---
_id: '12478'
abstract:
- lang: eng
text: In Gram negative bacteria, the multiple antibiotic resistance or mar operon,
is known to control the expression of multi-drug efflux genes that protect bacteria
from a wide range of drugs. As many different chemical compounds can induce this
operon, identifying the parameters that govern the dynamics of its induction is
crucial to better characterize the processes of tolerance and resistance. Most
experiments have assumed that the properties of the mar transcriptional network
can be inferred from population measurements. However, measurements from an asynchronous
population of cells can mask underlying phenotypic variations of single cells.
We monitored the activity of the mar promoter in single Escherichia coli cells
in linear micro-colonies and established that the response to a steady level of
inducer was most heterogeneous within individual colonies for an intermediate
value of inducer. Specifically, sub-lineages defined by contiguous daughter-cells
exhibited similar promoter activity, whereas activity was greatly variable between
different sub-lineages. Specific sub-trees of uniform promoter activity persisted
over several generations. Statistical analyses of the lineages suggest that the
presence of these sub-trees is the signature of an inducible memory of the promoter
state that is transmitted from mother to daughter cells. This single-cell study
reveals that the degree of epigenetic inheritance changes as a function of inducer
concentration, suggesting that phenotypic inheritance may be an inducible phenotype.
acknowledgement: This work was supported by NIH P50 award P50GM081892-02 to the University
of Chicago, a catalyst grant from the Chicago Biomedical Consortium with support
from The Searle Funds at The Chicago Community Trust to PC, and a Yen Fellowship
to CCG. MA was partially supported by PAPIIT-UNAM grant IN-11322.
article_number: '1049255'
article_processing_charge: Yes
article_type: original
author:
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
- first_name: L
full_name: Bruneaux, L
last_name: Bruneaux
- first_name: P
full_name: Oikonomou, P
last_name: Oikonomou
- first_name: M
full_name: Aldana, M
last_name: Aldana
- first_name: P
full_name: Cluzel, P
last_name: Cluzel
citation:
ama: Guet CC, Bruneaux L, Oikonomou P, Aldana M, Cluzel P. Monitoring lineages of
growing and dividing bacteria reveals an inducible memory of mar operon
expression. Frontiers in Microbiology. 2023;14. doi:10.3389/fmicb.2023.1049255
apa: Guet, C. C., Bruneaux, L., Oikonomou, P., Aldana, M., & Cluzel, P. (2023).
Monitoring lineages of growing and dividing bacteria reveals an inducible memory
of mar operon expression. Frontiers in Microbiology. Frontiers.
https://doi.org/10.3389/fmicb.2023.1049255
chicago: Guet, Calin C, L Bruneaux, P Oikonomou, M Aldana, and P Cluzel. “Monitoring
Lineages of Growing and Dividing Bacteria Reveals an Inducible Memory of Mar
Operon Expression.” Frontiers in Microbiology. Frontiers, 2023. https://doi.org/10.3389/fmicb.2023.1049255.
ieee: C. C. Guet, L. Bruneaux, P. Oikonomou, M. Aldana, and P. Cluzel, “Monitoring
lineages of growing and dividing bacteria reveals an inducible memory of mar
operon expression,” Frontiers in Microbiology, vol. 14. Frontiers, 2023.
ista: Guet CC, Bruneaux L, Oikonomou P, Aldana M, Cluzel P. 2023. Monitoring lineages
of growing and dividing bacteria reveals an inducible memory of mar operon
expression. Frontiers in Microbiology. 14, 1049255.
mla: Guet, Calin C., et al. “Monitoring Lineages of Growing and Dividing Bacteria
Reveals an Inducible Memory of Mar Operon Expression.” Frontiers in
Microbiology, vol. 14, 1049255, Frontiers, 2023, doi:10.3389/fmicb.2023.1049255.
short: C.C. Guet, L. Bruneaux, P. Oikonomou, M. Aldana, P. Cluzel, Frontiers in
Microbiology 14 (2023).
date_created: 2023-02-02T08:13:28Z
date_published: 2023-06-20T00:00:00Z
date_updated: 2023-08-02T06:25:04Z
day: '20'
ddc:
- '570'
department:
- _id: CaGu
doi: 10.3389/fmicb.2023.1049255
external_id:
isi:
- '001030002600001'
pmid:
- '37485524'
file:
- access_level: open_access
checksum: 7dd322347512afaa5daf72a0154f2f07
content_type: application/pdf
creator: dernst
date_created: 2023-07-31T07:16:34Z
date_updated: 2023-07-31T07:16:34Z
file_id: '13322'
file_name: 2023_FrontiersMicrobiology_Guet.pdf
file_size: 6452841
relation: main_file
success: 1
file_date_updated: 2023-07-31T07:16:34Z
has_accepted_license: '1'
intvolume: ' 14'
isi: 1
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
pmid: 1
publication: Frontiers in Microbiology
publication_identifier:
eissn:
- 1664-302X
publication_status: published
publisher: Frontiers
quality_controlled: '1'
scopus_import: '1'
status: public
title: Monitoring lineages of growing and dividing bacteria reveals an inducible memory
of mar operon expression
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: 14
year: '2023'
...
---
_id: '10736'
abstract:
- lang: eng
text: Predicting function from sequence is a central problem of biology. Currently,
this is possible only locally in a narrow mutational neighborhood around a wildtype
sequence rather than globally from any sequence. Using random mutant libraries,
we developed a biophysical model that accounts for multiple features of σ70 binding
bacterial promoters to predict constitutive gene expression levels from any sequence.
We experimentally and theoretically estimated that 10–20% of random sequences
lead to expression and ~80% of non-expressing sequences are one mutation away
from a functional promoter. The potential for generating expression from random
sequences is so pervasive that selection acts against σ70-RNA polymerase binding
sites even within inter-genic, promoter-containing regions. This pervasiveness
of σ70-binding sites implies that emergence of promoters is not the limiting step
in gene regulatory evolution. Ultimately, the inclusion of novel features of promoter
function into a mechanistic model enabled not only more accurate predictions of
gene expression levels, but also identified that promoters evolve more rapidly
than previously thought.
acknowledgement: 'We thank Hande Acar, Nicholas H Barton, Rok Grah, Tiago Paixao,
Maros Pleska, Anna Staron, and Murat Tugrul for insightful comments and input on
the manuscript. This work was supported by: Sir Henry Dale Fellowship jointly funded
by the Wellcome Trust and the Royal Society (grant number 216779/Z/19/Z) to ML;
IPC Grant from IST Austria to ML and SS; European Research Council Funding Programme
7 (2007–2013, grant agreement number 648440) to JPB.'
article_number: e64543
article_processing_charge: No
article_type: original
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: Magdalena
full_name: Steinrueck, Magdalena
last_name: Steinrueck
- first_name: David
full_name: Toledo-Aparicio, David
last_name: Toledo-Aparicio
- 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
- first_name: Gašper
full_name: Tkačik, Gašper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkačik
orcid: 0000-0002-6699-1455
citation:
ama: Lagator M, Sarikas S, Steinrueck M, et al. Predicting bacterial promoter function
and evolution from random sequences. eLife. 2022;11. doi:10.7554/eLife.64543
apa: Lagator, M., Sarikas, S., Steinrueck, M., Toledo-Aparicio, D., Bollback, J.
P., Guet, C. C., & Tkačik, G. (2022). Predicting bacterial promoter function
and evolution from random sequences. ELife. eLife Sciences Publications.
https://doi.org/10.7554/eLife.64543
chicago: Lagator, Mato, Srdjan Sarikas, Magdalena Steinrueck, David Toledo-Aparicio,
Jonathan P Bollback, Calin C Guet, and Gašper Tkačik. “Predicting Bacterial Promoter
Function and Evolution from Random Sequences.” ELife. eLife Sciences Publications,
2022. https://doi.org/10.7554/eLife.64543.
ieee: M. Lagator et al., “Predicting bacterial promoter function and evolution
from random sequences,” eLife, vol. 11. eLife Sciences Publications, 2022.
ista: Lagator M, Sarikas S, Steinrueck M, Toledo-Aparicio D, Bollback JP, Guet CC,
Tkačik G. 2022. Predicting bacterial promoter function and evolution from random
sequences. eLife. 11, e64543.
mla: Lagator, Mato, et al. “Predicting Bacterial Promoter Function and Evolution
from Random Sequences.” ELife, vol. 11, e64543, eLife Sciences Publications,
2022, doi:10.7554/eLife.64543.
short: M. Lagator, S. Sarikas, M. Steinrueck, D. Toledo-Aparicio, J.P. Bollback,
C.C. Guet, G. Tkačik, ELife 11 (2022).
date_created: 2022-02-06T23:01:32Z
date_published: 2022-01-26T00:00:00Z
date_updated: 2023-08-02T14:09:02Z
day: '26'
ddc:
- '576'
department:
- _id: CaGu
- _id: GaTk
- _id: NiBa
doi: 10.7554/eLife.64543
ec_funded: 1
external_id:
isi:
- '000751104400001'
pmid:
- '35080492'
file:
- access_level: open_access
checksum: decdcdf600ff51e9a9703b49ca114170
content_type: application/pdf
creator: cchlebak
date_created: 2022-02-07T07:14:09Z
date_updated: 2022-02-07T07:14:09Z
file_id: '10739'
file_name: 2022_ELife_Lagator.pdf
file_size: 5604343
relation: main_file
success: 1
file_date_updated: 2022-02-07T07:14:09Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 2578D616-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '648440'
name: Selective Barriers to Horizontal Gene Transfer
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Predicting bacterial promoter function and evolution from random sequences
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: 11
year: '2022'
...
