogous link between
micro- and macro-scale remains elusive, primarily due to the challenges involved
in setting up and analyzing multi-scale models. Here, we employ such a model to
investigate how stochasticity propagates from individual biochemical reaction
events in the bacterial innate immune system to the ecology of bacteria and bacterial
viruses. We show analytically how the dynamics of bacterial populations are shaped
by the activities of immunity-conferring enzymes in single cells and how the ecological
consequences imply optimal bacterial defense strategies against viruses. Our results
suggest that bacterial populations in the presence of viruses can either optimize
their initial growth rate or their population size, with the first strategy favoring
simple immunity featuring a single restriction modification system and the second
strategy favoring complex bacterial innate immunity featuring several simultaneously
active restriction modification systems.
article_number: e1007168
article_processing_charge: No
article_type: original
author:
- first_name: Jakob
full_name: Ruess, Jakob
id: 4A245D00-F248-11E8-B48F-1D18A9856A87
last_name: Ruess
orcid: 0000-0003-1615-3282
- 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
- first_name: Gašper
full_name: Tkačik, Gašper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkačik
orcid: 0000-0002-6699-1455
citation:
ama: Ruess J, Pleska M, Guet CC, Tkačik G. Molecular noise of innate immunity shapes
bacteria-phage ecologies. PLoS Computational Biology. 2019;15(7). doi:10.1371/journal.pcbi.1007168
apa: Ruess, J., Pleska, M., Guet, C. C., & Tkačik, G. (2019). Molecular noise
of innate immunity shapes bacteria-phage ecologies. PLoS Computational Biology.
Public Library of Science. https://doi.org/10.1371/journal.pcbi.1007168
chicago: Ruess, Jakob, Maros Pleska, Calin C Guet, and Gašper Tkačik. “Molecular
Noise of Innate Immunity Shapes Bacteria-Phage Ecologies.” PLoS Computational
Biology. Public Library of Science, 2019. https://doi.org/10.1371/journal.pcbi.1007168.
ieee: J. Ruess, M. Pleska, C. C. Guet, and G. Tkačik, “Molecular noise of innate
immunity shapes bacteria-phage ecologies,” PLoS Computational Biology,
vol. 15, no. 7. Public Library of Science, 2019.
ista: Ruess J, Pleska M, Guet CC, Tkačik G. 2019. Molecular noise of innate immunity
shapes bacteria-phage ecologies. PLoS Computational Biology. 15(7), e1007168.
mla: Ruess, Jakob, et al. “Molecular Noise of Innate Immunity Shapes Bacteria-Phage
Ecologies.” PLoS Computational Biology, vol. 15, no. 7, e1007168, Public
Library of Science, 2019, doi:10.1371/journal.pcbi.1007168.
short: J. Ruess, M. Pleska, C.C. Guet, G. Tkačik, PLoS Computational Biology 15
(2019).
date_created: 2019-08-11T21:59:19Z
date_published: 2019-07-02T00:00:00Z
date_updated: 2023-08-29T07:10:06Z
day: '02'
ddc:
- '570'
department:
- _id: CaGu
- _id: GaTk
doi: 10.1371/journal.pcbi.1007168
external_id:
isi:
- '000481577700032'
file:
- access_level: open_access
checksum: 7ded4721b41c2a0fc66a1c634540416a
content_type: application/pdf
creator: dernst
date_created: 2019-08-12T12:27:26Z
date_updated: 2020-07-14T12:47:40Z
file_id: '6803'
file_name: 2019_PlosComputBiology_Ruess.pdf
file_size: 2200003
relation: main_file
file_date_updated: 2020-07-14T12:47:40Z
has_accepted_license: '1'
intvolume: ' 15'
isi: 1
issue: '7'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
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
- _id: 251BCBEC-B435-11E9-9278-68D0E5697425
grant_number: RGY0079/2011
name: Multi-Level Conflicts in Evolutionary Dynamics of Restriction-Modification
Systems
publication: PLoS Computational Biology
publication_identifier:
eissn:
- 1553-7358
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
related_material:
record:
- id: '9786'
relation: research_data
status: public
scopus_import: '1'
status: public
title: Molecular noise of innate immunity shapes bacteria-phage ecologies
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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 15
year: '2019'
...
---
_id: '9786'
article_processing_charge: No
author:
- first_name: Jakob
full_name: Ruess, Jakob
id: 4A245D00-F248-11E8-B48F-1D18A9856A87
last_name: Ruess
orcid: 0000-0003-1615-3282
- 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
- first_name: Gašper
full_name: Tkačik, Gašper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkačik
orcid: 0000-0002-6699-1455
citation:
ama: Ruess J, Pleska M, Guet CC, Tkačik G. Supporting text and results. 2019. doi:10.1371/journal.pcbi.1007168.s001
apa: Ruess, J., Pleska, M., Guet, C. C., & Tkačik, G. (2019). Supporting text
and results. Public Library of Science. https://doi.org/10.1371/journal.pcbi.1007168.s001
chicago: Ruess, Jakob, Maros Pleska, Calin C Guet, and Gašper Tkačik. “Supporting
Text and Results.” Public Library of Science, 2019. https://doi.org/10.1371/journal.pcbi.1007168.s001.
ieee: J. Ruess, M. Pleska, C. C. Guet, and G. Tkačik, “Supporting text and results.”
Public Library of Science, 2019.
ista: Ruess J, Pleska M, Guet CC, Tkačik G. 2019. Supporting text and results, Public
Library of Science, 10.1371/journal.pcbi.1007168.s001.
mla: Ruess, Jakob, et al. Supporting Text and Results. Public Library of
Science, 2019, doi:10.1371/journal.pcbi.1007168.s001.
short: J. Ruess, M. Pleska, C.C. Guet, G. Tkačik, (2019).
date_created: 2021-08-06T08:23:43Z
date_published: 2019-07-02T00:00:00Z
date_updated: 2023-08-29T07:10:05Z
day: '02'
department:
- _id: CaGu
- _id: GaTk
doi: 10.1371/journal.pcbi.1007168.s001
month: '07'
oa_version: Published Version
publisher: Public Library of Science
related_material:
record:
- id: '6784'
relation: used_in_publication
status: public
status: public
title: Supporting text and results
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2019'
...
