---
_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).
corr_author: '1'
date_created: 2018-12-11T11:47:11Z
date_published: 2017-12-01T00:00:00Z
date_updated: 2026-06-18T18:54:20Z
day: '01'
ddc:
- '570'
department:
- _id: CaGu
doi: 10.1098/rsbl.2017.0646
external_id:
isi:
- '000418695400012'
pmid:
- '29237814'
fulldoi: https://doi.org/10.1098/rsbl.2017.0646
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isi: 1
issue: '12'
language:
- iso: eng
main_file_link:
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url: https://doi.org/10.1098/rsbl.2017.0646
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
- _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
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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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: '570'
abstract:
- lang: eng
text: 'Most phenotypes are determined by molecular systems composed of specifically
interacting molecules. However, unlike for individual components, little is known
about the distributions of mutational effects of molecular systems as a whole.
We ask how the distribution of mutational effects of a transcriptional regulatory
system differs from the distributions of its components, by first independently,
and then simultaneously, mutating a transcription factor and the associated promoter
it represses. We find that the system distribution exhibits increased phenotypic
variation compared to individual component distributions - an effect arising from
intermolecular epistasis between the transcription factor and its DNA-binding
site. In large part, this epistasis can be qualitatively attributed to the structure
of the transcriptional regulatory system and could therefore be a common feature
in prokaryotes. Counter-intuitively, intermolecular epistasis can alleviate the
constraints of individual components, thereby increasing phenotypic variation
that selection could act on and facilitating adaptive evolution. '
article_number: e28921
article_processing_charge: No
author:
- first_name: Mato
full_name: Lagator, Mato
id: 345D25EC-F248-11E8-B48F-1D18A9856A87
last_name: Lagator
- first_name: Srdjan
full_name: Sarikas, Srdjan
id: 35F0286E-F248-11E8-B48F-1D18A9856A87
last_name: Sarikas
- first_name: Hande
full_name: Acar, Hande
id: 2DDF136A-F248-11E8-B48F-1D18A9856A87
last_name: Acar
orcid: 0000-0003-1986-9753
- first_name: Jonathan P
full_name: Bollback, Jonathan P
id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
last_name: Bollback
orcid: 0000-0002-4624-4612
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Lagator M, Sarikas S, Acar H, Bollback JP, Guet CC. Regulatory network structure
determines patterns of intermolecular epistasis. eLife. 2017;6. doi:10.7554/eLife.28921
apa: Lagator, M., Sarikas, S., Acar, H., Bollback, J. P., & Guet, C. C. (2017).
Regulatory network structure determines patterns of intermolecular epistasis.
ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.28921
chicago: Lagator, Mato, Srdjan Sarikas, Hande Acar, Jonathan P Bollback, and Calin
C Guet. “Regulatory Network Structure Determines Patterns of Intermolecular Epistasis.”
ELife. eLife Sciences Publications, 2017. https://doi.org/10.7554/eLife.28921.
ieee: M. Lagator, S. Sarikas, H. Acar, J. P. Bollback, and C. C. Guet, “Regulatory
network structure determines patterns of intermolecular epistasis,” eLife,
vol. 6. eLife Sciences Publications, 2017.
ista: Lagator M, Sarikas S, Acar H, Bollback JP, Guet CC. 2017. Regulatory network
structure determines patterns of intermolecular epistasis. eLife. 6, e28921.
mla: Lagator, Mato, et al. “Regulatory Network Structure Determines Patterns of
Intermolecular Epistasis.” ELife, vol. 6, e28921, eLife Sciences Publications,
2017, doi:10.7554/eLife.28921.
short: M. Lagator, S. Sarikas, H. Acar, J.P. Bollback, C.C. Guet, ELife 6 (2017).
corr_author: '1'
date_created: 2018-12-11T11:47:14Z
date_published: 2017-11-13T00:00:00Z
date_updated: 2025-09-11T07:40:30Z
day: '13'
ddc:
- '576'
department:
- _id: CaGu
- _id: JoBo
- _id: NiBa
doi: 10.7554/eLife.28921
ec_funded: 1
external_id:
isi:
- '000425868200001'
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checksum: 273ab17f33305e4eaafd911ff88e7c5b
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creator: system
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content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:43Z
date_updated: 2020-07-14T12:47:10Z
file_id: '5097'
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file_size: 1953221
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fulldoi: https://doi.org/10.7554/eLife.28921
has_accepted_license: '1'
intvolume: ' 6'
isi: 1
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 2578D616-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '648440'
name: Selective Barriers to Horizontal Gene Transfer
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
publist_id: '7244'
pubrep_id: '918'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Regulatory network structure determines patterns of intermolecular epistasis
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 6
year: '2017'
...