---
_id: '11843'
abstract:
- lang: eng
text: A key attribute of persistent or recurring bacterial infections is the ability
of the pathogen to evade the host’s immune response. Many Enterobacteriaceae express
type 1 pili, a pre-adapted virulence trait, to invade host epithelial cells and
establish persistent infections. However, the molecular mechanisms and strategies
by which bacteria actively circumvent the immune response of the host remain poorly
understood. Here, we identified CD14, the major co-receptor for lipopolysaccharide
detection, on mouse dendritic cells (DCs) as a binding partner of FimH, the protein
located at the tip of the type 1 pilus of Escherichia coli. The FimH amino acids
involved in CD14 binding are highly conserved across pathogenic and non-pathogenic
strains. Binding of the pathogenic strain CFT073 to CD14 reduced DC migration
by overactivation of integrins and blunted expression of co-stimulatory molecules
by overactivating the NFAT (nuclear factor of activated T-cells) pathway, both
rate-limiting factors of T cell activation. This response was binary at the single-cell
level, but averaged in larger populations exposed to both piliated and non-piliated
pathogens, presumably via the exchange of immunomodulatory cytokines. While defining
an active molecular mechanism of immune evasion by pathogens, the interaction
between FimH and CD14 represents a potential target to interfere with persistent
and recurrent infections, such as urinary tract infections or Crohn’s disease.
acknowledged_ssus:
- _id: Bio
- _id: PreCl
- _id: EM-Fac
acknowledgement: We thank Ulrich Dobrindt for providing UPEC strains CFT073, UTI89,
and 536, Frank Assen, Vlad Gavra, Maximilian Götz, Bor Kavčič, Jonna Alanko, and
Eva Kiermaier for help with experiments and Robert Hauschild, Julian Stopp, and
Saren Tasciyan for help with data analysis. We thank the IST Austria Scientific
Service Units, especially the Bioimaging facility, the Preclinical facility and
the Electron microscopy facility for technical support, Jakob Wallner and all members
of the Guet and Sixt lab for fruitful discussions and Daria Siekhaus for critically
reading the manuscript. This work was supported by grants from the Austrian Research
Promotion Agency (FEMtech 868984) to IG, the European Research Council (CoG 724373),
and the Austrian Science Fund (FWF P29911) to MS.
article_number: e78995
article_processing_charge: Yes
article_type: original
author:
- first_name: Kathrin
full_name: Tomasek, Kathrin
id: 3AEC8556-F248-11E8-B48F-1D18A9856A87
last_name: Tomasek
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
- first_name: Ivana
full_name: Glatzová, Ivana
id: 727b3c7d-4939-11ec-89b3-b9b0750ab74d
last_name: Glatzová
- first_name: Michael S.
full_name: Lukesch, Michael S.
last_name: Lukesch
- 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: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Tomasek K, Leithner AF, Glatzová I, Lukesch MS, Guet CC, Sixt MK. Type 1 piliated
uropathogenic Escherichia coli hijack the host immune response by binding to CD14.
eLife. 2022;11. doi:10.7554/eLife.78995
apa: Tomasek, K., Leithner, A. F., Glatzová, I., Lukesch, M. S., Guet, C. C., &
Sixt, M. K. (2022). Type 1 piliated uropathogenic Escherichia coli hijack the
host immune response by binding to CD14. ELife. eLife Sciences Publications.
https://doi.org/10.7554/eLife.78995
chicago: Tomasek, Kathrin, Alexander F Leithner, Ivana Glatzová, Michael S. Lukesch,
Calin C Guet, and Michael K Sixt. “Type 1 Piliated Uropathogenic Escherichia Coli
Hijack the Host Immune Response by Binding to CD14.” ELife. eLife Sciences
Publications, 2022. https://doi.org/10.7554/eLife.78995.
ieee: K. Tomasek, A. F. Leithner, I. Glatzová, M. S. Lukesch, C. C. Guet, and M.
K. Sixt, “Type 1 piliated uropathogenic Escherichia coli hijack the host immune
response by binding to CD14,” eLife, vol. 11. eLife Sciences Publications,
2022.
ista: Tomasek K, Leithner AF, Glatzová I, Lukesch MS, Guet CC, Sixt MK. 2022. Type
1 piliated uropathogenic Escherichia coli hijack the host immune response by binding
to CD14. eLife. 11, e78995.
mla: Tomasek, Kathrin, et al. “Type 1 Piliated Uropathogenic Escherichia Coli Hijack
the Host Immune Response by Binding to CD14.” ELife, vol. 11, e78995, eLife
Sciences Publications, 2022, doi:10.7554/eLife.78995.
short: K. Tomasek, A.F. Leithner, I. Glatzová, M.S. Lukesch, C.C. Guet, M.K. Sixt,
ELife 11 (2022).
date_created: 2022-08-14T22:01:46Z
date_published: 2022-07-26T00:00:00Z
date_updated: 2023-08-03T12:54:21Z
day: '26'
ddc:
- '570'
department:
- _id: MiSi
- _id: CaGu
doi: 10.7554/eLife.78995
ec_funded: 1
external_id:
isi:
- '000838410200001'
file:
- access_level: open_access
checksum: 002a3c7c7ea5caa9af9cfbea308f6ea4
content_type: application/pdf
creator: cchlebak
date_created: 2022-08-16T08:57:37Z
date_updated: 2022-08-16T08:57:37Z
file_id: '11861'
file_name: 2022_eLife_Tomasek.pdf
file_size: 2057577
relation: main_file
success: 1
file_date_updated: 2022-08-16T08:57:37Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
project:
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular navigation along spatial gradients
- _id: 26018E70-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P29911
name: Mechanical adaptation of lamellipodial actin
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
related_material:
record:
- id: '10316'
relation: earlier_version
status: public
scopus_import: '1'
status: public
title: Type 1 piliated uropathogenic Escherichia coli hijack the host immune response
by binding to CD14
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: 11
year: '2022'
...
---
_id: '12333'
abstract:
- lang: eng
text: Together, copy-number and point mutations form the basis for most evolutionary
novelty, through the process of gene duplication and divergence. While a plethora
of genomic data reveals the long-term fate of diverging coding sequences and their
cis-regulatory elements, little is known about the early dynamics around the duplication
event itself. In microorganisms, selection for increased gene expression often
drives the expansion of gene copy-number mutations, which serves as a crude adaptation,
prior to divergence through refining point mutations. Using a simple synthetic
genetic reporter system that can distinguish between copy-number and point mutations,
we study their early and transient adaptive dynamics in real time in Escherichia
coli. We find two qualitatively different routes of adaptation, depending on the
level of functional improvement needed. In conditions of high gene expression
demand, the two mutation types occur as a combination. However, under low gene
expression demand, copy-number and point mutations are mutually exclusive; here,
owing to their higher frequency, adaptation is dominated by copy-number mutations,
in a process we term amplification hindrance. Ultimately, due to high reversal
rates and pleiotropic cost, copy-number mutations may not only serve as a crude
and transient adaptation, but also constrain sequence divergence over evolutionary
time scales.
acknowledgement: "We are grateful to N Barton, F Kondrashov, M Lagator, M Pleska,
R Roemhild, D Siekhaus, and G\r\nTkacik for input on the manuscript and to K Tomasek
for help with flow cytometry."
article_number: e82240
article_processing_charge: No
article_type: original
author:
- first_name: Isabella
full_name: Tomanek, Isabella
id: 3981F020-F248-11E8-B48F-1D18A9856A87
last_name: Tomanek
orcid: 0000-0001-6197-363X
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Tomanek I, Guet CC. Adaptation dynamics between copynumber and point mutations.
eLife. 2022;11. doi:10.7554/ELIFE.82240
apa: Tomanek, I., & Guet, C. C. (2022). Adaptation dynamics between copynumber
and point mutations. ELife. eLife Sciences Publications. https://doi.org/10.7554/ELIFE.82240
chicago: Tomanek, Isabella, and Calin C Guet. “Adaptation Dynamics between Copynumber
and Point Mutations.” ELife. eLife Sciences Publications, 2022. https://doi.org/10.7554/ELIFE.82240.
ieee: I. Tomanek and C. C. Guet, “Adaptation dynamics between copynumber and point
mutations,” eLife, vol. 11. eLife Sciences Publications, 2022.
ista: Tomanek I, Guet CC. 2022. Adaptation dynamics between copynumber and point
mutations. eLife. 11, e82240.
mla: Tomanek, Isabella, and Calin C. Guet. “Adaptation Dynamics between Copynumber
and Point Mutations.” ELife, vol. 11, e82240, eLife Sciences Publications,
2022, doi:10.7554/ELIFE.82240.
short: I. Tomanek, C.C. Guet, ELife 11 (2022).
date_created: 2023-01-22T23:00:55Z
date_published: 2022-12-22T00:00:00Z
date_updated: 2023-08-03T14:23:07Z
day: '22'
ddc:
- '570'
department:
- _id: CaGu
doi: 10.7554/ELIFE.82240
external_id:
isi:
- '000912674700001'
file:
- access_level: open_access
checksum: 9321fd5f06ff59d5e2d33daee84b3da1
content_type: application/pdf
creator: dernst
date_created: 2023-01-23T08:56:21Z
date_updated: 2023-01-23T08:56:21Z
file_id: '12338'
file_name: 2022_eLife_Tomanek.pdf
file_size: 8835954
relation: main_file
success: 1
file_date_updated: 2023-01-23T08:56:21Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
related_material:
link:
- relation: software
url: https://doi.org/10.5281/zenodo.6974122
record:
- id: '12339'
relation: research_data
status: public
scopus_import: '1'
status: public
title: Adaptation dynamics between copynumber and point mutations
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: 11
year: '2022'
...