---
_id: '7147'
abstract:
- lang: eng
text: "The expression of a gene is characterised by its transcription factors and
the function processing them. If the transcription factors are not affected by
gene products, the regulating function is often represented as a combinational
logic circuit, where the outputs (product) are determined by current input values
(transcription factors) only, and are hence independent on their relative arrival
times. However, the simultaneous arrival of transcription factors (TFs) in genetic
circuits is a strong assumption, given that the processes of transcription and
translation of a gene into a protein introduce intrinsic time delays and that
there is no global synchronisation among the arrival times of different molecular
species at molecular targets.\r\n\r\nIn this paper, we construct an experimentally
implementable genetic circuit with two inputs and a single output, such that,
in presence of small delays in input arrival, the circuit exhibits qualitatively
distinct observable phenotypes. In particular, these phenotypes are long lived
transients: they all converge to a single value, but so slowly, that they seem
stable for an extended time period, longer than typical experiment duration. We
used rule-based language to prototype our circuit, and we implemented a search
for finding the parameter combinations raising the phenotypes of interest.\r\n\r\nThe
behaviour of our prototype circuit has wide implications. First, it suggests that
GRNs can exploit event timing to create phenotypes. Second, it opens the possibility
that GRNs are using event timing to react to stimuli and memorise events, without
explicit feedback in regulation. From the modelling perspective, our prototype
circuit demonstrates the critical importance of analysing the transient dynamics
at the promoter binding sites of the DNA, before applying rapid equilibrium assumptions."
alternative_title:
- LNCS
article_processing_charge: No
author:
- 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: Thomas A
full_name: Henzinger, Thomas A
id: 40876CD8-F248-11E8-B48F-1D18A9856A87
last_name: Henzinger
orcid: 0000−0002−2985−7724
- first_name: Claudia
full_name: Igler, Claudia
id: 46613666-F248-11E8-B48F-1D18A9856A87
last_name: Igler
- first_name: Tatjana
full_name: Petrov, Tatjana
id: 3D5811FC-F248-11E8-B48F-1D18A9856A87
last_name: Petrov
orcid: 0000-0002-9041-0905
- first_name: Ali
full_name: Sezgin, Ali
id: 4C7638DA-F248-11E8-B48F-1D18A9856A87
last_name: Sezgin
citation:
ama: 'Guet CC, Henzinger TA, Igler C, Petrov T, Sezgin A. Transient memory in gene
regulation. In: 17th International Conference on Computational Methods in Systems
Biology. Vol 11773. Springer Nature; 2019:155-187. doi:10.1007/978-3-030-31304-3_9'
apa: 'Guet, C. C., Henzinger, T. A., Igler, C., Petrov, T., & Sezgin, A. (2019).
Transient memory in gene regulation. In 17th International Conference on Computational
Methods in Systems Biology (Vol. 11773, pp. 155–187). Trieste, Italy: Springer
Nature. https://doi.org/10.1007/978-3-030-31304-3_9'
chicago: Guet, Calin C, Thomas A Henzinger, Claudia Igler, Tatjana Petrov, and Ali
Sezgin. “Transient Memory in Gene Regulation.” In 17th International Conference
on Computational Methods in Systems Biology, 11773:155–87. Springer Nature,
2019. https://doi.org/10.1007/978-3-030-31304-3_9.
ieee: C. C. Guet, T. A. Henzinger, C. Igler, T. Petrov, and A. Sezgin, “Transient
memory in gene regulation,” in 17th International Conference on Computational
Methods in Systems Biology, Trieste, Italy, 2019, vol. 11773, pp. 155–187.
ista: 'Guet CC, Henzinger TA, Igler C, Petrov T, Sezgin A. 2019. Transient memory
in gene regulation. 17th International Conference on Computational Methods in
Systems Biology. CMSB: Computational Methods in Systems Biology, LNCS, vol. 11773,
155–187.'
mla: Guet, Calin C., et al. “Transient Memory in Gene Regulation.” 17th International
Conference on Computational Methods in Systems Biology, vol. 11773, Springer
Nature, 2019, pp. 155–87, doi:10.1007/978-3-030-31304-3_9.
short: C.C. Guet, T.A. Henzinger, C. Igler, T. Petrov, A. Sezgin, in:, 17th International
Conference on Computational Methods in Systems Biology, Springer Nature, 2019,
pp. 155–187.
conference:
end_date: 2019-09-20
location: Trieste, Italy
name: 'CMSB: Computational Methods in Systems Biology'
start_date: 2019-09-18
date_created: 2019-12-04T16:07:50Z
date_published: 2019-09-17T00:00:00Z
date_updated: 2023-09-06T11:18:08Z
day: '17'
department:
- _id: CaGu
- _id: ToHe
doi: 10.1007/978-3-030-31304-3_9
external_id:
isi:
- '000557875100009'
intvolume: ' 11773'
isi: 1
language:
- iso: eng
month: '09'
oa_version: None
page: 155-187
project:
- _id: 25F42A32-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Z211
name: The Wittgenstein Prize
- _id: 251EE76E-B435-11E9-9278-68D0E5697425
grant_number: '24573'
name: Design principles underlying genetic switch architecture
publication: 17th International Conference on Computational Methods in Systems Biology
publication_identifier:
eissn:
- 1611-3349
isbn:
- '9783030313036'
- '9783030313043'
issn:
- 0302-9743
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Transient memory in gene regulation
type: conference
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 11773
year: '2019'
...
---
_id: '138'
abstract:
- lang: eng
text: Autoregulation is the direct modulation of gene expression by the product
of the corresponding gene. Autoregulation of bacterial gene expression has been
mostly studied at the transcriptional level, when a protein acts as the cognate
transcriptional repressor. A recent study investigating dynamics of the bacterial
toxin–antitoxin MazEF system has shown how autoregulation at both the transcriptional
and post-transcriptional levels affects the heterogeneity of Escherichia coli
populations. Toxin–antitoxin systems hold a crucial but still elusive part in
bacterial response to stress. This perspective highlights how these modules can
also serve as a great model system for investigating basic concepts in gene regulation.
However, as the genomic background and environmental conditions substantially
influence toxin activation, it is important to study (auto)regulation of toxin–antitoxin
systems in well-defined setups as well as in conditions that resemble the environmental
niche.
article_processing_charge: Yes (via OA deal)
author:
- first_name: Nela
full_name: Nikolic, Nela
id: 42D9CABC-F248-11E8-B48F-1D18A9856A87
last_name: Nikolic
orcid: 0000-0001-9068-6090
citation:
ama: 'Nikolic N. Autoregulation of bacterial gene expression: lessons from the MazEF
toxin–antitoxin system. Current Genetics. 2019;65(1):133-138. doi:10.1007/s00294-018-0879-8'
apa: 'Nikolic, N. (2019). Autoregulation of bacterial gene expression: lessons from
the MazEF toxin–antitoxin system. Current Genetics. Springer. https://doi.org/10.1007/s00294-018-0879-8'
chicago: 'Nikolic, Nela. “Autoregulation of Bacterial Gene Expression: Lessons from
the MazEF Toxin–Antitoxin System.” Current Genetics. Springer, 2019. https://doi.org/10.1007/s00294-018-0879-8.'
ieee: 'N. Nikolic, “Autoregulation of bacterial gene expression: lessons from the
MazEF toxin–antitoxin system,” Current Genetics, vol. 65, no. 1. Springer,
pp. 133–138, 2019.'
ista: 'Nikolic N. 2019. Autoregulation of bacterial gene expression: lessons from
the MazEF toxin–antitoxin system. Current Genetics. 65(1), 133–138.'
mla: 'Nikolic, Nela. “Autoregulation of Bacterial Gene Expression: Lessons from
the MazEF Toxin–Antitoxin System.” Current Genetics, vol. 65, no. 1, Springer,
2019, pp. 133–38, doi:10.1007/s00294-018-0879-8.'
short: N. Nikolic, Current Genetics 65 (2019) 133–138.
date_created: 2018-12-11T11:44:50Z
date_published: 2019-02-01T00:00:00Z
date_updated: 2023-09-08T13:23:42Z
day: '01'
ddc:
- '570'
department:
- _id: CaGu
doi: 10.1007/s00294-018-0879-8
ec_funded: 1
external_id:
isi:
- '000456958800017'
file:
- access_level: open_access
checksum: 6779708b0b632a1a6ed28c56f5161142
content_type: application/pdf
creator: dernst
date_created: 2019-02-06T07:50:58Z
date_updated: 2020-07-14T12:44:47Z
file_id: '5930'
file_name: 2019_CurrentGenetics_Nikolic.pdf
file_size: 776399
relation: main_file
file_date_updated: 2020-07-14T12:44:47Z
has_accepted_license: '1'
intvolume: ' 65'
isi: 1
issue: '1'
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
page: 133-138
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
publication: Current Genetics
publication_status: published
publisher: Springer
publist_id: '7785'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Autoregulation of bacterial gene expression: lessons from the MazEF toxin–antitoxin
system'
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: 65
year: '2019'
...