---
_id: '613'
abstract:
- lang: eng
text: 'Bacteria in groups vary individually, and interact with other bacteria and
the environment to produce population-level patterns of gene expression. Investigating
such behavior in detail requires measuring and controlling populations at the
single-cell level alongside precisely specified interactions and environmental
characteristics. Here we present an automated, programmable platform that combines
image-based gene expression and growth measurements with on-line optogenetic expression
control for hundreds of individual Escherichia coli cells over days, in a dynamically
adjustable environment. This integrated platform broadly enables experiments that
bridge individual and population behaviors. We demonstrate: (i) population structuring
by independent closed-loop control of gene expression in many individual cells,
(ii) cell-cell variation control during antibiotic perturbation, (iii) hybrid
bio-digital circuits in single cells, and freely specifiable digital communication
between individual bacteria. These examples showcase the potential for real-time
integration of theoretical models with measurement and control of many individual
cells to investigate and engineer microbial population behavior.'
acknowledgement: We are grateful to M. Lang, H. Janovjak, M. Khammash, A. Milias-Argeitis,
M. Rullan, G. Batt, A. Bosma-Moody, Aryan, S. Leibler, and members of the Guet and
Tkačik groups for helpful discussion, comments, and suggestions. We thank A. Moglich,
T. Mathes, J. Tabor, and S. Schmidl for kind gifts of strains, and R. Hauschild,
B. Knep, M. Lang, T. Asenov, E. Papusheva, T. Menner, T. Adletzberger, and J. Merrin
for technical assistance. The research leading to these results has received funding
from the People Programme (Marie Curie Actions) of the European Union’s Seventh
Framework Programme (FP7/2007–2013) under REA grant agreement no. [291734]. (to
R.C. and J.R.), Austrian Science Fund grant FWF P28844 (to G.T.), and internal IST
Austria Interdisciplinary Project Support. J.R. acknowledges support from the Agence
Nationale de la Recherche (ANR) under Grant Nos. ANR-16-CE33-0018 (MEMIP), ANR-16-CE12-0025
(COGEX) and ANR-10-BINF-06-01 (ICEBERG).
article_number: '1535'
article_processing_charge: Yes (in subscription journal)
author:
- first_name: Remy P
full_name: Chait, Remy P
id: 3464AE84-F248-11E8-B48F-1D18A9856A87
last_name: Chait
orcid: 0000-0003-0876-3187
- first_name: Jakob
full_name: Ruess, Jakob
id: 4A245D00-F248-11E8-B48F-1D18A9856A87
last_name: Ruess
orcid: 0000-0003-1615-3282
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Gasper
full_name: Tkacik, Gasper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkacik
orcid: 0000-0002-6699-1455
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Chait RP, Ruess J, Bergmiller T, Tkačik G, Guet CC. Shaping bacterial population
behavior through computer interfaced control of individual cells. Nature Communications.
2017;8(1). doi:10.1038/s41467-017-01683-1
apa: Chait, R. P., Ruess, J., Bergmiller, T., Tkačik, G., & Guet, C. C. (2017).
Shaping bacterial population behavior through computer interfaced control of individual
cells. Nature Communications. Nature Publishing Group. https://doi.org/10.1038/s41467-017-01683-1
chicago: Chait, Remy P, Jakob Ruess, Tobias Bergmiller, Gašper Tkačik, and Calin
C Guet. “Shaping Bacterial Population Behavior through Computer Interfaced Control
of Individual Cells.” Nature Communications. Nature Publishing Group, 2017.
https://doi.org/10.1038/s41467-017-01683-1.
ieee: R. P. Chait, J. Ruess, T. Bergmiller, G. Tkačik, and C. C. Guet, “Shaping
bacterial population behavior through computer interfaced control of individual
cells,” Nature Communications, vol. 8, no. 1. Nature Publishing Group,
2017.
ista: Chait RP, Ruess J, Bergmiller T, Tkačik G, Guet CC. 2017. Shaping bacterial
population behavior through computer interfaced control of individual cells. Nature
Communications. 8(1), 1535.
mla: Chait, Remy P., et al. “Shaping Bacterial Population Behavior through Computer
Interfaced Control of Individual Cells.” Nature Communications, vol. 8,
no. 1, 1535, Nature Publishing Group, 2017, doi:10.1038/s41467-017-01683-1.
short: R.P. Chait, J. Ruess, T. Bergmiller, G. Tkačik, C.C. Guet, Nature Communications
8 (2017).