---
_id: '12339'
abstract:
- lang: eng
text: 'Copy-number and point mutations form the basis for most evolutionary novelty
through the process of gene duplication and divergence. While a plethora of genomic
sequence data reveals the long-term fate of diverging coding sequences and their
cis-regulatory elements, little is known about the early dynamics around the duplication
event itself. In microorganisms, selection for increased gene expression often
drives the expansion of gene copy-number mutations, which serves as a crude adaptation,
prior to divergence through refining point mutations. Using a simple synthetic
genetic system that allows us to distinguish copy-number and point mutations,
we study their early and transient adaptive dynamics in real-time in Escherichia
coli. We find two qualitatively different routes of adaptation depending on the
level of functional improvement selected for: In conditions of high gene expression
demand, the two types of mutations occur as a combination. Under low gene expression
demand, negative epistasis between the two types of mutations renders them mutually
exclusive. Thus, owing to their higher frequency, adaptation is dominated by copy-number
mutations. Ultimately, due to high rates of reversal and pleiotropic cost, copy-number
mutations may not only serve as a crude and transient adaptation but also constrain
sequence divergence over evolutionary time scales.'
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
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Tomanek I, Guet CC. Flow cytometry YFP and CFP data and deep sequencing data
of populations evolving in galactose. 2022. doi:10.5061/dryad.rfj6q57ds
apa: Tomanek, I., & Guet, C. C. (2022). Flow cytometry YFP and CFP data and
deep sequencing data of populations evolving in galactose. Dryad. https://doi.org/10.5061/dryad.rfj6q57ds
chicago: Tomanek, Isabella, and Calin C Guet. “Flow Cytometry YFP and CFP Data and
Deep Sequencing Data of Populations Evolving in Galactose.” Dryad, 2022. https://doi.org/10.5061/dryad.rfj6q57ds.
ieee: I. Tomanek and C. C. Guet, “Flow cytometry YFP and CFP data and deep sequencing
data of populations evolving in galactose.” Dryad, 2022.
ista: Tomanek I, Guet CC. 2022. Flow cytometry YFP and CFP data and deep sequencing
data of populations evolving in galactose, Dryad, 10.5061/dryad.rfj6q57ds.
mla: Tomanek, Isabella, and Calin C. Guet. Flow Cytometry YFP and CFP Data and
Deep Sequencing Data of Populations Evolving in Galactose. Dryad, 2022, doi:10.5061/dryad.rfj6q57ds.
short: I. Tomanek, C.C. Guet, (2022).
date_created: 2023-01-23T09:00:37Z
date_published: 2022-12-23T00:00:00Z
date_updated: 2023-08-03T14:23:06Z
day: '23'
ddc:
- '570'
department:
- _id: CaGu
doi: 10.5061/dryad.rfj6q57ds
main_file_link:
- open_access: '1'
url: https://doi.org/10.5061/dryad.rfj6q57ds
month: '12'
oa: 1
oa_version: Published Version
publisher: Dryad
related_material:
record:
- id: '12333'
relation: used_in_publication
status: public
status: public
title: Flow cytometry YFP and CFP data and deep sequencing data of populations evolving
in galactose
type: research_data_reference
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2022'
...
---
_id: '9283'
abstract:
- lang: eng
text: Gene expression levels are influenced by multiple coexisting molecular mechanisms.
Some of these interactions such as those of transcription factors and promoters
have been studied extensively. However, predicting phenotypes of gene regulatory
networks (GRNs) remains a major challenge. Here, we use a well-defined synthetic
GRN to study in Escherichia coli how network phenotypes depend on local genetic
context, i.e. the genetic neighborhood of a transcription factor and its relative
position. We show that one GRN with fixed topology can display not only quantitatively
but also qualitatively different phenotypes, depending solely on the local genetic
context of its components. Transcriptional read-through is the main molecular
mechanism that places one transcriptional unit (TU) within two separate regulons
without the need for complex regulatory sequences. We propose that relative order
of individual TUs, with its potential for combinatorial complexity, plays an important
role in shaping phenotypes of GRNs.
acknowledgement: "We thank J Bollback, L Hurst, M Lagator, C Nizak, O Rivoire, M Savageau,
G Tkacik, and B Vicozo\r\nfor helpful discussions; A Dolinar and A Greshnova for
technical assistance; T Bollenbach for supplying the strain JW0336; C Rusnac, and
members of the Guet lab for comments. 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 n˚\r\n628377
(ANS) and an Austrian Science Fund (FWF) grant n˚ I 3901-B32 (CCG)."
article_number: e65993
article_processing_charge: Yes
article_type: original
author:
- first_name: Anna A
full_name: Nagy-Staron, Anna A
id: 3ABC5BA6-F248-11E8-B48F-1D18A9856A87
last_name: Nagy-Staron
orcid: 0000-0002-1391-8377
- first_name: Kathrin
full_name: Tomasek, Kathrin
id: 3AEC8556-F248-11E8-B48F-1D18A9856A87
last_name: Tomasek
orcid: 0000-0003-3768-877X
- first_name: Caroline
full_name: Caruso Carter, Caroline
last_name: Caruso Carter
- first_name: Elisabeth
full_name: Sonnleitner, Elisabeth
last_name: Sonnleitner
- first_name: Bor
full_name: Kavcic, Bor
id: 350F91D2-F248-11E8-B48F-1D18A9856A87
last_name: Kavcic
orcid: 0000-0001-6041-254X
- first_name: Tiago
full_name: Paixão, Tiago
last_name: Paixão
- 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: Nagy-Staron AA, Tomasek K, Caruso Carter C, et al. Local genetic context shapes
the function of a gene regulatory network. eLife. 2021;10. doi:10.7554/elife.65993
apa: Nagy-Staron, A. A., Tomasek, K., Caruso Carter, C., Sonnleitner, E., Kavcic,
B., Paixão, T., & Guet, C. C. (2021). Local genetic context shapes the function
of a gene regulatory network. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.65993
chicago: Nagy-Staron, Anna A, Kathrin Tomasek, Caroline Caruso Carter, Elisabeth
Sonnleitner, Bor Kavcic, Tiago Paixão, and Calin C Guet. “Local Genetic Context
Shapes the Function of a Gene Regulatory Network.” ELife. eLife Sciences
Publications, 2021. https://doi.org/10.7554/elife.65993.
ieee: A. A. Nagy-Staron et al., “Local genetic context shapes the function
of a gene regulatory network,” eLife, vol. 10. eLife Sciences Publications,
2021.
ista: Nagy-Staron AA, Tomasek K, Caruso Carter C, Sonnleitner E, Kavcic B, Paixão
T, Guet CC. 2021. Local genetic context shapes the function of a gene regulatory
network. eLife. 10, e65993.
mla: Nagy-Staron, Anna A., et al. “Local Genetic Context Shapes the Function of
a Gene Regulatory Network.” ELife, vol. 10, e65993, eLife Sciences Publications,
2021, doi:10.7554/elife.65993.
short: A.A. Nagy-Staron, K. Tomasek, C. Caruso Carter, E. Sonnleitner, B. Kavcic,
T. Paixão, C.C. Guet, ELife 10 (2021).
date_created: 2021-03-23T10:11:46Z
date_published: 2021-03-08T00:00:00Z
date_updated: 2024-02-21T12:41:57Z
day: '08'
ddc:
- '570'
department:
- _id: GaTk
- _id: CaGu
doi: 10.7554/elife.65993
ec_funded: 1
external_id:
isi:
- '000631050900001'
file:
- access_level: open_access
checksum: 3c2f44058c2dd45a5a1027f09d263f8e
content_type: application/pdf
creator: bkavcic
date_created: 2021-03-23T10:12:58Z
date_updated: 2021-03-23T10:12:58Z
file_id: '9284'
file_name: elife-65993-v2.pdf
file_size: 1390469
relation: main_file
success: 1
file_date_updated: 2021-03-23T10:12:58Z
has_accepted_license: '1'
intvolume: ' 10'
isi: 1
keyword:
- Genetics and Molecular Biology
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
project:
- _id: 2517526A-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '628377'
name: 'The Systems Biology of Transcriptional Read-Through in Bacteria: from Synthetic
Networks to Genomic Studies'
- _id: 268BFA92-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: I03901
name: 'CyberCircuits: Cybergenetic circuits to test composability of gene networks'
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
related_material:
record:
- id: '8951'
relation: research_data
status: public
status: public
title: Local genetic context shapes the function of a gene regulatory network
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 10
year: '2021'
...