---
_id: '196'
abstract:
- lang: eng
text: 'The abelian sandpile serves as a model to study self-organized criticality,
a phenomenon occurring in biological, physical and social processes. The identity
of the abelian group is a fractal composed of self-similar patches, and its limit
is subject of extensive collaborative research. Here, we analyze the evolution
of the sandpile identity under harmonic fields of different orders. We show that
this evolution corresponds to periodic cycles through the abelian group characterized
by the smooth transformation and apparent conservation of the patches constituting
the identity. The dynamics induced by second and third order harmonics resemble
smooth stretchings, respectively translations, of the identity, while the ones
induced by fourth order harmonics resemble magnifications and rotations. Starting
with order three, the dynamics pass through extended regions of seemingly random
configurations which spontaneously reassemble into accentuated patterns. We show
that the space of harmonic functions projects to the extended analogue of the
sandpile group, thus providing a set of universal coordinates identifying configurations
between different domains. Since the original sandpile group is a subgroup of
the extended one, this directly implies that it admits a natural renormalization.
Furthermore, we show that the harmonic fields can be induced by simple Markov
processes, and that the corresponding stochastic dynamics show remarkable robustness
over hundreds of periods. Finally, we encode information into seemingly random
configurations, and decode this information with an algorithm requiring minimal
prior knowledge. Our results suggest that harmonic fields might split the sandpile
group into sub-sets showing different critical coefficients, and that it might
be possible to extend the fractal structure of the identity beyond the boundaries
of its domain. '
acknowledgement: "M.L. is grateful to the members of the C Guet and G Tkacik groups
for valuable comments and support. M.S. is grateful to Nikita Kalinin for inspiring
communications.\r\n"
article_processing_charge: No
article_type: original
author:
- first_name: Moritz
full_name: Lang, Moritz
id: 29E0800A-F248-11E8-B48F-1D18A9856A87
last_name: Lang
- first_name: Mikhail
full_name: Shkolnikov, Mikhail
id: 35084A62-F248-11E8-B48F-1D18A9856A87
last_name: Shkolnikov
orcid: 0000-0002-4310-178X
citation:
ama: Lang M, Shkolnikov M. Harmonic dynamics of the Abelian sandpile. Proceedings
of the National Academy of Sciences. 2019;116(8):2821-2830. doi:10.1073/pnas.1812015116
apa: Lang, M., & Shkolnikov, M. (2019). Harmonic dynamics of the Abelian sandpile.
Proceedings of the National Academy of Sciences. National Academy of Sciences.
https://doi.org/10.1073/pnas.1812015116
chicago: Lang, Moritz, and Mikhail Shkolnikov. “Harmonic Dynamics of the Abelian
Sandpile.” Proceedings of the National Academy of Sciences. National Academy
of Sciences, 2019. https://doi.org/10.1073/pnas.1812015116.
ieee: M. Lang and M. Shkolnikov, “Harmonic dynamics of the Abelian sandpile,” Proceedings
of the National Academy of Sciences, vol. 116, no. 8. National Academy of
Sciences, pp. 2821–2830, 2019.
ista: Lang M, Shkolnikov M. 2019. Harmonic dynamics of the Abelian sandpile. Proceedings
of the National Academy of Sciences. 116(8), 2821–2830.
mla: Lang, Moritz, and Mikhail Shkolnikov. “Harmonic Dynamics of the Abelian Sandpile.”
Proceedings of the National Academy of Sciences, vol. 116, no. 8, National
Academy of Sciences, 2019, pp. 2821–30, doi:10.1073/pnas.1812015116.
short: M. Lang, M. Shkolnikov, Proceedings of the National Academy of Sciences 116
(2019) 2821–2830.
date_created: 2018-12-11T11:45:08Z
date_published: 2019-02-19T00:00:00Z
date_updated: 2023-09-11T14:09:34Z
day: '19'
department:
- _id: CaGu
- _id: GaTk
- _id: TaHa
doi: 10.1073/pnas.1812015116
external_id:
arxiv:
- '1806.10823'
isi:
- '000459074400013'
pmid:
- ' 30728300'
intvolume: ' 116'
isi: 1
issue: '8'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1073/pnas.1812015116
month: '02'
oa: 1
oa_version: Published Version
page: 2821-2830
pmid: 1
publication: Proceedings of the National Academy of Sciences
publication_identifier:
eissn:
- 1091-6490
publication_status: published
publisher: National Academy of Sciences
quality_controlled: '1'
related_material:
link:
- description: News on IST Webpage
relation: press_release
url: https://ist.ac.at/en/news/famous-sandpile-model-shown-to-move-like-a-traveling-sand-dune/
scopus_import: '1'
status: public
title: Harmonic dynamics of the Abelian sandpile
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 116
year: '2019'
...
---
_id: '6371'
abstract:
- lang: eng
text: "Decades of studies have revealed the mechanisms of gene regulation in molecular
detail. We make use of such well-described regulatory systems to explore how the
molecular mechanisms of protein-protein and protein-DNA interactions shape the
dynamics and evolution of gene regulation. \r\n\r\ni) We uncover how the biophysics
of protein-DNA binding determines the potential of regulatory networks to evolve
and adapt, which can be captured using a simple mathematical model. \r\nii) The
evolution of regulatory connections can lead to a significant amount of crosstalk
between binding proteins. We explore the effect of crosstalk on gene expression
from a target promoter, which seems to be modulated through binding competition
at non-specific DNA sites. \r\niii) We investigate how the very same biophysical
characteristics as in i) can generate significant fitness costs for cells through
global crosstalk, meaning non-specific DNA binding across the genomic background.
\r\niv) Binding competition between proteins at a target promoter is a prevailing
regulatory feature due to the prevalence of co-regulation at bacterial promoters.
However, the dynamics of these systems are not always straightforward to determine
even if the molecular mechanisms of regulation are known. A detailed model of
the biophysical interactions reveals that interference between the regulatory
proteins can constitute a new, generic form of system memory that records the
history of the input signals at the promoter. \r\n\r\nWe demonstrate how the biophysics
of protein-DNA binding can be harnessed to investigate the principles that shape
and ultimately limit cellular gene regulation. These results provide a basis for
studies of higher-level functionality, which arises from the underlying regulation.