corr_author: '1'
date_created: 2018-12-11T11:47:30Z
date_published: 2017-12-01T00:00:00Z
date_updated: 2025-09-11T07:34:12Z
day: '01'
ddc:
- '576'
- '579'
department:
- _id: CaGu
- _id: GaTk
doi: 10.1038/s41467-017-01683-1
ec_funded: 1
external_id:
isi:
- '000415323000008'
file:
- access_level: open_access
checksum: 44bb5d0229926c23a9955d9fe0f9723f
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:16:05Z
date_updated: 2020-07-14T12:47:20Z
file_id: '5190'
file_name: IST-2017-911-v1+1_s41467-017-01683-1.pdf
file_size: 1951699
relation: main_file
file_date_updated: 2020-07-14T12:47:20Z
fulldoi: https://doi.org/10.1038/s41467-017-01683-1
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
issue: '1'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 254E9036-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P28844-B27
name: Biophysics of information processing in gene regulation
publication: Nature Communications
publication_identifier:
issn:
- 2041-1723
publication_status: published
publisher: Nature Publishing Group
publist_id: '7191'
pubrep_id: '911'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Shaping bacterial population behavior through computer interfaced control of
individual cells
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 8
year: '2017'
...
---
_id: '624'
abstract:
- lang: eng
text: Bacteria adapt to adverse environmental conditions by altering gene expression
patterns. Recently, a novel stress adaptation mechanism has been described that
allows Escherichia coli to alter gene expression at the post-transcriptional level.
The key player in this regulatory pathway is the endoribonuclease MazF, the toxin
component of the toxin-antitoxin module mazEF that is triggered by various stressful
conditions. In general, MazF degrades the majority of transcripts by cleaving
at ACA sites, which results in the retardation of bacterial growth. Furthermore,
MazF can process a small subset of mRNAs and render them leaderless by removing
their ribosome binding site. MazF concomitantly modifies ribosomes, making them
selective for the translation of leaderless mRNAs. In this study, we employed
fluorescent reporter-systems to investigate mazEF expression during stressful
conditions, and to infer consequences of the mRNA processing mediated by MazF
on gene expression at the single-cell level. Our results suggest that mazEF transcription
is maintained at low levels in single cells encountering adverse conditions, such
as antibiotic stress or amino acid starvation. Moreover, using the grcA mRNA as
a model for MazF-mediated mRNA processing, we found that MazF activation promotes
heterogeneity in the grcA reporter expression, resulting in a subpopulation of
cells with increased levels of GrcA reporter protein.
acknowledgement: 'Austrian Science Fund (FWF): M1697, P22249; Swiss National Science
Foundation (SNF): 145706; European Commission;FWF Special Research Program: RNA-REG
F43'
article_number: '3830'
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: Zrinka
full_name: Didara, Zrinka
last_name: Didara
- first_name: Isabella
full_name: Moll, Isabella
last_name: Moll
citation:
ama: Nikolic N, Didara Z, Moll I. MazF activation promotes translational heterogeneity
of the grcA mRNA in Escherichia coli populations. PeerJ. 2017;2017(9).
doi:10.7717/peerj.3830
apa: Nikolic, N., Didara, Z., & Moll, I. (2017). MazF activation promotes translational
heterogeneity of the grcA mRNA in Escherichia coli populations. PeerJ.
PeerJ. https://doi.org/10.7717/peerj.3830
chicago: Nikolic, Nela, Zrinka Didara, and Isabella Moll. “MazF Activation Promotes
Translational Heterogeneity of the GrcA MRNA in Escherichia Coli Populations.”
PeerJ. PeerJ, 2017. https://doi.org/10.7717/peerj.3830.
ieee: N. Nikolic, Z. Didara, and I. Moll, “MazF activation promotes translational
heterogeneity of the grcA mRNA in Escherichia coli populations,” PeerJ,
vol. 2017, no. 9. PeerJ, 2017.
ista: Nikolic N, Didara Z, Moll I. 2017. MazF activation promotes translational
heterogeneity of the grcA mRNA in Escherichia coli populations. PeerJ. 2017(9),
3830.
mla: Nikolic, Nela, et al. “MazF Activation Promotes Translational Heterogeneity
of the GrcA MRNA in Escherichia Coli Populations.” PeerJ, vol. 2017, no.