---
_id: '9647'
abstract:
- lang: eng
text: 'Gene expression is regulated by the set of transcription factors (TFs) that
bind to the promoter. The ensuing regulating function is often represented as
a combinational logic circuit, where output (gene expression) is determined by
current input values (promoter bound TFs) only. However, the simultaneous arrival
of TFs is a strong assumption, since transcription and translation of genes introduce
intrinsic time delays and there is no global synchronisation among the arrival
times of different molecular species at their targets. We present an experimentally
implementable genetic circuit with two inputs and one output, which in the presence
of small delays in input arrival, exhibits qualitatively distinct population-level
phenotypes, over timescales that are longer than typical cell doubling times.
From a dynamical systems point of view, these phenotypes represent long-lived
transients: although they converge to the same value eventually, they do so after
a very long time span. The key feature of this toy model genetic circuit is that,
despite having only two inputs and one output, it is regulated by twenty-three
distinct DNA-TF configurations, two of which are more stable than others (DNA
looped states), one promoting and another blocking the expression of the output
gene. Small delays in input arrival time result in a majority of cells in the
population quickly reaching the stable state associated with the first input,
while exiting of this stable state occurs at a slow timescale. In order to mechanistically
model the behaviour of this genetic circuit, we used a rule-based modelling language,
and implemented a grid-search to find parameter combinations giving rise to long-lived
transients. Our analysis shows that in the absence of feedback, there exist path-dependent
gene regulatory mechanisms based on the long timescale of transients. The behaviour
of this toy model circuit suggests that gene regulatory networks can exploit event
timing to create phenotypes, and it opens the possibility that they could use
event timing to memorise events, without regulatory feedback. The model reveals
the importance of (i) mechanistically modelling the transitions between the different
DNA-TF states, and (ii) employing transient analysis thereof.'
acknowledgement: 'Tatjana Petrov’s research was supported in part by SNSF Advanced
Postdoctoral Mobility Fellowship grant number P300P2 161067, the Ministry of Science,
Research and the Arts of the state of Baden-Wurttemberg, and the DFG Centre of Excellence
2117 ‘Centre for the Advanced Study of Collective Behaviour’ (ID: 422037984). Claudia
Igler is the recipient of a DOC Fellowship of the Austrian Academy of Sciences.
Thomas A. Henzinger’s research was supported in part by the Austrian Science Fund
(FWF) under grant Z211-N23 (Wittgenstein Award).'
article_processing_charge: No
article_type: original
author:
- first_name: Tatjana
full_name: Petrov, Tatjana
last_name: Petrov
- first_name: Claudia
full_name: Igler, Claudia
id: 46613666-F248-11E8-B48F-1D18A9856A87
last_name: Igler
- first_name: Ali
full_name: Sezgin, Ali
id: 4C7638DA-F248-11E8-B48F-1D18A9856A87
last_name: Sezgin
- first_name: Thomas A
full_name: Henzinger, Thomas A
id: 40876CD8-F248-11E8-B48F-1D18A9856A87
last_name: Henzinger
orcid: 0000-0002-2985-7724
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Petrov T, Igler C, Sezgin A, Henzinger TA, Guet CC. Long lived transients in
gene regulation. Theoretical Computer Science. 2021;893:1-16. doi:10.1016/j.tcs.2021.05.023
apa: Petrov, T., Igler, C., Sezgin, A., Henzinger, T. A., & Guet, C. C. (2021).
Long lived transients in gene regulation. Theoretical Computer Science.
Elsevier. https://doi.org/10.1016/j.tcs.2021.05.023
chicago: Petrov, Tatjana, Claudia Igler, Ali Sezgin, Thomas A Henzinger, and Calin
C Guet. “Long Lived Transients in Gene Regulation.” Theoretical Computer Science.
Elsevier, 2021. https://doi.org/10.1016/j.tcs.2021.05.023.
ieee: T. Petrov, C. Igler, A. Sezgin, T. A. Henzinger, and C. C. Guet, “Long lived
transients in gene regulation,” Theoretical Computer Science, vol. 893.
Elsevier, pp. 1–16, 2021.
ista: Petrov T, Igler C, Sezgin A, Henzinger TA, Guet CC. 2021. Long lived transients
in gene regulation. Theoretical Computer Science. 893, 1–16.
mla: Petrov, Tatjana, et al. “Long Lived Transients in Gene Regulation.” Theoretical
Computer Science, vol. 893, Elsevier, 2021, pp. 1–16, doi:10.1016/j.tcs.2021.05.023.
short: T. Petrov, C. Igler, A. Sezgin, T.A. Henzinger, C.C. Guet, Theoretical Computer
Science 893 (2021) 1–16.
date_created: 2021-07-11T22:01:18Z
date_published: 2021-06-04T00:00:00Z
date_updated: 2023-08-10T14:11:19Z
day: '04'
ddc:
- '004'
department:
- _id: ToHe
- _id: CaGu
doi: 10.1016/j.tcs.2021.05.023
external_id:
isi:
- '000710180500002'
file:
- access_level: open_access
checksum: d3aef34cfb13e53bba4cf44d01680793
content_type: application/pdf
creator: dernst
date_created: 2022-05-12T12:13:27Z
date_updated: 2022-05-12T12:13:27Z
file_id: '11364'
file_name: 2021_TheoreticalComputerScience_Petrov.pdf
file_size: 2566504
relation: main_file
success: 1
file_date_updated: 2022-05-12T12:13:27Z
has_accepted_license: '1'
intvolume: ' 893'
isi: 1
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-nd/4.0/
month: '06'
oa: 1
oa_version: Published Version
page: 1-16
project:
- _id: 25F42A32-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Z211
name: The Wittgenstein Prize
publication: Theoretical Computer Science
publication_identifier:
issn:
- 0304-3975
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Long lived transients in gene regulation
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 893
year: '2021'
...
---
_id: '10316'
abstract:
- lang: eng
text: A key attribute of persistent or recurring bacterial infections is the ability
of the pathogen to evade the host’s immune response. Many Enterobacteriaceae express
type 1 pili, a pre-adapted virulence trait, to invade host epithelial cells and
establish persistent infections. However, the molecular mechanisms and strategies
by which bacteria actively circumvent the immune response of the host remain poorly
understood. Here, we identified CD14, the major co-receptor for lipopolysaccharide
detection, on dendritic cells as a previously undescribed binding partner of FimH,
the protein located at the tip of the type 1 pilus of Escherichia coli. The FimH
amino acids involved in CD14 binding are highly conserved across pathogenic and
non-pathogenic strains. Binding of pathogenic bacteria to CD14 lead to reduced
dendritic cell migration and blunted expression of co-stimulatory molecules, both
rate-limiting factors of T cell activation. While defining an active molecular
mechanism of immune evasion by pathogens, the interaction between FimH and CD14
represents a potential target to interfere with persistent and recurrent infections,
such as urinary tract infections or Crohn’s disease.
acknowledged_ssus:
- _id: Bio
- _id: PreCl
- _id: EM-Fac
acknowledgement: We thank Ulrich Dobrindt for providing UPEC strain CFT073, Vlad Gavra
and Maximilian Götz, Bor Kavčič, Jonna Alanko and Eva Kiermaier for help with experiments
and Robert Hauschild, Julian Stopp and Saren Tasciyan for help with data analysis.
We thank the IST Austria Scientific Service Units, especially the Bioimaging facility,
the Preclinical facility and the Electron microscopy facility for technical support,
Jakob Wallner and all members of the Guet and Sixt lab for fruitful discussions
and Daria Siekhaus for critically reading the manuscript. This work was supported
by grants from the Austrian Research Promotion Agency (FEMtech 868984) to I.G.,
the European Research Council (CoG 724373) and the Austrian Science Fund (FWF P29911)
to M.S.
article_processing_charge: No
author:
- first_name: Kathrin
full_name: Tomasek, Kathrin
id: 3AEC8556-F248-11E8-B48F-1D18A9856A87
last_name: Tomasek
orcid: 0000-0003-3768-877X
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
- first_name: Ivana
full_name: Glatzová, Ivana
id: 727b3c7d-4939-11ec-89b3-b9b0750ab74d
last_name: Glatzová
- first_name: Michael S.
full_name: Lukesch, Michael S.
last_name: Lukesch
- 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: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-4561-241X
citation:
ama: Tomasek K, Leithner AF, Glatzová I, Lukesch MS, Guet CC, Sixt MK. Type 1 piliated
uropathogenic Escherichia coli hijack the host immune response by binding to CD14.
bioRxiv. doi:10.1101/2021.10.18.464770
apa: Tomasek, K., Leithner, A. F., Glatzová, I., Lukesch, M. S., Guet, C. C., &
Sixt, M. K. (n.d.). Type 1 piliated uropathogenic Escherichia coli hijack the
host immune response by binding to CD14. bioRxiv. Cold Spring Harbor Laboratory.
https://doi.org/10.1101/2021.10.18.464770
chicago: Tomasek, Kathrin, Alexander F Leithner, Ivana Glatzová, Michael S. Lukesch,
Calin C Guet, and Michael K Sixt. “Type 1 Piliated Uropathogenic Escherichia Coli
Hijack the Host Immune Response by Binding to CD14.” BioRxiv. Cold Spring
Harbor Laboratory, n.d. https://doi.org/10.1101/2021.10.18.464770.
ieee: K. Tomasek, A. F. Leithner, I. Glatzová, M. S. Lukesch, C. C. Guet, and M.
