---
_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. <i>PLoS Computational Biology</i>. 2019;15(7). doi:<a
    href="https://doi.org/10.1371/journal.pcbi.1007168">10.1371/journal.pcbi.1007168</a>
  apa: Ruess, J., Pleska, M., Guet, C. C., &#38; Tkačik, G. (2019). Molecular noise
    of innate immunity shapes bacteria-phage ecologies. <i>PLoS Computational Biology</i>.
    Public Library of Science. <a href="https://doi.org/10.1371/journal.pcbi.1007168">https://doi.org/10.1371/journal.pcbi.1007168</a>
  chicago: Ruess, Jakob, Maros Pleska, Calin C Guet, and Gašper Tkačik. “Molecular
    Noise of Innate Immunity Shapes Bacteria-Phage Ecologies.” <i>PLoS Computational
    Biology</i>. Public Library of Science, 2019. <a href="https://doi.org/10.1371/journal.pcbi.1007168">https://doi.org/10.1371/journal.pcbi.1007168</a>.
  ieee: J. Ruess, M. Pleska, C. C. Guet, and G. Tkačik, “Molecular noise of innate
    immunity shapes bacteria-phage ecologies,” <i>PLoS Computational Biology</i>,
    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.” <i>PLoS Computational Biology</i>, vol. 15, no. 7, e1007168, Public
    Library of Science, 2019, doi:<a href="https://doi.org/10.1371/journal.pcbi.1007168">10.1371/journal.pcbi.1007168</a>.
  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:
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isi: 1
issue: '7'
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license: https://creativecommons.org/licenses/by/4.0/
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'
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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: '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. <i>Nature Ecology
    and Evolution</i>. 2018;2(2):359-366. doi:<a href="https://doi.org/10.1038/s41559-017-0424-z">10.1038/s41559-017-0424-z</a>
  apa: Pleska, M., Lang, M., Refardt, D., Levin, B., &#38; Guet, C. C. (2018). Phage-host
    population dynamics promotes prophage acquisition in bacteria with innate immunity.
    <i>Nature Ecology and Evolution</i>. Springer Nature. <a href="https://doi.org/10.1038/s41559-017-0424-z">https://doi.org/10.1038/s41559-017-0424-z</a>
  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.” <i>Nature Ecology and Evolution</i>. Springer Nature, 2018.
    <a href="https://doi.org/10.1038/s41559-017-0424-z">https://doi.org/10.1038/s41559-017-0424-z</a>.
  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,” <i>Nature
    Ecology and Evolution</i>, 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.” <i>Nature Ecology and Evolution</i>, vol. 2,
    no. 2, Springer Nature, 2018, pp. 359–66, doi:<a href="https://doi.org/10.1038/s41559-017-0424-z">10.1038/s41559-017-0424-z</a>.
  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: '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:<a href="https://doi.org/10.15479/AT:ISTA:th_916">10.15479/AT:ISTA:th_916</a>
  apa: Pleska, M. (2017). <i>Biology of restriction-modification systems at the single-cell
    and population level</i>. Institute of Science and Technology Austria. <a href="https://doi.org/10.15479/AT:ISTA:th_916">https://doi.org/10.15479/AT:ISTA:th_916</a>
  chicago: Pleska, Maros. “Biology of Restriction-Modification Systems at the Single-Cell
    and Population Level.” Institute of Science and Technology Austria, 2017. <a href="https://doi.org/10.15479/AT:ISTA:th_916">https://doi.org/10.15479/AT:ISTA:th_916</a>.
  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. <i>Biology of Restriction-Modification Systems at the Single-Cell
    and Population Level</i>. Institute of Science and Technology Austria, 2017, doi:<a
    href="https://doi.org/10.15479/AT:ISTA:th_916">10.15479/AT:ISTA:th_916</a>.
  short: M. Pleska, Biology of Restriction-Modification Systems at the Single-Cell
    and Population Level, Institute of Science and Technology Austria, 2017.
date_created: 2018-12-11T11:45:10Z
date_published: 2017-10-01T00:00:00Z
date_updated: 2023-09-15T12:04:56Z
day: '01'
ddc:
- '576'
- '579'
degree_awarded: PhD
department:
- _id: CaGu
doi: 10.15479/AT:ISTA:th_916
file:
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month: '10'
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page: '126'
project:
- _id: 251D65D8-B435-11E9-9278-68D0E5697425
  grant_number: '24210'
  name: Effects of Stochasticity on the Function of Restriction-Modi cation Systems
    at the Single-Cell Level (DOC Fellowship)
publication_identifier:
  issn:
  - 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '7711'
pubrep_id: '916'
related_material:
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  - id: '561'
    relation: part_of_dissertation
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    relation: part_of_dissertation
    status: public
status: public
supervisor:
- first_name: Calin C
  full_name: Guet, Calin C
  id: 47F8433E-F248-11E8-B48F-1D18A9856A87
  last_name: Guet
  orcid: 0000-0001-6220-2052
title: Biology of restriction-modification systems at the single-cell and population
  level
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2017'
...