9, 3830, PeerJ, 2017, doi:10.7717/peerj.3830.
short: N. Nikolic, Z. Didara, I. Moll, PeerJ 2017 (2017).
corr_author: '1'
date_created: 2018-12-11T11:47:33Z
date_published: 2017-09-21T00:00:00Z
date_updated: 2025-09-11T07:30:06Z
day: '21'
ddc:
- '579'
department:
- _id: CaGu
doi: 10.7717/peerj.3830
external_id:
isi:
- '000411665900002'
file:
- access_level: open_access
checksum: 3d79ae6b6eabc90b0eaaed82ff3493b0
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:11:51Z
date_updated: 2020-07-14T12:47:24Z
file_id: '4908'
file_name: IST-2017-909-v1+1_peerj-3830.pdf
file_size: 682064
relation: main_file
file_date_updated: 2020-07-14T12:47:24Z
fulldoi: https://doi.org/10.7717/peerj.3830
has_accepted_license: '1'
intvolume: ' 2017'
isi: 1
issue: '9'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
publication: PeerJ
publication_identifier:
issn:
- 2167-8359
publication_status: published
publisher: PeerJ
publist_id: '7172'
pubrep_id: '909'
quality_controlled: '1'
scopus_import: '1'
status: public
title: MazF activation promotes translational heterogeneity of the grcA mRNA in Escherichia
coli populations
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 2017
year: '2017'
...
---
OA_place: publisher
_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.
corr_author: '1'
date_created: 2018-12-11T11:45:10Z
date_published: 2017-10-01T00:00:00Z
date_updated: 2026-06-18T18:54:19Z
day: '01'
ddc:
- '576'
- '579'
degree_awarded: PhD
department:
- _id: CaGu
doi: 10.15479/AT:ISTA:th_916
file:
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creator: system
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creator: dernst
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date_updated: 2020-07-14T12:45:24Z
file_id: '6204'
file_name: 2017_Pleska_Maros_Thesis.docx
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fulldoi: https://doi.org/10.15479/AT:ISTA:th_916
has_accepted_license: '1'
language:
- iso: eng
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
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: '457'
relation: part_of_dissertation
status: public
- id: '1243'
relation: part_of_dissertation
status: public
- id: '561'
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: ba8df636-2132-11f1-aed0-ed93e2281fdd
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: 2025-04-15T06:50:01Z
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
fulldoi: https://doi.org/10.1016/j.automatica.2017.03.030
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: '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: 2025-07-10T12:01:50Z
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
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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
fulldoi: https://doi.org/10.7554/eLife.25192
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:
- 2050-084X
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: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 6
year: '2017'
...
---
_id: '655'
abstract:
- lang: eng
text: 'The bacterial flagellum is a self-assembling nanomachine. The external flagellar
filament, several times longer than a bacterial cell body, is made of a few tens
of thousands subunits of a single protein: flagellin. A fundamental problem concerns
the molecular mechanism of how the flagellum grows outside the cell, where no
discernible energy source is available. Here, we monitored the dynamic assembly
of individual flagella using in situ labelling and real-time immunostaining of
elongating flagellar filaments. We report that the rate of flagellum growth, initially
~1,700 amino acids per second, decreases with length and that the previously proposed
chain mechanism does not contribute to the filament elongation dynamics. Inhibition
of the proton motive force-dependent export apparatus revealed a major contribution
of substrate injection in driving filament elongation. The combination of experimental
and mathematical evidence demonstrates that a simple, injection-diffusion mechanism
controls bacterial flagella growth outside the cell.'
article_number: e23136
article_processing_charge: No
author:
- first_name: Thibaud
full_name: Renault, Thibaud
last_name: Renault
- first_name: Anthony
full_name: Abraham, Anthony
last_name: Abraham
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Guillaume
full_name: Paradis, Guillaume
last_name: Paradis
- first_name: Simon
full_name: Rainville, Simon
last_name: Rainville
- first_name: Emmanuelle
full_name: Charpentier, Emmanuelle
last_name: Charpentier
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
- first_name: Yuhai
full_name: Tu, Yuhai
last_name: Tu
- first_name: Keiichi
full_name: Namba, Keiichi
last_name: Namba
- first_name: James
full_name: Keener, James
last_name: Keener
- first_name: Tohru
full_name: Minamino, Tohru
last_name: Minamino
- first_name: Marc
full_name: Erhardt, Marc
last_name: Erhardt
citation:
ama: Renault T, Abraham A, Bergmiller T, et al. Bacterial flagella grow through
an injection diffusion mechanism. eLife. 2017;6. doi:10.7554/eLife.23136
apa: Renault, T., Abraham, A., Bergmiller, T., Paradis, G., Rainville, S., Charpentier,
E., … Erhardt, M. (2017). Bacterial flagella grow through an injection diffusion
mechanism. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.23136
chicago: Renault, Thibaud, Anthony Abraham, Tobias Bergmiller, Guillaume Paradis,
Simon Rainville, Emmanuelle Charpentier, Calin C Guet, et al. “Bacterial Flagella
Grow through an Injection Diffusion Mechanism.” ELife. eLife Sciences Publications,
2017. https://doi.org/10.7554/eLife.23136.
