---
_id: '10307'
abstract:
- lang: eng
text: Bacteria-host interactions represent a continuous trade-off between benefit
and risk. Thus, the host immune response is faced with a non-trivial problem –
accommodate beneficial commensals and remove harmful pathogens. This is especially
difficult as molecular patterns, such as lipopolysaccharide or specific surface
organelles such as pili, are conserved in both, commensal and pathogenic bacteria.
Type 1 pili, tightly regulated by phase variation, are considered an important
virulence factor of pathogenic bacteria as they facilitate invasion into host
cells. While invasion represents a de facto passive mechanism for pathogens to
escape the host immune response, we demonstrate a fundamental role of type 1 pili
as active modulators of the innate and adaptive immune response.
acknowledged_ssus:
- _id: LifeSc
- _id: Bio
- _id: PreCl
- _id: EM-Fac
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Kathrin
full_name: Tomasek, Kathrin
id: 3AEC8556-F248-11E8-B48F-1D18A9856A87
last_name: Tomasek
orcid: 0000-0003-3768-877X
citation:
ama: Tomasek K. Pathogenic Escherichia coli hijack the host immune response. 2021.
doi:10.15479/at:ista:10307
apa: Tomasek, K. (2021). Pathogenic Escherichia coli hijack the host immune response.
Institute of Science and Technology Austria. https://doi.org/10.15479/at:ista:10307
chicago: Tomasek, Kathrin. “Pathogenic Escherichia Coli Hijack the Host Immune Response.”
Institute of Science and Technology Austria, 2021. https://doi.org/10.15479/at:ista:10307.
ieee: K. Tomasek, “Pathogenic Escherichia coli hijack the host immune response,”
Institute of Science and Technology Austria, 2021.
ista: Tomasek K. 2021. Pathogenic Escherichia coli hijack the host immune response.
Institute of Science and Technology Austria.
mla: Tomasek, Kathrin. Pathogenic Escherichia Coli Hijack the Host Immune Response.
Institute of Science and Technology Austria, 2021, doi:10.15479/at:ista:10307.
short: K. Tomasek, Pathogenic Escherichia Coli Hijack the Host Immune Response,
Institute of Science and Technology Austria, 2021.
date_created: 2021-11-18T15:05:06Z
date_published: 2021-11-18T00:00:00Z
date_updated: 2023-09-07T13:34:38Z
day: '18'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: MiSi
- _id: CaGu
- _id: GradSch
doi: 10.15479/at:ista:10307
file:
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issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
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relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-4561-241X
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
title: Pathogenic Escherichia coli hijack the host immune response
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2021'
...
---
_id: '8155'
abstract:
- lang: eng
text: "In the thesis we focus on the interplay of the biophysics and evolution of
gene regulation. We start by addressing how the type of prokaryotic gene regulation
– activation and repression – affects spurious binding to DNA, also known as\r\ntranscriptional
crosstalk. We propose that regulatory interference caused by excess regulatory
proteins in the dense cellular medium – global crosstalk – could be a factor in
determining which type of gene regulatory network is evolutionarily preferred.
Next,we use a normative approach in eukaryotic gene regulation to describe minimal\r\nnon-equilibrium
enhancer models that optimize so-called regulatory phenotypes. We find a class
of models that differ from standard thermodynamic equilibrium models by a single
parameter that notably increases the regulatory performance. Next chapter addresses
the question of genotype-phenotype-fitness maps of higher dimensional phenotypes.
We show that our biophysically realistic approach allows us to understand how
the mechanisms of promoter function constrain genotypephenotype maps, and how
they affect the evolutionary trajectories of promoters.\r\nIn the last chapter
we ask whether the intrinsic instability of gene duplication and amplification
provides a generic alternative to canonical gene regulation. Using mathematical
modeling, we show that amplifications can tune gene expression in many environments,
including those where transcription factor-based schemes are\r\nhard to evolve
or maintain. "
acknowledgement: For the duration of his PhD, Rok was a recipient of a DOC fellowship
of the Austrian Academy of Sciences.
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Rok
full_name: Grah, Rok
id: 483E70DE-F248-11E8-B48F-1D18A9856A87
last_name: Grah
orcid: 0000-0003-2539-3560
citation:
ama: Grah R. Gene regulation across scales – how biophysical constraints shape evolution.