\ \r\n"
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Claudia
full_name: Igler, Claudia
id: 46613666-F248-11E8-B48F-1D18A9856A87
last_name: Igler
citation:
ama: Igler C. On the nature of gene regulatory design - The biophysics of transcription
factor binding shapes gene regulation. 2019. doi:10.15479/AT:ISTA:6371
apa: Igler, C. (2019). On the nature of gene regulatory design - The biophysics
of transcription factor binding shapes gene regulation. Institute of Science
and Technology Austria. https://doi.org/10.15479/AT:ISTA:6371
chicago: Igler, Claudia. “On the Nature of Gene Regulatory Design - The Biophysics
of Transcription Factor Binding Shapes Gene Regulation.” Institute of Science
and Technology Austria, 2019. https://doi.org/10.15479/AT:ISTA:6371.
ieee: C. Igler, “On the nature of gene regulatory design - The biophysics of transcription
factor binding shapes gene regulation,” Institute of Science and Technology Austria,
2019.
ista: Igler C. 2019. On the nature of gene regulatory design - The biophysics of
transcription factor binding shapes gene regulation. Institute of Science and
Technology Austria.
mla: Igler, Claudia. On the Nature of Gene Regulatory Design - The Biophysics
of Transcription Factor Binding Shapes Gene Regulation. Institute of Science
and Technology Austria, 2019, doi:10.15479/AT:ISTA:6371.
short: C. Igler, On the Nature of Gene Regulatory Design - The Biophysics of Transcription
Factor Binding Shapes Gene Regulation, Institute of Science and Technology Austria,
2019.
date_created: 2019-05-03T11:55:51Z
date_published: 2019-05-03T00:00:00Z
date_updated: 2024-02-21T13:45:52Z
day: '03'
ddc:
- '576'
- '579'
degree_awarded: PhD
department:
- _id: CaGu
doi: 10.15479/AT:ISTA:6371
file:
- access_level: open_access
checksum: c0085d47c58c9cbcab1b0a783480f6da
content_type: application/pdf
creator: cigler
date_created: 2019-05-03T11:54:52Z
date_updated: 2021-02-11T11:17:13Z
embargo: 2020-05-02
file_id: '6373'
file_name: IglerClaudia_OntheNatureofGeneRegulatoryDesign.pdf
file_size: 12597663
relation: main_file
- access_level: closed
checksum: 2eac954de1c8bbf7e6fb35ed0221ae8c
content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
creator: cigler
date_created: 2019-05-03T11:54:54Z
date_updated: 2020-07-14T12:47:28Z
embargo_to: open_access
file_id: '6374'
file_name: IglerClaudia_OntheNatureofGeneRegulatoryDesign.docx
file_size: 34644426
relation: source_file
file_date_updated: 2021-02-11T11:17:13Z
has_accepted_license: '1'
keyword:
- gene regulation
- biophysics
- transcription factor binding
- bacteria
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: '152'
project:
- _id: 251EE76E-B435-11E9-9278-68D0E5697425
grant_number: '24573'
name: Design principles underlying genetic switch architecture (DOC Fellowship)
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '67'
relation: part_of_dissertation
status: public
- id: '5585'
relation: popular_science
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: On the nature of gene regulatory design - The biophysics of transcription factor
binding shapes gene regulation
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2019'
...
---
_id: '305'
abstract:
- lang: eng
text: The hanging-drop network (HDN) is a technology platform based on a completely
open microfluidic network at the bottom of an inverted, surface-patterned substrate.
The platform is predominantly used for the formation, culturing, and interaction
of self-assembled spherical microtissues (spheroids) under precisely controlled
flow conditions. Here, we describe design, fabrication, and operation of microfluidic
hanging-drop networks.
acknowledgement: This work was financially supported by FP7 of the EU through the
project “Body on a chip,” ICT-FET-296257, and the ERC Advanced Grant “NeuroCMOS”
(contract 267351), as well as by an individual Ambizione Grant 142440 from the Swiss
National Science Foundation for Olivier Frey. The research leading to these results
also 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]. We would like to thank Alexander Stettler, ETH Zurich for his expertise
and support in the cleanroom, and we acknowledge the Single Cell Unit of D-BSSE,
ETH Zurich for assistance in microscopy issues. M.L. is grateful to the members
of the Guet and Tkačik groups, IST Austria, for valuable comments and support.
alternative_title:
- MIMB
author:
- first_name: Patrick
full_name: Misun, Patrick
last_name: Misun
- first_name: Axel
full_name: Birchler, Axel
last_name: Birchler
- first_name: Moritz
full_name: Lang, Moritz
id: 29E0800A-F248-11E8-B48F-1D18A9856A87
last_name: Lang
- first_name: Andreas
full_name: Hierlemann, Andreas
last_name: Hierlemann
- first_name: Olivier
full_name: Frey, Olivier
last_name: Frey
citation:
ama: Misun P, Birchler A, Lang M, Hierlemann A, Frey O. Fabrication and operation
of microfluidic hanging drop networks. Methods in Molecular Biology. 2018;1771:183-202.
doi:10.1007/978-1-4939-7792-5_15
apa: Misun, P., Birchler, A., Lang, M., Hierlemann, A., & Frey, O. (2018). Fabrication
and operation of microfluidic hanging drop networks. Methods in Molecular Biology.
Springer. https://doi.org/10.1007/978-1-4939-7792-5_15
chicago: Misun, Patrick, Axel Birchler, Moritz Lang, Andreas Hierlemann, and Olivier
Frey. “Fabrication and Operation of Microfluidic Hanging Drop Networks.” Methods
in Molecular Biology. Springer, 2018. https://doi.org/10.1007/978-1-4939-7792-5_15.
ieee: P. Misun, A. Birchler, M. Lang, A. Hierlemann, and O. Frey, “Fabrication and
operation of microfluidic hanging drop networks,” Methods in Molecular Biology,
vol. 1771. Springer, pp. 183–202, 2018.
ista: Misun P, Birchler A, Lang M, Hierlemann A, Frey O. 2018. Fabrication and operation
of microfluidic hanging drop networks. Methods in Molecular Biology. 1771, 183–202.
mla: Misun, Patrick, et al. “Fabrication and Operation of Microfluidic Hanging Drop
Networks.” Methods in Molecular Biology, vol. 1771, Springer, 2018, pp.
183–202, doi:10.1007/978-1-4939-7792-5_15.
short: P. Misun, A. Birchler, M. Lang, A. Hierlemann, O. Frey, Methods in Molecular
Biology 1771 (2018) 183–202.
date_created: 2018-12-11T11:45:43Z
date_published: 2018-01-01T00:00:00Z
date_updated: 2021-01-12T07:40:42Z
day: '01'
department:
- _id: CaGu
- _id: GaTk
doi: 10.1007/978-1-4939-7792-5_15
ec_funded: 1
intvolume: ' 1771'
language:
- iso: eng
month: '01'
oa_version: None
page: 183 - 202
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
publication: Methods in Molecular Biology
publication_status: published
publisher: Springer
publist_id: '7574'
quality_controlled: '1'
scopus_import: 1
status: public
title: Fabrication and operation of microfluidic hanging drop networks
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 1771
year: '2018'
...
---
_id: '723'
abstract:
- lang: eng
text: Escaping local optima is one of the major obstacles to function optimisation.