K. Sixt, “Type 1 piliated uropathogenic Escherichia coli hijack the host immune
response by binding to CD14,” bioRxiv. Cold Spring Harbor Laboratory.
ista: Tomasek K, Leithner AF, Glatzová I, Lukesch MS, Guet CC, Sixt MK. Type 1 piliated
uropathogenic Escherichia coli hijack the host immune response by binding to CD14.
bioRxiv, 10.1101/2021.10.18.464770.
mla: Tomasek, Kathrin, et al. “Type 1 Piliated Uropathogenic Escherichia Coli Hijack
the Host Immune Response by Binding to CD14.” BioRxiv, Cold Spring Harbor
Laboratory, doi:10.1101/2021.10.18.464770.
short: K. Tomasek, A.F. Leithner, I. Glatzová, M.S. Lukesch, C.C. Guet, M.K. Sixt,
BioRxiv (n.d.).
date_created: 2021-11-19T12:24:16Z
date_published: 2021-10-18T00:00:00Z
date_updated: 2024-03-25T23:30:19Z
day: '18'
department:
- _id: CaGu
- _id: MiSi
doi: 10.1101/2021.10.18.464770
ec_funded: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.biorxiv.org/content/10.1101/2021.10.18.464770v1
month: '10'
oa: 1
oa_version: Preprint
project:
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular navigation along spatial gradients
- _id: 26018E70-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P29911
name: Mechanical adaptation of lamellipodial actin
publication: bioRxiv
publication_status: submitted
publisher: Cold Spring Harbor Laboratory
related_material:
record:
- id: '11843'
relation: later_version
status: public
- id: '10307'
relation: dissertation_contains
status: public
status: public
title: Type 1 piliated uropathogenic Escherichia coli hijack the host immune response
by binding to CD14
type: preprint
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
year: '2021'
...
---
_id: '9822'
abstract:
- lang: eng
text: Attachment of adhesive molecules on cell culture surfaces to restrict cell
adhesion to defined areas and shapes has been vital for the progress of in vitro
research. In currently existing patterning methods, a combination of pattern properties
such as stability, precision, specificity, high-throughput outcome, and spatiotemporal
control is highly desirable but challenging to achieve. Here, we introduce a versatile
and high-throughput covalent photoimmobilization technique, comprising a light-dose-dependent
patterning step and a subsequent functionalization of the pattern via click chemistry.
This two-step process is feasible on arbitrary surfaces and allows for generation
of sustainable patterns and gradients. The method is validated in different biological
systems by patterning adhesive ligands on cell-repellent surfaces, thereby constraining
the growth and migration of cells to the designated areas. We then implement a
sequential photopatterning approach by adding a second switchable patterning step,
allowing for spatiotemporal control over two distinct surface patterns. As a proof
of concept, we reconstruct the dynamics of the tip/stalk cell switch during angiogenesis.
Our results show that the spatiotemporal control provided by our “sequential photopatterning”
system is essential for mimicking dynamic biological processes and that our innovative
approach has great potential for further applications in cell science.
acknowledgement: We would like to thank Charlott Leu for the production of our chromium
wafers, Louise Ritter for her contribution of the IF stainings in Figure 4, Shokoufeh
Teymouri for her help with the Bioinert coated slides, and finally Prof. Dr. Joachim
Rädler for his valuable scientific guidance.
article_processing_charge: Yes (in subscription journal)
article_type: original
author:
- first_name: Themistoklis
full_name: Zisis, Themistoklis
last_name: Zisis
- first_name: Jan
full_name: Schwarz, Jan
id: 346C1EC6-F248-11E8-B48F-1D18A9856A87
last_name: Schwarz
- first_name: Miriam
full_name: Balles, Miriam
last_name: Balles
- first_name: Maibritt
full_name: Kretschmer, Maibritt
last_name: Kretschmer
- first_name: Maria
full_name: Nemethova, Maria
id: 34E27F1C-F248-11E8-B48F-1D18A9856A87
last_name: Nemethova
- 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: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Janina
full_name: Lange, Janina
last_name: Lange
- 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: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-4561-241X
- first_name: Stefan
full_name: Zahler, Stefan
last_name: Zahler
citation:
ama: Zisis T, Schwarz J, Balles M, et al. Sequential and switchable patterning for
studying cellular processes under spatiotemporal control. ACS Applied Materials
and Interfaces. 2021;13(30):35545–35560. doi:10.1021/acsami.1c09850
apa: Zisis, T., Schwarz, J., Balles, M., Kretschmer, M., Nemethova, M., Chait, R.
P., … Zahler, S. (2021). Sequential and switchable patterning for studying cellular
processes under spatiotemporal control. ACS Applied Materials and Interfaces.
American Chemical Society. https://doi.org/10.1021/acsami.1c09850
chicago: Zisis, Themistoklis, Jan Schwarz, Miriam Balles, Maibritt Kretschmer, Maria
Nemethova, Remy P Chait, Robert Hauschild, et al. “Sequential and Switchable Patterning
for Studying Cellular Processes under Spatiotemporal Control.” ACS Applied
Materials and Interfaces. American Chemical Society, 2021. https://doi.org/10.1021/acsami.1c09850.
ieee: T. Zisis et al., “Sequential and switchable patterning for studying
cellular processes under spatiotemporal control,” ACS Applied Materials and
Interfaces, vol. 13, no. 30. American Chemical Society, pp. 35545–35560, 2021.
ista: Zisis T, Schwarz J, Balles M, Kretschmer M, Nemethova M, Chait RP, Hauschild
R, Lange J, Guet CC, Sixt MK, Zahler S. 2021. Sequential and switchable patterning
for studying cellular processes under spatiotemporal control. ACS Applied Materials
and Interfaces. 13(30), 35545–35560.
mla: Zisis, Themistoklis, et al. “Sequential and Switchable Patterning for Studying
Cellular Processes under Spatiotemporal Control.” ACS Applied Materials and
Interfaces, vol. 13, no. 30, American Chemical Society, 2021, pp. 35545–35560,
doi:10.1021/acsami.1c09850.
short: T. Zisis, J. Schwarz, M. Balles, M. Kretschmer, M. Nemethova, R.P. Chait,
R. Hauschild, J. Lange, C.C. Guet, M.K. Sixt, S. Zahler, ACS Applied Materials
and Interfaces 13 (2021) 35545–35560.
date_created: 2021-08-08T22:01:28Z
date_published: 2021-08-04T00:00:00Z
date_updated: 2023-08-10T14:22:48Z
day: '04'
ddc:
- '620'
- '570'
department:
- _id: MiSi
- _id: GaTk
- _id: Bio
- _id: CaGu
doi: 10.1021/acsami.1c09850
ec_funded: 1
external_id:
isi:
- '000683741400026'
pmid:
- '34283577'
file:
- access_level: open_access
checksum: b043a91d9f9200e467b970b692687ed3
content_type: application/pdf
creator: asandaue
date_created: 2021-08-09T09:44:03Z
date_updated: 2021-08-09T09:44:03Z
file_id: '9833'
file_name: 2021_ACSAppliedMaterialsAndInterfaces_Zisis.pdf
file_size: 7123293
relation: main_file
success: 1
file_date_updated: 2021-08-09T09:44:03Z
has_accepted_license: '1'
intvolume: ' 13'
isi: 1
issue: '30'
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
page: 35545–35560
pmid: 1
project:
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular navigation along spatial gradients
publication: ACS Applied Materials and Interfaces
publication_identifier:
eissn:
- '19448252'
issn:
- '19448244'
publication_status: published
publisher: American Chemical Society
quality_controlled: '1'
scopus_import: '1'
status: public
title: Sequential and switchable patterning for studying cellular processes under
spatiotemporal control
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 13
year: '2021'
...
---
_id: '7652'
abstract:
- lang: eng
text: Organisms cope with change by taking advantage of transcriptional regulators.