ieee: T. Renault et al., “Bacterial flagella grow through an injection diffusion
mechanism,” eLife, vol. 6. eLife Sciences Publications, 2017.
ista: Renault T, Abraham A, Bergmiller T, Paradis G, Rainville S, Charpentier E,
Guet CC, Tu Y, Namba K, Keener J, Minamino T, Erhardt M. 2017. Bacterial flagella
grow through an injection diffusion mechanism. eLife. 6, e23136.
mla: Renault, Thibaud, et al. “Bacterial Flagella Grow through an Injection Diffusion
Mechanism.” ELife, vol. 6, e23136, eLife Sciences Publications, 2017, doi:10.7554/eLife.23136.
short: T. Renault, A. Abraham, T. Bergmiller, G. Paradis, S. Rainville, E. Charpentier,
C.C. Guet, Y. Tu, K. Namba, J. Keener, T. Minamino, M. Erhardt, ELife 6 (2017).
date_created: 2018-12-11T11:47:44Z
date_published: 2017-03-06T00:00:00Z
date_updated: 2025-09-11T07:11:19Z
day: '06'
ddc:
- '579'
department:
- _id: CaGu
doi: 10.7554/eLife.23136
external_id:
isi:
- '000398680700001'
file:
- access_level: open_access
checksum: 39e1c3e82ddac83a30422fa72fa1a383
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:08:53Z
date_updated: 2020-07-14T12:47:33Z
file_id: '4716'
file_name: IST-2017-904-v1+1_elife-23136-v2.pdf
file_size: 5520359
relation: main_file
- access_level: open_access
checksum: a6d542253028f52e00aa29739ddffe8f
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:08:54Z
date_updated: 2020-07-14T12:47:33Z
file_id: '4717'
file_name: IST-2017-904-v1+2_elife-23136-figures-v2.pdf
file_size: 11242920
relation: main_file
file_date_updated: 2020-07-14T12:47:33Z
fulldoi: https://doi.org/10.7554/eLife.23136
has_accepted_license: '1'
intvolume: ' 6'
isi: 1
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
publist_id: '7082'
pubrep_id: '904'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Bacterial flagella grow through an injection diffusion mechanism
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 6
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.
corr_author: '1'
date_created: 2018-12-11T11:47:48Z
date_published: 2017-04-21T00:00:00Z
date_updated: 2025-09-11T07:05:04Z
day: '21'
department:
- _id: CaGu
- _id: GaTk
- _id: Bio
doi: 10.1126/science.aaf4762
external_id:
isi:
- '000399540100060'
fulldoi: https://doi.org/10.1126/science.aaf4762
intvolume: ' 356'
isi: 1
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:
- 0036-8075
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '7064'
quality_controlled: '1'
related_material:
record:
- id: '5560'
relation: popular_science
status: public
scopus_import: '1'
status: public
title: Biased partitioning of the multidrug efflux pump AcrAB TolC underlies long
lived phenotypic heterogeneity
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 356
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: 2025-09-18T09:42:08Z
day: '18'
department:
- _id: CaGu
doi: 10.1371/journal.pgen.1007122.s018
fulldoi: https://doi.org/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: '9845'
abstract:
- lang: eng
text: "Estimates of 13 C-arabinose and 2 H-glucose uptake from the fractions of
heavy isotopes measured\tin single cells"
article_processing_charge: No
author:
- first_name: Nela
full_name: Nikolic, Nela
id: 42D9CABC-F248-11E8-B48F-1D18A9856A87
last_name: Nikolic
orcid: 0000-0001-9068-6090
- first_name: Frank
full_name: Schreiber, Frank
last_name: Schreiber
- first_name: Alma
full_name: Dal Co, Alma
last_name: Dal Co
- first_name: Daniel
full_name: Kiviet, Daniel
last_name: Kiviet
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Sten
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. Mathematical model. 2017. doi:10.1371/journal.pgen.1007122.s017
apa: Nikolic, N., Schreiber, F., Dal Co, A., Kiviet, D., Bergmiller, T., Littmann,
S., … Ackermann, M. (2017). Mathematical model. Public Library of Science. https://doi.org/10.1371/journal.pgen.1007122.s017
chicago: Nikolic, Nela, Frank Schreiber, Alma Dal Co, Daniel Kiviet, Tobias Bergmiller,
Sten Littmann, Marcel Kuypers, and Martin Ackermann. “Mathematical Model.” Public
Library of Science, 2017. https://doi.org/10.1371/journal.pgen.1007122.s017.