Using the metaphor of a fitness landscape, local optima correspond to hills separated
by fitness valleys that have to be overcome. We define a class of fitness valleys
of tunable difficulty by considering their length, representing the Hamming path
between the two optima and their depth, the drop in fitness. For this function
class we present a runtime comparison between stochastic search algorithms using
different search strategies. The (1+1) EA is a simple and well-studied evolutionary
algorithm that has to jump across the valley to a point of higher fitness because
it does not accept worsening moves (elitism). In contrast, the Metropolis algorithm
and the Strong Selection Weak Mutation (SSWM) algorithm, a famous process in population
genetics, are both able to cross the fitness valley by accepting worsening moves.
We show that the runtime of the (1+1) EA depends critically on the length of the
valley while the runtimes of the non-elitist algorithms depend crucially on the
depth of the valley. Moreover, we show that both SSWM and Metropolis can also
efficiently optimise a rugged function consisting of consecutive valleys.
article_processing_charge: No
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: 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: Oliveto P, Paixao T, Pérez Heredia J, Sudholt D, Trubenova B. How to escape
local optima in black box optimisation when non elitism outperforms elitism. Algorithmica.
2018;80(5):1604-1633. doi:10.1007/s00453-017-0369-2
apa: Oliveto, P., Paixao, T., Pérez Heredia, J., Sudholt, D., & Trubenova, B.
(2018). How to escape local optima in black box optimisation when non elitism
outperforms elitism. Algorithmica. Springer. https://doi.org/10.1007/s00453-017-0369-2
chicago: Oliveto, Pietro, Tiago Paixao, Jorge Pérez Heredia, Dirk Sudholt, and Barbora
Trubenova. “How to Escape Local Optima in Black Box Optimisation When Non Elitism
Outperforms Elitism.” Algorithmica. Springer, 2018. https://doi.org/10.1007/s00453-017-0369-2.
ieee: P. Oliveto, T. Paixao, J. Pérez Heredia, D. Sudholt, and B. Trubenova, “How
to escape local optima in black box optimisation when non elitism outperforms
elitism,” Algorithmica, vol. 80, no. 5. Springer, pp. 1604–1633, 2018.
ista: Oliveto P, Paixao T, Pérez Heredia J, Sudholt D, Trubenova B. 2018. How to
escape local optima in black box optimisation when non elitism outperforms elitism.
Algorithmica. 80(5), 1604–1633.
mla: Oliveto, Pietro, et al. “How to Escape Local Optima in Black Box Optimisation
When Non Elitism Outperforms Elitism.” Algorithmica, vol. 80, no. 5, Springer,
2018, pp. 1604–33, doi:10.1007/s00453-017-0369-2.
short: P. Oliveto, T. Paixao, J. Pérez Heredia, D. Sudholt, B. Trubenova, Algorithmica
80 (2018) 1604–1633.
date_created: 2018-12-11T11:48:09Z
date_published: 2018-05-01T00:00:00Z
date_updated: 2023-09-11T14:11:35Z
day: '01'
ddc:
- '576'
department:
- _id: NiBa
- _id: CaGu
doi: 10.1007/s00453-017-0369-2
ec_funded: 1
external_id:
isi:
- '000428239300010'
file:
- access_level: open_access
checksum: 7d92f5d7be81e387edeec4f06442791c
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:08:14Z
date_updated: 2020-07-14T12:47:54Z
file_id: '4674'
file_name: IST-2018-1014-v1+1_2018_Paixao_Escape.pdf
file_size: 691245
relation: main_file
file_date_updated: 2020-07-14T12:47:54Z
has_accepted_license: '1'
intvolume: ' 80'
isi: 1
issue: '5'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: 1604 - 1633
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_status: published
publisher: Springer
publist_id: '6957'
pubrep_id: '1014'
quality_controlled: '1'
scopus_import: '1'
status: public
title: How to escape local optima in black box optimisation when non elitism outperforms
elitism
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: 80
year: '2018'
...
---
_id: '503'
abstract:
- lang: eng
text: Buffers are essential for diluting bacterial cultures for flow cytometry analysis
in order to study bacterial physiology and gene expression parameters based on
fluorescence signals. Using a variety of constitutively expressed fluorescent
proteins in Escherichia coli K-12 strain MG1655, we found strong artifactual changes
in fluorescence levels after dilution into the commonly used flow cytometry buffer
phosphate-buffered saline (PBS) and two other buffer solutions, Tris-HCl and M9
salts. These changes appeared very rapidly after dilution, and were linked to
increased membrane permeability and loss in cell viability. We observed buffer-related
effects in several different E. coli strains, K-12, C and W, but not E. coli B,
which can be partially explained by differences in lipopolysaccharide (LPS) and
outer membrane composition. Supplementing the buffers with divalent cations responsible
for outer membrane stability, Mg2+ and Ca2+, preserved fluorescence signals, membrane
integrity and viability of E. coli. Thus, stabilizing the bacterial outer membrane
is essential for precise and unbiased measurements of fluorescence parameters
using flow cytometry.
acknowledged_ssus:
- _id: Bio
acknowledgement: "We thank R Chait and M Lagator for sharing Bacillus subtilis CR_Y1
and pZS*_2R-cIPtet-Venus-Prm, respectively. We are grateful to T Pilizota and all
members of the Guet lab for critically reading the manuscript. We also thank the
Bioimaging facility at IST Austria for assistance using the FACSAria III system.\r\n\r\n"
article_processing_charge: No
author:
- first_name: Kathrin
full_name: Tomasek, Kathrin
id: 3AEC8556-F248-11E8-B48F-1D18A9856A87
last_name: Tomasek
orcid: 0000-0003-3768-877X
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- 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: Tomasek K, Bergmiller T, Guet CC. Lack of cations in flow cytometry buffers
affect fluorescence signals by reducing membrane stability and viability of Escherichia
coli strains. Journal of Biotechnology. 2018;268:40-52. doi:10.1016/j.jbiotec.2018.01.008
apa: Tomasek, K., Bergmiller, T., & Guet, C. C. (2018). Lack of cations in flow
cytometry buffers affect fluorescence signals by reducing membrane stability and
viability of Escherichia coli strains. Journal of Biotechnology. Elsevier.
https://doi.org/10.1016/j.jbiotec.2018.01.008
chicago: Tomasek, Kathrin, Tobias Bergmiller, and Calin C Guet. “Lack of Cations
in Flow Cytometry Buffers Affect Fluorescence Signals by Reducing Membrane Stability
and Viability of Escherichia Coli Strains.” Journal of Biotechnology. Elsevier,
2018. https://doi.org/10.1016/j.jbiotec.2018.01.008.
ieee: K. Tomasek, T. Bergmiller, and C. C. Guet, “Lack of cations in flow cytometry
buffers affect fluorescence signals by reducing membrane stability and viability
of Escherichia coli strains,” Journal of Biotechnology, vol. 268. Elsevier,
pp. 40–52, 2018.
ista: Tomasek K, Bergmiller T, Guet CC. 2018. Lack of cations in flow cytometry
buffers affect fluorescence signals by reducing membrane stability and viability
of Escherichia coli strains. Journal of Biotechnology. 268, 40–52.
mla: Tomasek, Kathrin, et al. “Lack of Cations in Flow Cytometry Buffers Affect
Fluorescence Signals by Reducing Membrane Stability and Viability of Escherichia
Coli Strains.” Journal of Biotechnology, vol. 268, Elsevier, 2018, pp.