However, when faced with rare environments, the evolution of transcriptional regulators
and their promoters may be too slow. Here, we investigate whether the intrinsic
instability of gene duplication and amplification provides a generic alternative
to canonical gene regulation. Using real-time monitoring of gene-copy-number mutations
in Escherichia coli, we show that gene duplications and amplifications enable
adaptation to fluctuating environments by rapidly generating copy-number and,
therefore, expression-level polymorphisms. This amplification-mediated gene expression
tuning (AMGET) occurs on timescales that are similar to canonical gene regulation
and can respond to rapid environmental changes. Mathematical modelling shows that
amplifications also tune gene expression in stochastic environments in which transcription-factor-based
schemes are hard to evolve or maintain. The fleeting nature of gene amplifications
gives rise to a generic population-level mechanism that relies on genetic heterogeneity
to rapidly tune the expression of any gene, without leaving any genomic signature.
acknowledgement: We thank L. Hurst, N. Barton, M. Pleska, M. Steinrück, B. Kavcic
and A. Staron for input on the manuscript, and To. Bergmiller and R. Chait for help
with microfluidics experiments. I.T. is a recipient the OMV fellowship. R.G. is
a recipient of a DOC (Doctoral Fellowship Programme of the Austrian Academy of Sciences)
Fellowship of the Austrian Academy of Sciences.
article_processing_charge: No
article_type: original
author:
- first_name: Isabella
full_name: Tomanek, Isabella
id: 3981F020-F248-11E8-B48F-1D18A9856A87
last_name: Tomanek
orcid: 0000-0001-6197-363X
- first_name: Rok
full_name: Grah, Rok
id: 483E70DE-F248-11E8-B48F-1D18A9856A87
last_name: Grah
orcid: 0000-0003-2539-3560
- first_name: M.
full_name: Lagator, M.
last_name: Lagator
- first_name: A. M. C.
full_name: Andersson, A. M. C.
last_name: Andersson
- first_name: Jonathan P
full_name: Bollback, Jonathan P
id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
last_name: Bollback
orcid: 0000-0002-4624-4612
- first_name: Gašper
full_name: Tkačik, Gašper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkačik
orcid: 0000-0002-6699-1455
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Tomanek I, Grah R, Lagator M, et al. Gene amplification as a form of population-level
gene expression regulation. Nature Ecology & Evolution. 2020;4(4):612-625.
doi:10.1038/s41559-020-1132-7
apa: Tomanek, I., Grah, R., Lagator, M., Andersson, A. M. C., Bollback, J. P., Tkačik,
G., & Guet, C. C. (2020). Gene amplification as a form of population-level
gene expression regulation. Nature Ecology & Evolution. Springer Nature.
https://doi.org/10.1038/s41559-020-1132-7
chicago: Tomanek, Isabella, Rok Grah, M. Lagator, A. M. C. Andersson, Jonathan P
Bollback, Gašper Tkačik, and Calin C Guet. “Gene Amplification as a Form of Population-Level
Gene Expression Regulation.” Nature Ecology & Evolution. Springer Nature,
2020. https://doi.org/10.1038/s41559-020-1132-7.
ieee: I. Tomanek et al., “Gene amplification as a form of population-level
gene expression regulation,” Nature Ecology & Evolution, vol. 4, no.
4. Springer Nature, pp. 612–625, 2020.
ista: Tomanek I, Grah R, Lagator M, Andersson AMC, Bollback JP, Tkačik G, Guet CC.
2020. Gene amplification as a form of population-level gene expression regulation.
Nature Ecology & Evolution. 4(4), 612–625.
mla: Tomanek, Isabella, et al. “Gene Amplification as a Form of Population-Level
Gene Expression Regulation.” Nature Ecology & Evolution, vol. 4, no.
4, Springer Nature, 2020, pp. 612–25, doi:10.1038/s41559-020-1132-7.
short: I. Tomanek, R. Grah, M. Lagator, A.M.C. Andersson, J.P. Bollback, G. Tkačik,
C.C. Guet, Nature Ecology & Evolution 4 (2020) 612–625.
date_created: 2020-04-08T15:20:53Z
date_published: 2020-04-01T00:00:00Z
date_updated: 2024-03-25T23:30:20Z
day: '01'
ddc:
- '570'
department:
- _id: GaTk
- _id: CaGu
doi: 10.1038/s41559-020-1132-7
external_id:
isi:
- '000519008300005'
file:
- access_level: open_access
checksum: ef3bbf42023e30b2c24a6278025d2040
content_type: application/pdf
creator: dernst
date_created: 2020-10-09T09:56:01Z
date_updated: 2020-10-09T09:56:01Z
file_id: '8640'
file_name: 2020_NatureEcolEvo_Tomanek.pdf
file_size: 745242
relation: main_file
success: 1
file_date_updated: 2020-10-09T09:56:01Z
has_accepted_license: '1'
intvolume: ' 4'
isi: 1
issue: '4'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Submitted Version
page: 612-625
project:
- _id: 267C84F4-B435-11E9-9278-68D0E5697425
name: Biophysically realistic genotype-phenotype maps for regulatory networks
publication: Nature Ecology & Evolution
publication_identifier:
issn:
- 2397-334X
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/how-to-thrive-without-gene-regulation/
record:
- id: '8155'
relation: dissertation_contains
status: public
- id: '7383'
relation: research_data
status: public
- id: '7016'
relation: research_data
status: public
- id: '8653'
relation: used_in_publication
status: public
scopus_import: '1'
status: public
title: Gene amplification as a form of population-level gene expression regulation
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 4
year: '2020'
...
---
_id: '6784'
abstract:
- lang: eng
text: Mathematical models have been used successfully at diverse scales of biological
organization, ranging from ecology and population dynamics to stochastic reaction
events occurring between individual molecules in single cells. Generally, many
biological processes unfold across multiple scales, with mutations being the best
studied example of how stochasticity at the molecular scale can influence outcomes
at the population scale. In many other contexts, however, an analogous link between
micro- and macro-scale remains elusive, primarily due to the challenges involved
in setting up and analyzing multi-scale models. Here, we employ such a model to
investigate how stochasticity propagates from individual biochemical reaction
events in the bacterial innate immune system to the ecology of bacteria and bacterial
viruses. We show analytically how the dynamics of bacterial populations are shaped
by the activities of immunity-conferring enzymes in single cells and how the ecological
consequences imply optimal bacterial defense strategies against viruses. Our results
suggest that bacterial populations in the presence of viruses can either optimize
their initial growth rate or their population size, with the first strategy favoring
simple immunity featuring a single restriction modification system and the second
strategy favoring complex bacterial innate immunity featuring several simultaneously
active restriction modification systems.
article_number: e1007168
article_processing_charge: No
article_type: original
author:
- first_name: Jakob
full_name: Ruess, Jakob
id: 4A245D00-F248-11E8-B48F-1D18A9856A87
last_name: Ruess
orcid: 0000-0003-1615-3282
- first_name: Maros
full_name: Pleska, Maros
id: 4569785E-F248-11E8-B48F-1D18A9856A87
last_name: Pleska
orcid: 0000-0001-7460-7479
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
- first_name: Gašper
full_name: Tkačik, Gašper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkačik
orcid: 0000-0002-6699-1455
citation:
ama: Ruess J, Pleska M, Guet CC, Tkačik G. Molecular noise of innate immunity shapes
bacteria-phage ecologies. PLoS Computational Biology. 2019;15(7). doi:10.1371/journal.pcbi.1007168
apa: Ruess, J., Pleska, M., Guet, C. C., & Tkačik, G. (2019). Molecular noise
of innate immunity shapes bacteria-phage ecologies. PLoS Computational Biology.
Public Library of Science. https://doi.org/10.1371/journal.pcbi.1007168
chicago: Ruess, Jakob, Maros Pleska, Calin C Guet, and Gašper Tkačik. “Molecular
Noise of Innate Immunity Shapes Bacteria-Phage Ecologies.” PLoS Computational
Biology. Public Library of Science, 2019. https://doi.org/10.1371/journal.pcbi.1007168.
ieee: J. Ruess, M. Pleska, C. C. Guet, and G. Tkačik, “Molecular noise of innate
immunity shapes bacteria-phage ecologies,” PLoS Computational Biology,
vol. 15, no. 7. Public Library of Science, 2019.
ista: Ruess J, Pleska M, Guet CC, Tkačik G. 2019. Molecular noise of innate immunity
shapes bacteria-phage ecologies. PLoS Computational Biology. 15(7), e1007168.
mla: Ruess, Jakob, et al. “Molecular Noise of Innate Immunity Shapes Bacteria-Phage
Ecologies.” PLoS Computational Biology, vol. 15, no. 7, e1007168, Public
Library of Science, 2019, doi:10.1371/journal.pcbi.1007168.
short: J. Ruess, M. Pleska, C.C. Guet, G. Tkačik, PLoS Computational Biology 15
(2019).
date_created: 2019-08-11T21:59:19Z
date_published: 2019-07-02T00:00:00Z
date_updated: 2023-08-29T07:10:06Z
day: '02'
ddc:
- '570'
department:
- _id: CaGu
- _id: GaTk
doi: 10.1371/journal.pcbi.1007168
external_id:
isi:
- '000481577700032'
file:
- access_level: open_access
checksum: 7ded4721b41c2a0fc66a1c634540416a
content_type: application/pdf
creator: dernst
date_created: 2019-08-12T12:27:26Z
date_updated: 2020-07-14T12:47:40Z
file_id: '6803'
file_name: 2019_PlosComputBiology_Ruess.pdf
file_size: 2200003
relation: main_file
file_date_updated: 2020-07-14T12:47:40Z
has_accepted_license: '1'
intvolume: ' 15'
isi: 1
issue: '7'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
project:
- _id: 251D65D8-B435-11E9-9278-68D0E5697425
grant_number: '24210'
name: Effects of Stochasticity on the Function of Restriction-Modi cation Systems
at the Single-Cell Level
- _id: 251BCBEC-B435-11E9-9278-68D0E5697425
grant_number: RGY0079/2011
name: Multi-Level Conflicts in Evolutionary Dynamics of Restriction-Modification
Systems
publication: PLoS Computational Biology
publication_identifier:
eissn:
- 1553-7358
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
related_material:
record:
- id: '9786'
relation: research_data
status: public
scopus_import: '1'
status: public
title: Molecular noise of innate immunity shapes bacteria-phage ecologies
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 15
year: '2019'
...