---
_id: '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. <i>Biology Letters</i>. 2017;13(12). doi:<a href="https://doi.org/10.1098/rsbl.2017.0646">10.1098/rsbl.2017.0646</a>
  apa: Pleska, M., &#38; Guet, C. C. (2017). Effects of mutations in phage restriction
    sites during escape from restriction–modification. <i>Biology Letters</i>. The
    Royal Society. <a href="https://doi.org/10.1098/rsbl.2017.0646">https://doi.org/10.1098/rsbl.2017.0646</a>
  chicago: Pleska, Maros, and Calin C Guet. “Effects of Mutations in Phage Restriction
    Sites during Escape from Restriction–Modification.” <i>Biology Letters</i>. The
    Royal Society, 2017. <a href="https://doi.org/10.1098/rsbl.2017.0646">https://doi.org/10.1098/rsbl.2017.0646</a>.
  ieee: M. Pleska and C. C. Guet, “Effects of mutations in phage restriction sites
    during escape from restriction–modification,” <i>Biology Letters</i>, 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.” <i>Biology Letters</i>, vol.
    13, no. 12, 20170646, The Royal Society, 2017, doi:<a href="https://doi.org/10.1098/rsbl.2017.0646">10.1098/rsbl.2017.0646</a>.
  short: M. Pleska, C.C. Guet, Biology Letters 13 (2017).
date_created: 2018-12-11T11:47:11Z
date_published: 2017-12-01T00:00:00Z
date_updated: 2023-09-07T11:59:32Z
day: '01'
department:
- _id: CaGu
doi: 10.1098/rsbl.2017.0646
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intvolume: '        13'
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- 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 (HFSP Young investigators' grant)
- _id: 251D65D8-B435-11E9-9278-68D0E5697425
  grant_number: '24210'
  name: Effects of Stochasticity on the Function of Restriction-Modi cation Systems
    at the Single-Cell Level (DOC Fellowship)
publication: Biology Letters
publication_identifier:
  issn:
  - 1744-9561
publication_status: published
publisher: The Royal Society
publist_id: '7253'
quality_controlled: '1'
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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: '1243'
abstract:
- lang: eng
  text: Restriction-modification (RM) systems represent a minimal and ubiquitous biological
    system of self/non-self discrimination in prokaryotes [1], which protects hosts
    from exogenous DNA [2]. The mechanism is based on the balance between methyltransferase
    (M) and cognate restriction endonuclease (R). M tags endogenous DNA as self by
    methylating short specific DNA sequences called restriction sites, whereas R recognizes
    unmethylated restriction sites as non-self and introduces a double-stranded DNA
    break [3]. Restriction sites are significantly underrepresented in prokaryotic
    genomes [4-7], suggesting that the discrimination mechanism is imperfect and occasionally
    leads to autoimmunity due to self-DNA cleavage (self-restriction) [8]. Furthermore,
    RM systems can promote DNA recombination [9] and contribute to genetic variation
    in microbial populations, thus facilitating adaptive evolution [10]. However,
    cleavage of self-DNA by RM systems as elements shaping prokaryotic genomes has
    not been directly detected, and its cause, frequency, and outcome are unknown.
    We quantify self-restriction caused by two RM systems of Escherichia coli and
    find that, in agreement with levels of restriction site avoidance, EcoRI, but
    not EcoRV, cleaves self-DNA at a measurable rate. Self-restriction is a stochastic
    process, which temporarily induces the SOS response, and is followed by DNA repair,
    maintaining cell viability. We find that RM systems with higher restriction efficiency
    against bacteriophage infections exhibit a higher rate of self-restriction, and
    that this rate can be further increased by stochastic imbalance between R and
    M. Our results identify molecular noise in RM systems as a factor shaping prokaryotic
    genomes.
acknowledgement: This work was funded by an HFSP Young Investigators’ grant. M.P.