2020. doi:10.15479/AT:ISTA:8155
apa: Grah, R. (2020). Gene regulation across scales – how biophysical constraints
shape evolution. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:8155
chicago: Grah, Rok. “Gene Regulation across Scales – How Biophysical Constraints
Shape Evolution.” Institute of Science and Technology Austria, 2020. https://doi.org/10.15479/AT:ISTA:8155.
ieee: R. Grah, “Gene regulation across scales – how biophysical constraints shape
evolution,” Institute of Science and Technology Austria, 2020.
ista: Grah R. 2020. Gene regulation across scales – how biophysical constraints
shape evolution. Institute of Science and Technology Austria.
mla: Grah, Rok. Gene Regulation across Scales – How Biophysical Constraints Shape
Evolution. Institute of Science and Technology Austria, 2020, doi:10.15479/AT:ISTA:8155.
short: R. Grah, Gene Regulation across Scales – How Biophysical Constraints Shape
Evolution, Institute of Science and Technology Austria, 2020.
date_created: 2020-07-23T09:51:28Z
date_published: 2020-07-24T00:00:00Z
date_updated: 2023-09-07T13:13:27Z
day: '24'
ddc:
- '530'
- '570'
degree_awarded: PhD
department:
- _id: CaGu
- _id: GaTk
doi: 10.15479/AT:ISTA:8155
file:
- access_level: open_access
content_type: application/pdf
creator: rgrah
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date_updated: 2020-07-27T12:00:07Z
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oa: 1
oa_version: Published Version
page: '310'
project:
- _id: 267C84F4-B435-11E9-9278-68D0E5697425
name: Biophysically realistic genotype-phenotype maps for regulatory networks
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '7675'
relation: part_of_dissertation
status: public
- id: '7569'
relation: part_of_dissertation
status: public
- id: '7652'
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
- first_name: Gašper
full_name: Tkačik, Gašper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkačik
orcid: 0000-0002-6699-1455
title: Gene regulation across scales – how biophysical constraints shape evolution
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2020'
...
---
_id: '8653'
abstract:
- lang: eng
text: "Mutations are the raw material of evolution and come in many different flavors.
Point mutations change a single letter in the DNA sequence, while copy number
mutations like duplications or deletions add or remove many letters of the DNA
sequence simultaneously. Each type of mutation exhibits specific properties like
its rate of formation and reversal. \r\nGene expression is a fundamental phenotype
that can be altered by both, point and copy number mutations. The following thesis
is concerned with the dynamics of gene expression evolution and how it is affected
by the properties exhibited by point and copy number mutations. Specifically,
we are considering i) copy number mutations during adaptation to fluctuating environments
and ii) the interaction of copy number and point mutations during adaptation to
constant environments. "
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Isabella
full_name: Tomanek, Isabella
id: 3981F020-F248-11E8-B48F-1D18A9856A87
last_name: Tomanek
orcid: 0000-0001-6197-363X
citation:
ama: Tomanek I. The evolution of gene expression by copy number and point mutations.
2020. doi:10.15479/AT:ISTA:8653
apa: Tomanek, I. (2020). The evolution of gene expression by copy number and
point mutations. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:8653
chicago: Tomanek, Isabella. “The Evolution of Gene Expression by Copy Number and
Point Mutations.” Institute of Science and Technology Austria, 2020. https://doi.org/10.15479/AT:ISTA:8653.
ieee: I. Tomanek, “The evolution of gene expression by copy number and point mutations,”
Institute of Science and Technology Austria, 2020.
ista: Tomanek I. 2020. The evolution of gene expression by copy number and point
mutations. Institute of Science and Technology Austria.
mla: Tomanek, Isabella. The Evolution of Gene Expression by Copy Number and Point
Mutations. Institute of Science and Technology Austria, 2020, doi:10.15479/AT:ISTA:8653.
short: I. Tomanek, The Evolution of Gene Expression by Copy Number and Point Mutations,
Institute of Science and Technology Austria, 2020.
date_created: 2020-10-13T13:02:33Z
date_published: 2020-10-13T00:00:00Z
date_updated: 2023-09-07T13:22:42Z
day: '13'
ddc:
- '576'
degree_awarded: PhD
department:
- _id: CaGu
doi: 10.15479/AT:ISTA:8653
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file_date_updated: 2021-10-20T22:30:03Z
has_accepted_license: '1'
keyword:
- duplication
- amplification
- promoter
- CNV
- AMGET
- experimental evolution
- Escherichia coli
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
page: '117'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '7652'
relation: research_data
status: public
status: public
supervisor:
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
title: The evolution of gene expression by copy number and point mutations
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2020'
...