---
_id: '7147'
abstract:
- lang: eng
text: "The expression of a gene is characterised by its transcription factors and
the function processing them. If the transcription factors are not affected by
gene products, the regulating function is often represented as a combinational
logic circuit, where the outputs (product) are determined by current input values
(transcription factors) only, and are hence independent on their relative arrival
times. However, the simultaneous arrival of transcription factors (TFs) in genetic
circuits is a strong assumption, given that the processes of transcription and
translation of a gene into a protein introduce intrinsic time delays and that
there is no global synchronisation among the arrival times of different molecular
species at molecular targets.\r\n\r\nIn this paper, we construct an experimentally
implementable genetic circuit with two inputs and a single output, such that,
in presence of small delays in input arrival, the circuit exhibits qualitatively
distinct observable phenotypes. In particular, these phenotypes are long lived
transients: they all converge to a single value, but so slowly, that they seem
stable for an extended time period, longer than typical experiment duration. We
used rule-based language to prototype our circuit, and we implemented a search
for finding the parameter combinations raising the phenotypes of interest.\r\n\r\nThe
behaviour of our prototype circuit has wide implications. First, it suggests that
GRNs can exploit event timing to create phenotypes. Second, it opens the possibility
that GRNs are using event timing to react to stimuli and memorise events, without
explicit feedback in regulation. From the modelling perspective, our prototype
circuit demonstrates the critical importance of analysing the transient dynamics
at the promoter binding sites of the DNA, before applying rapid equilibrium assumptions."
alternative_title:
- LNCS
article_processing_charge: No
author:
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
- first_name: Thomas A
full_name: Henzinger, Thomas A
id: 40876CD8-F248-11E8-B48F-1D18A9856A87
last_name: Henzinger
orcid: 0000−0002−2985−7724
- first_name: Claudia
full_name: Igler, Claudia
id: 46613666-F248-11E8-B48F-1D18A9856A87
last_name: Igler
- first_name: Tatjana
full_name: Petrov, Tatjana
id: 3D5811FC-F248-11E8-B48F-1D18A9856A87
last_name: Petrov
orcid: 0000-0002-9041-0905
- first_name: Ali
full_name: Sezgin, Ali
id: 4C7638DA-F248-11E8-B48F-1D18A9856A87
last_name: Sezgin
citation:
ama: 'Guet CC, Henzinger TA, Igler C, Petrov T, Sezgin A. Transient memory in gene
regulation. In: 17th International Conference on Computational Methods in Systems
Biology. Vol 11773. Springer Nature; 2019:155-187. doi:10.1007/978-3-030-31304-3_9'
apa: 'Guet, C. C., Henzinger, T. A., Igler, C., Petrov, T., & Sezgin, A. (2019).
Transient memory in gene regulation. In 17th International Conference on Computational
Methods in Systems Biology (Vol. 11773, pp. 155–187). Trieste, Italy: Springer
Nature. https://doi.org/10.1007/978-3-030-31304-3_9'
chicago: Guet, Calin C, Thomas A Henzinger, Claudia Igler, Tatjana Petrov, and Ali
Sezgin. “Transient Memory in Gene Regulation.” In 17th International Conference
on Computational Methods in Systems Biology, 11773:155–87. Springer Nature,
2019. https://doi.org/10.1007/978-3-030-31304-3_9.
ieee: C. C. Guet, T. A. Henzinger, C. Igler, T. Petrov, and A. Sezgin, “Transient
memory in gene regulation,” in 17th International Conference on Computational
Methods in Systems Biology, Trieste, Italy, 2019, vol. 11773, pp. 155–187.
ista: 'Guet CC, Henzinger TA, Igler C, Petrov T, Sezgin A. 2019. Transient memory
in gene regulation. 17th International Conference on Computational Methods in
Systems Biology. CMSB: Computational Methods in Systems Biology, LNCS, vol. 11773,
155–187.'
mla: Guet, Calin C., et al. “Transient Memory in Gene Regulation.” 17th International
Conference on Computational Methods in Systems Biology, vol. 11773, Springer
Nature, 2019, pp. 155–87, doi:10.1007/978-3-030-31304-3_9.
short: C.C. Guet, T.A. Henzinger, C. Igler, T. Petrov, A. Sezgin, in:, 17th International
Conference on Computational Methods in Systems Biology, Springer Nature, 2019,
pp. 155–187.
conference:
end_date: 2019-09-20
location: Trieste, Italy
name: 'CMSB: Computational Methods in Systems Biology'
start_date: 2019-09-18
date_created: 2019-12-04T16:07:50Z
date_published: 2019-09-17T00:00:00Z
date_updated: 2023-09-06T11:18:08Z
day: '17'
department:
- _id: CaGu
- _id: ToHe
doi: 10.1007/978-3-030-31304-3_9
external_id:
isi:
- '000557875100009'
intvolume: ' 11773'
isi: 1
language:
- iso: eng
month: '09'
oa_version: None
page: 155-187
project:
- _id: 25F42A32-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Z211
name: The Wittgenstein Prize
- _id: 251EE76E-B435-11E9-9278-68D0E5697425
grant_number: '24573'
name: Design principles underlying genetic switch architecture
publication: 17th International Conference on Computational Methods in Systems Biology
publication_identifier:
eissn:
- 1611-3349
isbn:
- '9783030313036'
- '9783030313043'
issn:
- 0302-9743
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Transient memory in gene regulation
type: conference
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 11773
year: '2019'
...
---
_id: '9786'
article_processing_charge: No
author:
- first_name: Jakob
full_name: Ruess, Jakob
id: 4A245D00-F248-11E8-B48F-1D18A9856A87
last_name: Ruess
orcid: 0000-0003-1615-3282
- first_name: Maros
full_name: Pleska, Maros
id: 4569785E-F248-11E8-B48F-1D18A9856A87
last_name: Pleska
orcid: 0000-0001-7460-7479
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
- first_name: Gašper
full_name: Tkačik, Gašper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkačik
orcid: 0000-0002-6699-1455
citation:
ama: Ruess J, Pleska M, Guet CC, Tkačik G. Supporting text and results. 2019. doi:10.1371/journal.pcbi.1007168.s001
apa: Ruess, J., Pleska, M., Guet, C. C., & Tkačik, G. (2019). Supporting text
and results. Public Library of Science. https://doi.org/10.1371/journal.pcbi.1007168.s001
chicago: Ruess, Jakob, Maros Pleska, Calin C Guet, and Gašper Tkačik. “Supporting
Text and Results.” Public Library of Science, 2019. https://doi.org/10.1371/journal.pcbi.1007168.s001.
ieee: J. Ruess, M. Pleska, C. C. Guet, and G. Tkačik, “Supporting text and results.”
Public Library of Science, 2019.
ista: Ruess J, Pleska M, Guet CC, Tkačik G. 2019. Supporting text and results, Public
Library of Science, 10.1371/journal.pcbi.1007168.s001.
mla: Ruess, Jakob, et al. Supporting Text and Results. Public Library of
Science, 2019, doi:10.1371/journal.pcbi.1007168.s001.
short: J. Ruess, M. Pleska, C.C. Guet, G. Tkačik, (2019).
date_created: 2021-08-06T08:23:43Z
date_published: 2019-07-02T00:00:00Z
date_updated: 2023-08-29T07:10:05Z
day: '02'
department:
- _id: CaGu
- _id: GaTk
doi: 10.1371/journal.pcbi.1007168.s001
month: '07'
oa_version: Published Version
publisher: Public Library of Science
related_material:
record:
- id: '6784'
relation: used_in_publication
status: public
status: public
title: Supporting text and results
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2019'
...