40–52, doi:10.1016/j.jbiotec.2018.01.008.
short: K. Tomasek, T. Bergmiller, C.C. Guet, Journal of Biotechnology 268 (2018)
40–52.
date_created: 2018-12-11T11:46:50Z
date_published: 2018-02-20T00:00:00Z
date_updated: 2023-09-13T08:24:51Z
day: '20'
department:
- _id: CaGu
doi: 10.1016/j.jbiotec.2018.01.008
external_id:
isi:
- '000425715100006'
intvolume: ' 268'
isi: 1
language:
- iso: eng
month: '02'
oa_version: None
page: 40 - 52
publication: Journal of Biotechnology
publication_status: published
publisher: Elsevier
publist_id: '7317'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Lack of cations in flow cytometry buffers affect fluorescence signals by reducing
membrane stability and viability of Escherichia coli strains
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 268
year: '2018'
...
---
_id: '82'
abstract:
- lang: eng
text: In experimental cultures, when bacteria are mixed with lytic (virulent) bacteriophage,
bacterial cells resistant to the phage commonly emerge and become the dominant
population of bacteria. Following the ascent of resistant mutants, the densities
of bacteria in these simple communities become limited by resources rather than
the phage. Despite the evolution of resistant hosts, upon which the phage cannot
replicate, the lytic phage population is most commonly maintained in an apparently
stable state with the resistant bacteria. Several mechanisms have been put forward
to account for this result. Here we report the results of population dynamic/evolution
experiments with a virulent mutant of phage Lambda, λVIR, and Escherichia coli
in serial transfer cultures. We show that, following the ascent of λVIR-resistant
bacteria, λVIRis maintained in the majority of cases in maltose-limited minimal
media and in all cases in nutrient-rich broth. Using mathematical models and experiments,
we show that the dominant mechanism responsible for maintenance of λVIRin these
resource-limited populations dominated by resistant E. coli is a high rate of
either phenotypic or genetic transition from resistance to susceptibility—a hitherto
undemonstrated mechanism we term "leaky resistance." We discuss the
implications of leaky resistance to our understanding of the conditions for the
maintenance of phage in populations of bacteria—their “existence conditions.”.
article_number: '2005971'
article_processing_charge: Yes
author:
- first_name: Waqas
full_name: Chaudhry, Waqas
last_name: Chaudhry
- first_name: Maros
full_name: Pleska, Maros
id: 4569785E-F248-11E8-B48F-1D18A9856A87
last_name: Pleska
orcid: 0000-0001-7460-7479
- first_name: Nilang
full_name: Shah, Nilang
last_name: Shah
- first_name: Howard
full_name: Weiss, Howard
last_name: Weiss
- first_name: Ingrid
full_name: Mccall, Ingrid
last_name: Mccall
- first_name: Justin
full_name: Meyer, Justin
last_name: Meyer
- first_name: Animesh
full_name: Gupta, Animesh
last_name: Gupta
- 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: Bruce
full_name: Levin, Bruce
last_name: Levin
citation:
ama: Chaudhry W, Pleska M, Shah N, et al. Leaky resistance and the conditions for
the existence of lytic bacteriophage. PLoS Biology. 2018;16(8). doi:10.1371/journal.pbio.2005971
apa: Chaudhry, W., Pleska, M., Shah, N., Weiss, H., Mccall, I., Meyer, J., … Levin,
B. (2018). Leaky resistance and the conditions for the existence of lytic bacteriophage.
PLoS Biology. Public Library of Science. https://doi.org/10.1371/journal.pbio.2005971
chicago: Chaudhry, Waqas, Maros Pleska, Nilang Shah, Howard Weiss, Ingrid Mccall,
Justin Meyer, Animesh Gupta, Calin C Guet, and Bruce Levin. “Leaky Resistance
and the Conditions for the Existence of Lytic Bacteriophage.” PLoS Biology.
Public Library of Science, 2018. https://doi.org/10.1371/journal.pbio.2005971.
ieee: W. Chaudhry et al., “Leaky resistance and the conditions for the existence
of lytic bacteriophage,” PLoS Biology, vol. 16, no. 8. Public Library of
Science, 2018.
ista: Chaudhry W, Pleska M, Shah N, Weiss H, Mccall I, Meyer J, Gupta A, Guet CC,
Levin B. 2018. Leaky resistance and the conditions for the existence of lytic
bacteriophage. PLoS Biology. 16(8), 2005971.
mla: Chaudhry, Waqas, et al. “Leaky Resistance and the Conditions for the Existence
of Lytic Bacteriophage.” PLoS Biology, vol. 16, no. 8, 2005971, Public
Library of Science, 2018, doi:10.1371/journal.pbio.2005971.
short: W. Chaudhry, M. Pleska, N. Shah, H. Weiss, I. Mccall, J. Meyer, A. Gupta,
C.C. Guet, B. Levin, PLoS Biology 16 (2018).
date_created: 2018-12-11T11:44:32Z
date_published: 2018-08-16T00:00:00Z
date_updated: 2023-09-13T08:45:41Z
day: '16'
ddc:
- '570'
department:
- _id: CaGu
doi: 10.1371/journal.pbio.2005971
external_id:
isi:
- '000443383300024'
file:
- access_level: open_access
checksum: 527076f78265cd4ea192cd1569851587
content_type: application/pdf
creator: dernst
date_created: 2018-12-17T12:55:31Z
date_updated: 2020-07-14T12:48:10Z
file_id: '5706'
file_name: 2018_Plos_Chaudhry.pdf
file_size: 4007095
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has_accepted_license: '1'
intvolume: ' 16'
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issue: '8'
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
publication: PLoS Biology
publication_status: published
publisher: Public Library of Science
publist_id: '7972'
quality_controlled: '1'
related_material:
record:
- id: '9810'
relation: research_data
status: public
scopus_import: '1'
status: public
title: Leaky resistance and the conditions for the existence of lytic bacteriophage
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: 16
year: '2018'
...
---
_id: '9810'
article_processing_charge: No
author:
- first_name: Waqas
full_name: Chaudhry, Waqas
last_name: Chaudhry
- first_name: Maros
full_name: Pleska, Maros
id: 4569785E-F248-11E8-B48F-1D18A9856A87
last_name: Pleska
orcid: 0000-0001-7460-7479
- first_name: Nilang
full_name: Shah, Nilang
last_name: Shah
- first_name: Howard
full_name: Weiss, Howard
last_name: Weiss
- first_name: Ingrid
full_name: Mccall, Ingrid
last_name: Mccall
- first_name: Justin
full_name: Meyer, Justin
last_name: Meyer
- first_name: Animesh
full_name: Gupta, Animesh
last_name: Gupta
- 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: Bruce
full_name: Levin, Bruce
last_name: Levin
citation:
ama: Chaudhry W, Pleska M, Shah N, et al. Numerical data used in figures. 2018.
doi:10.1371/journal.pbio.2005971.s008
apa: Chaudhry, W., Pleska, M., Shah, N., Weiss, H., Mccall, I., Meyer, J., … Levin,
B. (2018). Numerical data used in figures. Public Library of Science. https://doi.org/10.1371/journal.pbio.2005971.s008
chicago: Chaudhry, Waqas, Maros Pleska, Nilang Shah, Howard Weiss, Ingrid Mccall,
Justin Meyer, Animesh Gupta, Calin C Guet, and Bruce Levin. “Numerical Data Used
in Figures.” Public Library of Science, 2018. https://doi.org/10.1371/journal.pbio.2005971.s008.