  is a recipient of a DOC Fellowship of the Austrian Academy of Science at the Institute
  of Science and Technology Austria. R.O. and Y.W. were supported by the Platform
  for Dynamic Approaches to Living System from MEXT, Japan. We wish to thank I. Kobayashi
  for providing us with the EcoRI and EcoRV plasmids, and A. Campbell for providing
  us with the λ vir phage. We thank D. Siekhaus and C. Uhler and members of the C.C.G.
  and J.P. Bollback laboratories for in-depth discussions. We thank B. Stern for comments
  on an earlier version of the manuscript. We especially thank B.R. Levin for advice
  and comments, and the anonymous reviewers for significantly improving the manuscript.
author:
- first_name: Maros
  full_name: Pleska, Maros
  id: 4569785E-F248-11E8-B48F-1D18A9856A87
  last_name: Pleska
  orcid: 0000-0001-7460-7479
- first_name: Long
  full_name: Qian, Long
  last_name: Qian
- first_name: Reiko
  full_name: Okura, Reiko
  last_name: Okura
- first_name: Tobias
  full_name: Bergmiller, Tobias
  id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
  last_name: Bergmiller
  orcid: 0000-0001-5396-4346
- first_name: Yuichi
  full_name: Wakamoto, Yuichi
  last_name: Wakamoto
- first_name: Edo
  full_name: Kussell, Edo
  last_name: Kussell
- first_name: Calin C
  full_name: Guet, Calin C
  id: 47F8433E-F248-11E8-B48F-1D18A9856A87
  last_name: Guet
  orcid: 0000-0001-6220-2052
citation:
  ama: Pleska M, Qian L, Okura R, et al. Bacterial autoimmunity due to a restriction-modification
    system. <i>Current Biology</i>. 2016;26(3):404-409. doi:<a href="https://doi.org/10.1016/j.cub.2015.12.041">10.1016/j.cub.2015.12.041</a>
  apa: Pleska, M., Qian, L., Okura, R., Bergmiller, T., Wakamoto, Y., Kussell, E.,
    &#38; Guet, C. C. (2016). Bacterial autoimmunity due to a restriction-modification
    system. <i>Current Biology</i>. Cell Press. <a href="https://doi.org/10.1016/j.cub.2015.12.041">https://doi.org/10.1016/j.cub.2015.12.041</a>
  chicago: Pleska, Maros, Long Qian, Reiko Okura, Tobias Bergmiller, Yuichi Wakamoto,
    Edo Kussell, and Calin C Guet. “Bacterial Autoimmunity Due to a Restriction-Modification
    System.” <i>Current Biology</i>. Cell Press, 2016. <a href="https://doi.org/10.1016/j.cub.2015.12.041">https://doi.org/10.1016/j.cub.2015.12.041</a>.
  ieee: M. Pleska <i>et al.</i>, “Bacterial autoimmunity due to a restriction-modification
    system,” <i>Current Biology</i>, vol. 26, no. 3. Cell Press, pp. 404–409, 2016.
  ista: Pleska M, Qian L, Okura R, Bergmiller T, Wakamoto Y, Kussell E, Guet CC. 2016.
    Bacterial autoimmunity due to a restriction-modification system. Current Biology.
    26(3), 404–409.
  mla: Pleska, Maros, et al. “Bacterial Autoimmunity Due to a Restriction-Modification
    System.” <i>Current Biology</i>, vol. 26, no. 3, Cell Press, 2016, pp. 404–09,
    doi:<a href="https://doi.org/10.1016/j.cub.2015.12.041">10.1016/j.cub.2015.12.041</a>.
  short: M. Pleska, L. Qian, R. Okura, T. Bergmiller, Y. Wakamoto, E. Kussell, C.C.
    Guet, Current Biology 26 (2016) 404–409.
date_created: 2018-12-11T11:50:54Z
date_published: 2016-02-08T00:00:00Z
date_updated: 2023-09-07T11:59:32Z
day: '08'
department:
- _id: CaGu
doi: 10.1016/j.cub.2015.12.041
intvolume: '        26'
issue: '3'
language:
- iso: eng
month: '02'
oa_version: None
page: 404 - 409
project:
- _id: 251D65D8-B435-11E9-9278-68D0E5697425
  grant_number: '24210'
  name: Effects of Stochasticity on the Function of Restriction-Modi cation Systems
    at the Single-Cell Level (DOC Fellowship)
publication: Current Biology
publication_status: published
publisher: Cell Press
publist_id: '6087'
quality_controlled: '1'
related_material:
  record:
  - id: '202'
    relation: dissertation_contains
    status: public
scopus_import: 1
status: public
title: Bacterial autoimmunity due to a restriction-modification system
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 26
year: '2016'
...