---
_id: '6371'
abstract:
- lang: eng
text: "Decades of studies have revealed the mechanisms of gene regulation in molecular
detail. We make use of such well-described regulatory systems to explore how the
molecular mechanisms of protein-protein and protein-DNA interactions shape the
dynamics and evolution of gene regulation. \r\n\r\ni) We uncover how the biophysics
of protein-DNA binding determines the potential of regulatory networks to evolve
and adapt, which can be captured using a simple mathematical model. \r\nii) The
evolution of regulatory connections can lead to a significant amount of crosstalk
between binding proteins. We explore the effect of crosstalk on gene expression
from a target promoter, which seems to be modulated through binding competition
at non-specific DNA sites. \r\niii) We investigate how the very same biophysical
characteristics as in i) can generate significant fitness costs for cells through
global crosstalk, meaning non-specific DNA binding across the genomic background.
\r\niv) Binding competition between proteins at a target promoter is a prevailing
regulatory feature due to the prevalence of co-regulation at bacterial promoters.
However, the dynamics of these systems are not always straightforward to determine
even if the molecular mechanisms of regulation are known. A detailed model of
the biophysical interactions reveals that interference between the regulatory
proteins can constitute a new, generic form of system memory that records the
history of the input signals at the promoter. \r\n\r\nWe demonstrate how the biophysics
of protein-DNA binding can be harnessed to investigate the principles that shape
and ultimately limit cellular gene regulation. These results provide a basis for
studies of higher-level functionality, which arises from the underlying regulation.
\ \r\n"
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Claudia
full_name: Igler, Claudia
id: 46613666-F248-11E8-B48F-1D18A9856A87
last_name: Igler
citation:
ama: Igler C. On the nature of gene regulatory design - The biophysics of transcription
factor binding shapes gene regulation. 2019. doi:10.15479/AT:ISTA:6371
apa: Igler, C. (2019). On the nature of gene regulatory design - The biophysics
of transcription factor binding shapes gene regulation. Institute of Science
and Technology Austria. https://doi.org/10.15479/AT:ISTA:6371
chicago: Igler, Claudia. “On the Nature of Gene Regulatory Design - The Biophysics
of Transcription Factor Binding Shapes Gene Regulation.” Institute of Science
and Technology Austria, 2019. https://doi.org/10.15479/AT:ISTA:6371.
ieee: C. Igler, “On the nature of gene regulatory design - The biophysics of transcription
factor binding shapes gene regulation,” Institute of Science and Technology Austria,
2019.
ista: Igler C. 2019. On the nature of gene regulatory design - The biophysics of
transcription factor binding shapes gene regulation. Institute of Science and
Technology Austria.
mla: Igler, Claudia. On the Nature of Gene Regulatory Design - The Biophysics
of Transcription Factor Binding Shapes Gene Regulation. Institute of Science
and Technology Austria, 2019, doi:10.15479/AT:ISTA:6371.
short: C. Igler, On the Nature of Gene Regulatory Design - The Biophysics of Transcription
Factor Binding Shapes Gene Regulation, Institute of Science and Technology Austria,
2019.
date_created: 2019-05-03T11:55:51Z
date_published: 2019-05-03T00:00:00Z
date_updated: 2024-02-21T13:45:52Z
day: '03'
ddc:
- '576'
- '579'
degree_awarded: PhD
department:
- _id: CaGu
doi: 10.15479/AT:ISTA:6371
file:
- access_level: open_access
checksum: c0085d47c58c9cbcab1b0a783480f6da
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creator: cigler
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date_updated: 2021-02-11T11:17:13Z
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file_name: IglerClaudia_OntheNatureofGeneRegulatoryDesign.pdf
file_size: 12597663
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date_updated: 2020-07-14T12:47:28Z
embargo_to: open_access
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file_size: 34644426
relation: source_file
file_date_updated: 2021-02-11T11:17:13Z
has_accepted_license: '1'
keyword:
- gene regulation
- biophysics
- transcription factor binding
- bacteria
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: '152'
project:
- _id: 251EE76E-B435-11E9-9278-68D0E5697425
grant_number: '24573'
name: Design principles underlying genetic switch architecture (DOC Fellowship)
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '67'
relation: part_of_dissertation
status: public
- id: '5585'
relation: popular_science
status: public
status: public
supervisor:
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
title: On the nature of gene regulatory design - The biophysics of transcription factor
binding shapes gene regulation
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2019'
...