ieee: W. Chaudhry et al., “Numerical data used in figures.” Public Library
of Science, 2018.
ista: Chaudhry W, Pleska M, Shah N, Weiss H, Mccall I, Meyer J, Gupta A, Guet CC,
Levin B. 2018. Numerical data used in figures, Public Library of Science, 10.1371/journal.pbio.2005971.s008.
mla: Chaudhry, Waqas, et al. Numerical Data Used in Figures. Public Library
of Science, 2018, doi:10.1371/journal.pbio.2005971.s008.
short: W. Chaudhry, M. Pleska, N. Shah, H. Weiss, I. Mccall, J. Meyer, A. Gupta,
C.C. Guet, B. Levin, (2018).
date_created: 2021-08-06T12:43:44Z
date_published: 2018-08-16T00:00:00Z
date_updated: 2023-09-13T08:45:41Z
day: '16'
department:
- _id: CaGu
doi: 10.1371/journal.pbio.2005971.s008
month: '08'
oa_version: Published Version
publisher: Public Library of Science
related_material:
record:
- id: '82'
relation: used_in_publication
status: public
status: public
title: Numerical data used in figures
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2018'
...
---
_id: '457'
abstract:
- lang: eng
text: Temperate bacteriophages integrate in bacterial genomes as prophages and represent
an important source of genetic variation for bacterial evolution, frequently transmitting
fitness-augmenting genes such as toxins responsible for virulence of major pathogens.
However, only a fraction of bacteriophage infections are lysogenic and lead to
prophage acquisition, whereas the majority are lytic and kill the infected bacteria.
Unless able to discriminate lytic from lysogenic infections, mechanisms of immunity
to bacteriophages are expected to act as a double-edged sword and increase the
odds of survival at the cost of depriving bacteria of potentially beneficial prophages.
We show that although restriction-modification systems as mechanisms of innate
immunity prevent both lytic and lysogenic infections indiscriminately in individual
bacteria, they increase the number of prophage-acquiring individuals at the population
level. We find that this counterintuitive result is a consequence of phage-host
population dynamics, in which restriction-modification systems delay infection
onset until bacteria reach densities at which the probability of lysogeny increases.
These results underscore the importance of population-level dynamics as a key
factor modulating costs and benefits of immunity to temperate bacteriophages
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
- first_name: Moritz
full_name: Lang, Moritz
id: 29E0800A-F248-11E8-B48F-1D18A9856A87
last_name: Lang
- first_name: Dominik
full_name: Refardt, Dominik
last_name: Refardt
- first_name: Bruce
full_name: Levin, Bruce
last_name: Levin
- 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, Lang M, Refardt D, Levin B, Guet CC. Phage-host population dynamics
promotes prophage acquisition in bacteria with innate immunity. Nature Ecology
and Evolution. 2018;2(2):359-366. doi:10.1038/s41559-017-0424-z
apa: Pleska, M., Lang, M., Refardt, D., Levin, B., & Guet, C. C. (2018). Phage-host
population dynamics promotes prophage acquisition in bacteria with innate immunity.
Nature Ecology and Evolution. Springer Nature. https://doi.org/10.1038/s41559-017-0424-z
chicago: Pleska, Maros, Moritz Lang, Dominik Refardt, Bruce Levin, and Calin C Guet.
“Phage-Host Population Dynamics Promotes Prophage Acquisition in Bacteria with
Innate Immunity.” Nature Ecology and Evolution. Springer Nature, 2018.
https://doi.org/10.1038/s41559-017-0424-z.
ieee: M. Pleska, M. Lang, D. Refardt, B. Levin, and C. C. Guet, “Phage-host population
dynamics promotes prophage acquisition in bacteria with innate immunity,” Nature
Ecology and Evolution, vol. 2, no. 2. Springer Nature, pp. 359–366, 2018.
ista: Pleska M, Lang M, Refardt D, Levin B, Guet CC. 2018. Phage-host population
dynamics promotes prophage acquisition in bacteria with innate immunity. Nature
Ecology and Evolution. 2(2), 359–366.
mla: Pleska, Maros, et al. “Phage-Host Population Dynamics Promotes Prophage Acquisition
in Bacteria with Innate Immunity.” Nature Ecology and Evolution, vol. 2,
no. 2, Springer Nature, 2018, pp. 359–66, doi:10.1038/s41559-017-0424-z.
short: M. Pleska, M. Lang, D. Refardt, B. Levin, C.C. Guet, Nature Ecology and Evolution
2 (2018) 359–366.
date_created: 2018-12-11T11:46:35Z
date_published: 2018-02-01T00:00:00Z
date_updated: 2023-09-15T12:04:57Z
day: '01'
department:
- _id: CaGu
- _id: GaTk
doi: 10.1038/s41559-017-0424-z
ec_funded: 1
external_id:
isi:
- '000426516400027'
intvolume: ' 2'
isi: 1
issue: '2'
language:
- iso: eng
month: '02'
oa_version: None
page: 359 - 366
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _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: Nature Ecology and Evolution
publication_status: published
publisher: Springer Nature
publist_id: '7364'
quality_controlled: '1'
related_material:
record:
- id: '202'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Phage-host population dynamics promotes prophage acquisition in bacteria with
innate immunity
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 2
year: '2018'
...
---
_id: '5984'
abstract:
- lang: eng
text: G-protein-coupled receptors (GPCRs) form the largest receptor family, relay
environmental stimuli to changes in cell behavior and represent prime drug targets.
Many GPCRs are classified as orphan receptors because of the limited knowledge
on their ligands and coupling to cellular signaling machineries. Here, we engineer
a library of 63 chimeric receptors that contain the signaling domains of human
orphan and understudied GPCRs functionally linked to the light-sensing domain
of rhodopsin. Upon stimulation with visible light, we identify activation of canonical
cell signaling pathways, including cAMP-, Ca2+-, MAPK/ERK-, and Rho-dependent
pathways, downstream of the engineered receptors. For the human pseudogene GPR33,
we resurrect a signaling function that supports its hypothesized role as a pathogen
entry site. These results demonstrate that substituting unknown chemical activators
with a light switch can reveal information about protein function and provide
an optically controlled protein library for exploring the physiology and therapeutic
potential of understudied GPCRs.
article_number: '1950'
article_processing_charge: No
author:
- first_name: Maurizio
full_name: Morri, Maurizio
id: 4863116E-F248-11E8-B48F-1D18A9856A87
last_name: Morri
- first_name: Inmaculada
full_name: Sanchez-Romero, Inmaculada
id: 3D9C5D30-F248-11E8-B48F-1D18A9856A87
last_name: Sanchez-Romero
- first_name: Alexandra-Madelaine
full_name: Tichy, Alexandra-Madelaine
id: 29D8BB2C-F248-11E8-B48F-1D18A9856A87
last_name: Tichy
- first_name: Stephanie
full_name: Kainrath, Stephanie
id: 32CFBA64-F248-11E8-B48F-1D18A9856A87
last_name: Kainrath
- first_name: Elliot J.
full_name: Gerrard, Elliot J.