ieee: N. Nikolic et al., “Mathematical model.” Public Library of Science,
2017.
ista: Nikolic N, Schreiber F, Dal Co A, Kiviet D, Bergmiller T, Littmann S, Kuypers
M, Ackermann M. 2017. Mathematical model, Public Library of Science, 10.1371/journal.pgen.1007122.s017.
mla: Nikolic, Nela, et al. Mathematical Model. Public Library of Science,
2017, doi:10.1371/journal.pgen.1007122.s017.
short: N. Nikolic, F. Schreiber, A. Dal Co, D. Kiviet, T. Bergmiller, S. Littmann,
M. Kuypers, M. Ackermann, (2017).
date_created: 2021-08-09T13:31:51Z
date_published: 2017-12-18T00:00:00Z
date_updated: 2025-09-18T09:42:08Z
day: '18'
department:
- _id: CaGu
doi: 10.1371/journal.pgen.1007122.s017
fulldoi: https://doi.org/10.1371/journal.pgen.1007122.s017
month: '12'
oa_version: None
publisher: Public Library of Science
related_material:
record:
- id: '541'
relation: used_in_publication
status: public
status: public
title: Mathematical model
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2017'
...
---
_id: '9846'
article_processing_charge: No
author:
- first_name: Nela
full_name: Nikolic, Nela
id: 42D9CABC-F248-11E8-B48F-1D18A9856A87
last_name: Nikolic
orcid: 0000-0001-9068-6090
- first_name: Frank
full_name: Schreiber, Frank
last_name: Schreiber
- first_name: Alma
full_name: Dal Co, Alma
last_name: Dal Co
- first_name: Daniel
full_name: Kiviet, Daniel
last_name: Kiviet
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Sten
full_name: Littmann, Sten
last_name: Littmann
- first_name: Marcel
full_name: Kuypers, Marcel
last_name: Kuypers
- first_name: Martin
full_name: Ackermann, Martin
last_name: Ackermann
citation:
ama: Nikolic N, Schreiber F, Dal Co A, et al. Supplementary methods. 2017. doi:10.1371/journal.pgen.1007122.s016
apa: Nikolic, N., Schreiber, F., Dal Co, A., Kiviet, D., Bergmiller, T., Littmann,
S., … Ackermann, M. (2017). Supplementary methods. Public Library of Science.
https://doi.org/10.1371/journal.pgen.1007122.s016
chicago: Nikolic, Nela, Frank Schreiber, Alma Dal Co, Daniel Kiviet, Tobias Bergmiller,
Sten Littmann, Marcel Kuypers, and Martin Ackermann. “Supplementary Methods.”
Public Library of Science, 2017. https://doi.org/10.1371/journal.pgen.1007122.s016.
ieee: N. Nikolic et al., “Supplementary methods.” Public Library of Science,
2017.
ista: Nikolic N, Schreiber F, Dal Co A, Kiviet D, Bergmiller T, Littmann S, Kuypers
M, Ackermann M. 2017. Supplementary methods, Public Library of Science, 10.1371/journal.pgen.1007122.s016.
mla: Nikolic, Nela, et al. Supplementary Methods. Public Library of Science,
2017, doi:10.1371/journal.pgen.1007122.s016.
short: N. Nikolic, F. Schreiber, A. Dal Co, D. Kiviet, T. Bergmiller, S. Littmann,
M. Kuypers, M. Ackermann, (2017).
date_created: 2021-08-09T13:35:17Z
date_published: 2017-12-18T00:00:00Z
date_updated: 2025-09-18T09:42:08Z
day: '18'
department:
- _id: CaGu
doi: 10.1371/journal.pgen.1007122.s016
fulldoi: https://doi.org/10.1371/journal.pgen.1007122.s016
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: Supplementary methods
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2017'
...
---
_id: '9847'
abstract:
- lang: eng
text: information on culture conditions, phage mutagenesis, verification and lysate
preparation; Raw data
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: 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. Supplementary materials and methods; Full data set from
effects of mutations in phage restriction sites during escape from restriction–modification.