---
_id: '26'
abstract:
- lang: eng
text: Expression of genes is a fundamental molecular phenotype that is subject to
evolution by different types of mutations. Both the rate and the effect of mutations
may depend on the DNA sequence context of a particular gene or a particular promoter
sequence. In this thesis I investigate the nature of this dependence using simple
genetic systems in Escherichia coli. With these systems I explore the evolution
of constitutive gene expression from random starting sequences at different loci
on the chromosome and at different locations in sequence space. First, I dissect
chromosomal neighborhood effects that underlie locus-dependent differences in
the potential of a gene under selection to become more highly expressed. Next,
I find that the effects of point mutations in promoter sequences are dependent
on sequence context, and that an existing energy matrix model performs poorly
in predicting relative expression of unrelated sequences. Finally, I show that
a substantial fraction of random sequences contain functional promoters and I
present an extended thermodynamic model that predicts promoter strength in full
sequence space. Taken together, these results provide new insights and guides
on how to integrate information on sequence context to improve our qualitative
and quantitative understanding of bacterial gene expression, with implications
for rapid evolution of drug resistance, de novo evolution of genes, and horizontal
gene transfer.
alternative_title:
- ISTA Thesis
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
citation:
ama: Steinrück M. The influence of sequence context on the evolution of bacterial
gene expression. 2018. doi:10.15479/AT:ISTA:th1059
apa: Steinrück, M. (2018). The influence of sequence context on the evolution
of bacterial gene expression. Institute of Science and Technology Austria.
https://doi.org/10.15479/AT:ISTA:th1059
chicago: Steinrück, Magdalena. “The Influence of Sequence Context on the Evolution
of Bacterial Gene Expression.” Institute of Science and Technology Austria, 2018.
https://doi.org/10.15479/AT:ISTA:th1059.
ieee: M. Steinrück, “The influence of sequence context on the evolution of bacterial
gene expression,” Institute of Science and Technology Austria, 2018.
ista: Steinrück M. 2018. The influence of sequence context on the evolution of bacterial
gene expression. Institute of Science and Technology Austria.
mla: Steinrück, Magdalena. The Influence of Sequence Context on the Evolution
of Bacterial Gene Expression. Institute of Science and Technology Austria,
2018, doi:10.15479/AT:ISTA:th1059.
short: M. Steinrück, The Influence of Sequence Context on the Evolution of Bacterial
Gene Expression, Institute of Science and Technology Austria, 2018.
date_created: 2018-12-11T11:44:14Z
date_published: 2018-10-30T00:00:00Z
date_updated: 2023-09-07T12:48:43Z
day: '30'
ddc:
- '576'
- '579'
degree_awarded: PhD
department:
- _id: CaGu
doi: 10.15479/AT:ISTA:th1059
file:
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checksum: 413cbce1cd1debeae3abe2a25dbc70d1
content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
creator: dernst
date_created: 2019-02-08T10:51:22Z
date_updated: 2020-07-14T12:45:43Z
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file_size: 9190845
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creator: dernst
date_created: 2019-02-08T10:51:22Z
date_updated: 2021-02-11T11:17:14Z
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file_id: '5942'
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file_date_updated: 2021-02-11T11:17:14Z
has_accepted_license: '1'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
page: '109'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '8029'
pubrep_id: '1059'
related_material:
record:
- id: '704'
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: The influence of sequence context on the evolution of bacterial gene expression
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
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
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author:
- first_name: Maros
full_name: Pleska, Maros
id: 4569785E-F248-11E8-B48F-1D18A9856A87
last_name: Pleska
orcid: 0000-0001-7460-7479
citation:
ama: Pleska M. Biology of restriction-modification systems at the single-cell and
population level. 2017. doi:10.15479/AT:ISTA:th_916
apa: Pleska, M. (2017). Biology of restriction-modification systems at the single-cell
and population level. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th_916
chicago: Pleska, Maros. “Biology of Restriction-Modification Systems at the Single-Cell
and Population Level.” Institute of Science and Technology Austria, 2017. https://doi.org/10.15479/AT:ISTA:th_916.
ieee: M. Pleska, “Biology of restriction-modification systems at the single-cell
and population level,” Institute of Science and Technology Austria, 2017.
ista: Pleska M. 2017. Biology of restriction-modification systems at the single-cell
and population level. Institute of Science and Technology Austria.
mla: Pleska, Maros. Biology of Restriction-Modification Systems at the Single-Cell
and Population Level. Institute of Science and Technology Austria, 2017, doi:10.15479/AT:ISTA:th_916.
short: M. Pleska, Biology of Restriction-Modification Systems at the Single-Cell
and Population Level, Institute of Science and Technology Austria, 2017.
date_created: 2018-12-11T11:45:10Z
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id: 47F8433E-F248-11E8-B48F-1D18A9856A87
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orcid: 0000-0001-6220-2052
title: Biology of restriction-modification systems at the single-cell and population
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