last_name: Gerrard
- first_name: Priscila
full_name: Hirschfeld, Priscila
id: 435ACB3A-F248-11E8-B48F-1D18A9856A87
last_name: Hirschfeld
- first_name: Jan
full_name: Schwarz, Jan
id: 346C1EC6-F248-11E8-B48F-1D18A9856A87
last_name: Schwarz
- 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: Morri M, Sanchez-Romero I, Tichy A-M, et al. Optical functionalization of human
class A orphan G-protein-coupled receptors. Nature Communications. 2018;9(1).
doi:10.1038/s41467-018-04342-1
apa: Morri, M., Sanchez-Romero, I., Tichy, A.-M., Kainrath, S., Gerrard, E. J.,
Hirschfeld, P., … Janovjak, H. L. (2018). Optical functionalization of human class
A orphan G-protein-coupled receptors. Nature Communications. Springer Nature.
https://doi.org/10.1038/s41467-018-04342-1
chicago: Morri, Maurizio, Inmaculada Sanchez-Romero, Alexandra-Madelaine Tichy,
Stephanie Kainrath, Elliot J. Gerrard, Priscila Hirschfeld, Jan Schwarz, and Harald
L Janovjak. “Optical Functionalization of Human Class A Orphan G-Protein-Coupled
Receptors.” Nature Communications. Springer Nature, 2018. https://doi.org/10.1038/s41467-018-04342-1.
ieee: M. Morri et al., “Optical functionalization of human class A orphan
G-protein-coupled receptors,” Nature Communications, vol. 9, no. 1. Springer
Nature, 2018.
ista: Morri M, Sanchez-Romero I, Tichy A-M, Kainrath S, Gerrard EJ, Hirschfeld P,
Schwarz J, Janovjak HL. 2018. Optical functionalization of human class A orphan
G-protein-coupled receptors. Nature Communications. 9(1), 1950.
mla: Morri, Maurizio, et al. “Optical Functionalization of Human Class A Orphan
G-Protein-Coupled Receptors.” Nature Communications, vol. 9, no. 1, 1950,
Springer Nature, 2018, doi:10.1038/s41467-018-04342-1.
short: M. Morri, I. Sanchez-Romero, A.-M. Tichy, S. Kainrath, E.J. Gerrard, P. Hirschfeld,
J. Schwarz, H.L. Janovjak, Nature Communications 9 (2018).
date_created: 2019-02-14T10:50:24Z
date_published: 2018-12-01T00:00:00Z
date_updated: 2023-09-19T14:29:32Z
day: '01'
ddc:
- '570'
department:
- _id: HaJa
- _id: CaGu
- _id: MiSi
doi: 10.1038/s41467-018-04342-1
ec_funded: 1
external_id:
isi:
- '000432280000006'
file:
- access_level: open_access
checksum: 8325fcc194264af4749e662a73bf66b5
content_type: application/pdf
creator: kschuh
date_created: 2019-02-14T10:58:29Z
date_updated: 2020-07-14T12:47:14Z
file_id: '5985'
file_name: 2018_Springer_Morri.pdf
file_size: 1349914
relation: main_file
file_date_updated: 2020-07-14T12:47:14Z
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
issue: '1'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
project:
- _id: 25548C20-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '303564'
name: Microbial Ion Channels for Synthetic Neurobiology
- _id: 255A6082-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: W1232-B24
name: Molecular Drug Targets
publication: Nature Communications
publication_identifier:
issn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Optical functionalization of human class A orphan G-protein-coupled receptors
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: 9
year: '2018'
...
---
_id: '19'
abstract:
- lang: eng
text: Bacteria regulate genes to survive antibiotic stress, but regulation can be
far from perfect. When regulation is not optimal, mutations that change gene expression
can contribute to antibiotic resistance. It is not systematically understood to
what extent natural gene regulation is or is not optimal for distinct antibiotics,
and how changes in expression of specific genes quantitatively affect antibiotic
resistance. Here we discover a simple quantitative relation between fitness, gene
expression, and antibiotic potency, which rationalizes our observation that a
multitude of genes and even innate antibiotic defense mechanisms have expression
that is critically nonoptimal under antibiotic treatment. First, we developed
a pooled-strain drug-diffusion assay and screened Escherichia coli overexpression
and knockout libraries, finding that resistance to a range of 31 antibiotics could
result from changing expression of a large and functionally diverse set of genes,
in a primarily but not exclusively drug-specific manner. Second, by synthetically
controlling the expression of single-drug and multidrug resistance genes, we observed
that their fitness-expression functions changed dramatically under antibiotic
treatment in accordance with a log-sensitivity relation. Thus, because many genes
are nonoptimally expressed under antibiotic treatment, many regulatory mutations
can contribute to resistance by altering expression and by activating latent defenses.
article_processing_charge: No
article_type: original
author:
- first_name: Adam
full_name: Palmer, Adam
last_name: Palmer
- 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: Roy
full_name: Kishony, Roy
last_name: Kishony
citation:
ama: Palmer A, Chait RP, Kishony R. Nonoptimal gene expression creates latent potential
for antibiotic resistance. Molecular Biology and Evolution. 2018;35(11):2669-2684.
doi:10.1093/molbev/msy163
apa: Palmer, A., Chait, R. P., & Kishony, R. (2018). Nonoptimal gene expression
creates latent potential for antibiotic resistance. Molecular Biology and Evolution.
Oxford University Press. https://doi.org/10.1093/molbev/msy163
chicago: Palmer, Adam, Remy P Chait, and Roy Kishony. “Nonoptimal Gene Expression
Creates Latent Potential for Antibiotic Resistance.” Molecular Biology and
Evolution. Oxford University Press, 2018. https://doi.org/10.1093/molbev/msy163.
ieee: A. Palmer, R. P. Chait, and R. Kishony, “Nonoptimal gene expression creates
latent potential for antibiotic resistance,” Molecular Biology and Evolution,
vol. 35, no. 11. Oxford University Press, pp. 2669–2684, 2018.
ista: Palmer A, Chait RP, Kishony R. 2018. Nonoptimal gene expression creates latent
potential for antibiotic resistance. Molecular Biology and Evolution. 35(11),
2669–2684.
mla: Palmer, Adam, et al. “Nonoptimal Gene Expression Creates Latent Potential for
Antibiotic Resistance.” Molecular Biology and Evolution, vol. 35, no. 11,
Oxford University Press, 2018, pp. 2669–84, doi:10.1093/molbev/msy163.
short: A. Palmer, R.P. Chait, R. Kishony, Molecular Biology and Evolution 35 (2018)
2669–2684.
date_created: 2018-12-11T11:44:11Z
date_published: 2018-08-28T00:00:00Z
date_updated: 2023-10-17T11:51:06Z
day: '28'
department:
- _id: CaGu
- _id: GaTk
doi: 10.1093/molbev/msy163
external_id:
isi:
- '000452567200006'
pmid:
- '30169679'
intvolume: ' 35'
isi: 1
issue: '11'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pubmed/30169679
month: '08'
oa: 1
oa_version: Submitted Version
page: 2669 - 2684
pmid: 1
publication: Molecular Biology and Evolution
publication_identifier:
issn:
- 0737-4038
publication_status: published
publisher: Oxford University Press
publist_id: '8036'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nonoptimal gene expression creates latent potential for antibiotic resistance
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 35
year: '2018'
...