2017. doi:10.6084/m9.figshare.5633917.v1
apa: Pleska, M., & Guet, C. C. (2017). Supplementary materials and methods;
Full data set from effects of mutations in phage restriction sites during escape
from restriction–modification. The Royal Society. https://doi.org/10.6084/m9.figshare.5633917.v1
chicago: Pleska, Maros, and Calin C Guet. “Supplementary Materials and Methods;
Full Data Set from Effects of Mutations in Phage Restriction Sites during Escape
from Restriction–Modification.” The Royal Society, 2017. https://doi.org/10.6084/m9.figshare.5633917.v1.
ieee: M. Pleska and C. C. Guet, “Supplementary materials and methods; Full data
set from effects of mutations in phage restriction sites during escape from restriction–modification.”
The Royal Society, 2017.
ista: Pleska M, Guet CC. 2017. Supplementary materials and methods; Full data set
from effects of mutations in phage restriction sites during escape from restriction–modification,
The Royal Society, 10.6084/m9.figshare.5633917.v1.
mla: Pleska, Maros, and Calin C. Guet. Supplementary Materials and Methods; Full
Data Set from Effects of Mutations in Phage Restriction Sites during Escape from
Restriction–Modification. The Royal Society, 2017, doi:10.6084/m9.figshare.5633917.v1.
short: M. Pleska, C.C. Guet, (2017).
corr_author: '1'
date_created: 2021-08-09T13:54:38Z
date_published: 2017-11-27T00:00:00Z
date_updated: 2026-06-18T18:54:19Z
day: '27'
department:
- _id: CaGu
doi: 10.6084/m9.figshare.5633917.v1
fulldoi: https://doi.org/10.6084/m9.figshare.5633917.v1
main_file_link:
- open_access: '1'
url: https://doi.org/10.6084/m9.figshare.5633917.v1
month: '11'
oa: 1
oa_version: Published Version
publisher: The Royal Society
related_material:
record:
- id: '561'
relation: used_in_publication
status: public
status: public
title: Supplementary materials and methods; Full data set from effects of mutations
in phage restriction sites during escape from restriction–modification
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2017'
...
---
_id: '9849'
abstract:
- lang: eng
text: This text provides additional information about the model, a derivation of
the analytic results in Eq (4), and details about simulations of an additional
parameter set.
article_processing_charge: No
author:
- first_name: Marta
full_name: Lukacisinova, Marta
id: 4342E402-F248-11E8-B48F-1D18A9856A87
last_name: Lukacisinova
orcid: 0000-0002-2519-8004
- first_name: Sebastian
full_name: Novak, Sebastian
id: 461468AE-F248-11E8-B48F-1D18A9856A87
last_name: Novak
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. Modelling and simulation details. 2017.
doi:10.1371/journal.pcbi.1005609.s001
apa: Lukacisinova, M., Novak, S., & Paixao, T. (2017). Modelling and simulation
details. Public Library of Science. https://doi.org/10.1371/journal.pcbi.1005609.s001
chicago: Lukacisinova, Marta, Sebastian Novak, and Tiago Paixao. “Modelling and
Simulation Details.” Public Library of Science, 2017. https://doi.org/10.1371/journal.pcbi.1005609.s001.
ieee: M. Lukacisinova, S. Novak, and T. Paixao, “Modelling and simulation details.”
Public Library of Science, 2017.
ista: Lukacisinova M, Novak S, Paixao T. 2017. Modelling and simulation details,
Public Library of Science, 10.1371/journal.pcbi.1005609.s001.
mla: Lukacisinova, Marta, et al. Modelling and Simulation Details. Public
Library of Science, 2017, doi:10.1371/journal.pcbi.1005609.s001.
short: M. Lukacisinova, S. Novak, T. Paixao, (2017).
date_created: 2021-08-09T14:02:34Z
date_published: 2017-07-18T00:00:00Z
date_updated: 2025-09-10T11:11:52Z
day: '18'
department:
- _id: ToBo
- _id: NiBa
- _id: CaGu
doi: 10.1371/journal.pcbi.1005609.s001
fulldoi: https://doi.org/10.1371/journal.pcbi.1005609.s001
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: Modelling and simulation details
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2017'
...
---
_id: '9850'
abstract:
- lang: eng
text: In this text, we discuss how a cost of resistance and the possibility of lethal
mutations impact our model.
article_processing_charge: No
author:
- first_name: Marta
full_name: Lukacisinova, Marta
id: 4342E402-F248-11E8-B48F-1D18A9856A87
last_name: Lukacisinova
orcid: 0000-0002-2519-8004
- first_name: Sebastian
full_name: Novak, Sebastian
id: 461468AE-F248-11E8-B48F-1D18A9856A87
last_name: Novak
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. Extensions of the model. 2017. doi:10.1371/journal.pcbi.1005609.s002
apa: Lukacisinova, M., Novak, S., & Paixao, T. (2017). Extensions of the model.
Public Library of Science. https://doi.org/10.1371/journal.pcbi.1005609.s002
chicago: Lukacisinova, Marta, Sebastian Novak, and Tiago Paixao. “Extensions of
the Model.” Public Library of Science, 2017. https://doi.org/10.1371/journal.pcbi.1005609.s002.
ieee: M. Lukacisinova, S. Novak, and T. Paixao, “Extensions of the model.” Public
Library of Science, 2017.
ista: Lukacisinova M, Novak S, Paixao T. 2017. Extensions of the model, Public Library
of Science, 10.1371/journal.pcbi.1005609.s002.
mla: Lukacisinova, Marta, et al. Extensions of the Model. Public Library
of Science, 2017, doi:10.1371/journal.pcbi.1005609.s002.
short: M. Lukacisinova, S. Novak, T. Paixao, (2017).
date_created: 2021-08-09T14:05:24Z
date_published: 2017-07-18T00:00:00Z
date_updated: 2025-09-10T11:11:52Z
day: '18'
department:
- _id: ToBo
- _id: CaGu
- _id: NiBa
doi: 10.1371/journal.pcbi.1005609.s002
fulldoi: https://doi.org/10.1371/journal.pcbi.1005609.s002
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: Extensions of the model
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2017'
...
---
_id: '9851'
abstract:
- lang: eng
text: Based on the intuitive derivation of the dynamics of SIM allele frequency
pM in the main text, we present a heuristic prediction for the long-term SIM allele
frequencies with χ > 1 stresses and compare it to numerical simulations.
article_processing_charge: No
author:
- first_name: Marta
full_name: Lukacisinova, Marta
id: 4342E402-F248-11E8-B48F-1D18A9856A87
last_name: Lukacisinova
orcid: 0000-0002-2519-8004
- first_name: Sebastian
full_name: Novak, Sebastian
id: 461468AE-F248-11E8-B48F-1D18A9856A87
last_name: Novak
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. 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: 2025-09-10T11:11:52Z
day: '18'
department:
- _id: ToBo
- _id: CaGu
- _id: NiBa
doi: 10.1371/journal.pcbi.1005609.s003
fulldoi: https://doi.org/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
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. 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: 2025-09-10T11:11:52Z
day: '18'
department:
- _id: ToBo
- _id: CaGu
- _id: NiBa
doi: 10.1371/journal.pcbi.1005609.s004
fulldoi: https://doi.org/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: '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
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. 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).
corr_author: '1'
date_created: 2018-12-11T11:48:01Z
date_published: 2017-07-25T00:00:00Z
date_updated: 2026-10-17T22:30:19Z
day: '25'
ddc:
- '576'
department:
- _id: CaGu
doi: 10.7554/eLife.25100
external_id:
isi:
- '000406183700001'
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date_created: 2018-12-12T10:12:55Z
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file_id: '4976'
file_name: IST-2017-890-v1+2_elife-25100-figures-v1.pdf
file_size: 3428681
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fulldoi: https://doi.org/10.7554/eLife.25100
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intvolume: ' 6'
isi: 1
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
publist_id: '6990'
pubrep_id: '890'
quality_controlled: '1'
related_material:
record:
- id: '5564'
relation: popular_science
status: public
- id: '26'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Complex chromosomal neighborhood effects determine the adaptive potential of
a gene under selection
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 6
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.
corr_author: '1'
date_created: 2018-12-11T11:48:13Z
date_published: 2017-10-23T00:00:00Z
date_updated: 2026-10-17T22:30:25Z
day: '23'
department:
- _id: CaHe
- _id: CaGu
- _id: GaTk
doi: 10.1016/j.devcel.2017.09.014
ec_funded: 1
external_id:
isi:
- '000413443700011'
fulldoi: https://doi.org/10.1016/j.devcel.2017.09.014
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:
- 1534-5807
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: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 43
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_processing_charge: No
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).
corr_author: '1'
date_created: 2018-12-11T11:47:58Z
date_published: 2017-07-18T00:00:00Z
date_updated: 2026-10-17T22:31:07Z
day: '18'
ddc:
- '576'
department:
- _id: ToBo
- _id: NiBa
- _id: CaGu
doi: 10.1371/journal.pcbi.1005609
ec_funded: 1
external_id:
isi:
- '000406619800014'
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
fulldoi: https://doi.org/10.1371/journal.pcbi.1005609
has_accepted_license: '1'
intvolume: ' 13'
isi: 1
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:
- 1553-734X
publication_status: published
publisher: Public Library of Science
publist_id: '7004'
pubrep_id: '894'
quality_controlled: '1'
related_material:
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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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 13
year: '2017'
...