---
_id: '82'
abstract:
- lang: eng
text: In experimental cultures, when bacteria are mixed with lytic (virulent) bacteriophage,
bacterial cells resistant to the phage commonly emerge and become the dominant
population of bacteria. Following the ascent of resistant mutants, the densities
of bacteria in these simple communities become limited by resources rather than
the phage. Despite the evolution of resistant hosts, upon which the phage cannot
replicate, the lytic phage population is most commonly maintained in an apparently
stable state with the resistant bacteria. Several mechanisms have been put forward
to account for this result. Here we report the results of population dynamic/evolution
experiments with a virulent mutant of phage Lambda, λVIR, and Escherichia coli
in serial transfer cultures. We show that, following the ascent of λVIR-resistant
bacteria, λVIRis maintained in the majority of cases in maltose-limited minimal
media and in all cases in nutrient-rich broth. Using mathematical models and experiments,
we show that the dominant mechanism responsible for maintenance of λVIRin these
resource-limited populations dominated by resistant E. coli is a high rate of
either phenotypic or genetic transition from resistance to susceptibility—a hitherto
undemonstrated mechanism we term "leaky resistance." We discuss the
implications of leaky resistance to our understanding of the conditions for the
maintenance of phage in populations of bacteria—their “existence conditions.”.
article_number: '2005971'
article_processing_charge: Yes
author:
- first_name: Waqas
full_name: Chaudhry, Waqas
last_name: Chaudhry
- first_name: Maros
full_name: Pleska, Maros
id: 4569785E-F248-11E8-B48F-1D18A9856A87
last_name: Pleska
orcid: 0000-0001-7460-7479
- first_name: Nilang
full_name: Shah, Nilang
last_name: Shah
- first_name: Howard
full_name: Weiss, Howard
last_name: Weiss
- first_name: Ingrid
full_name: Mccall, Ingrid
last_name: Mccall
- first_name: Justin
full_name: Meyer, Justin
last_name: Meyer
- first_name: Animesh
full_name: Gupta, Animesh
last_name: Gupta
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
- first_name: Bruce
full_name: Levin, Bruce
last_name: Levin
citation:
ama: Chaudhry W, Pleska M, Shah N, et al. Leaky resistance and the conditions for
the existence of lytic bacteriophage. PLoS Biology. 2018;16(8). doi:10.1371/journal.pbio.2005971
apa: Chaudhry, W., Pleska, M., Shah, N., Weiss, H., Mccall, I., Meyer, J., … Levin,
B. (2018). Leaky resistance and the conditions for the existence of lytic bacteriophage.
PLoS Biology. Public Library of Science. https://doi.org/10.1371/journal.pbio.2005971
chicago: Chaudhry, Waqas, Maros Pleska, Nilang Shah, Howard Weiss, Ingrid Mccall,
Justin Meyer, Animesh Gupta, Calin C Guet, and Bruce Levin. “Leaky Resistance
and the Conditions for the Existence of Lytic Bacteriophage.” PLoS Biology.
Public Library of Science, 2018. https://doi.org/10.1371/journal.pbio.2005971.
ieee: W. Chaudhry et al., “Leaky resistance and the conditions for the existence
of lytic bacteriophage,” PLoS Biology, vol. 16, no. 8. Public Library of
Science, 2018.
ista: Chaudhry W, Pleska M, Shah N, Weiss H, Mccall I, Meyer J, Gupta A, Guet CC,
Levin B. 2018. Leaky resistance and the conditions for the existence of lytic
bacteriophage. PLoS Biology. 16(8), 2005971.
mla: Chaudhry, Waqas, et al. “Leaky Resistance and the Conditions for the Existence
of Lytic Bacteriophage.” PLoS Biology, vol. 16, no. 8, 2005971, Public
Library of Science, 2018, doi:10.1371/journal.pbio.2005971.
short: W. Chaudhry, M. Pleska, N. Shah, H. Weiss, I. Mccall, J. Meyer, A. Gupta,
C.C. Guet, B. Levin, PLoS Biology 16 (2018).
date_created: 2018-12-11T11:44:32Z
date_published: 2018-08-16T00:00:00Z
date_updated: 2023-09-13T08:45:41Z
day: '16'
ddc:
- '570'
department:
- _id: CaGu
doi: 10.1371/journal.pbio.2005971
external_id:
isi:
- '000443383300024'
file:
- access_level: open_access
checksum: 527076f78265cd4ea192cd1569851587
content_type: application/pdf
creator: dernst
date_created: 2018-12-17T12:55:31Z
date_updated: 2020-07-14T12:48:10Z
file_id: '5706'
file_name: 2018_Plos_Chaudhry.pdf
file_size: 4007095
relation: main_file
file_date_updated: 2020-07-14T12:48:10Z
has_accepted_license: '1'
intvolume: ' 16'
isi: 1
issue: '8'
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
publication: PLoS Biology
publication_status: published
publisher: Public Library of Science
publist_id: '7972'
quality_controlled: '1'
related_material:
record:
- id: '9810'
relation: research_data
status: public
scopus_import: '1'
status: public
title: Leaky resistance and the conditions for the existence of lytic bacteriophage
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 16
year: '2018'
...
---
_id: '67'
abstract:
- lang: eng
text: 'Gene regulatory networks evolve through rewiring of individual components—that
is, through changes in regulatory connections. However, the mechanistic basis
of regulatory rewiring is poorly understood. Using a canonical gene regulatory
system, we quantify the properties of transcription factors that determine the
evolutionary potential for rewiring of regulatory connections: robustness, tunability
and evolvability. In vivo repression measurements of two repressors at mutated
operator sites reveal their contrasting evolutionary potential: while robustness
and evolvability were positively correlated, both were in trade-off with tunability.
Epistatic interactions between adjacent operators alleviated this trade-off. A
thermodynamic model explains how the differences in robustness, tunability and
evolvability arise from biophysical characteristics of repressor–DNA binding.
The model also uncovers that the energy matrix, which describes how mutations
affect repressor–DNA binding, encodes crucial information about the evolutionary
potential of a repressor. The biophysical determinants of evolutionary potential
for regulatory rewiring constitute a mechanistic framework for understanding network
evolution.'
article_processing_charge: No
article_type: original
author:
- first_name: Claudia
full_name: Igler, Claudia
id: 46613666-F248-11E8-B48F-1D18A9856A87
last_name: Igler
- first_name: Mato
full_name: Lagator, Mato
id: 345D25EC-F248-11E8-B48F-1D18A9856A87
last_name: Lagator
- first_name: Gasper
full_name: Tkacik, Gasper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkacik
orcid: 0000-0002-6699-1455
- 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: Igler C, Lagator M, Tkačik G, Bollback JP, Guet CC. Evolutionary potential
of transcription factors for gene regulatory rewiring. Nature Ecology and Evolution.
2018;2(10):1633-1643. doi:10.1038/s41559-018-0651-y
apa: Igler, C., Lagator, M., Tkačik, G., Bollback, J. P., & Guet, C. C. (2018).
Evolutionary potential of transcription factors for gene regulatory rewiring.
Nature Ecology and Evolution. Nature Publishing Group. https://doi.org/10.1038/s41559-018-0651-y
chicago: Igler, Claudia, Mato Lagator, Gašper Tkačik, Jonathan P Bollback, and Calin
C Guet. “Evolutionary Potential of Transcription Factors for Gene Regulatory Rewiring.”
Nature Ecology and Evolution. Nature Publishing Group, 2018. https://doi.org/10.1038/s41559-018-0651-y.
ieee: C. Igler, M. Lagator, G. Tkačik, J. P. Bollback, and C. C. Guet, “Evolutionary
potential of transcription factors for gene regulatory rewiring,” Nature Ecology
and Evolution, vol. 2, no. 10. Nature Publishing Group, pp. 1633–1643, 2018.
ista: Igler C, Lagator M, Tkačik G, Bollback JP, Guet CC. 2018. Evolutionary potential
of transcription factors for gene regulatory rewiring. Nature Ecology and Evolution.
2(10), 1633–1643.
mla: Igler, Claudia, et al. “Evolutionary Potential of Transcription Factors for
Gene Regulatory Rewiring.” Nature Ecology and Evolution, vol. 2, no. 10,
Nature Publishing Group, 2018, pp. 1633–43, doi:10.1038/s41559-018-0651-y.
short: C. Igler, M. Lagator, G. Tkačik, J.P. Bollback, C.C. Guet, Nature Ecology
and Evolution 2 (2018) 1633–1643.
date_created: 2018-12-11T11:44:27Z
date_published: 2018-09-10T00:00:00Z
date_updated: 2024-03-25T23:30:27Z
day: '10'
ddc:
- '570'
department:
- _id: CaGu
- _id: GaTk
- _id: JoBo
doi: 10.1038/s41559-018-0651-y
ec_funded: 1
external_id:
isi:
- '000447947600021'
file:
- access_level: open_access
checksum: 383a2e2c944a856e2e821ec8e7bf71b6
content_type: application/pdf
creator: dernst
date_created: 2020-05-14T11:28:52Z
date_updated: 2020-07-14T12:47:37Z
file_id: '7830'
file_name: 2018_NatureEcology_Igler.pdf
file_size: 1135973
relation: main_file
file_date_updated: 2020-07-14T12:47:37Z
has_accepted_license: '1'
intvolume: ' 2'
isi: 1
issue: '10'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Submitted Version
page: 1633 - 1643
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
- _id: 251EE76E-B435-11E9-9278-68D0E5697425
grant_number: '24573'
name: Design principles underlying genetic switch architecture (DOC Fellowship)
publication: Nature Ecology and Evolution
publication_status: published
publisher: Nature Publishing Group
publist_id: '7987'
quality_controlled: '1'
related_material:
record:
- id: '5585'
relation: popular_science
status: public
- id: '6371'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Evolutionary potential of transcription factors for gene regulatory rewiring
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 2
year: '2018'
...
---
_id: '457'
abstract:
- lang: eng
text: Temperate bacteriophages integrate in bacterial genomes as prophages and represent
an important source of genetic variation for bacterial evolution, frequently transmitting
fitness-augmenting genes such as toxins responsible for virulence of major pathogens.
However, only a fraction of bacteriophage infections are lysogenic and lead to
prophage acquisition, whereas the majority are lytic and kill the infected bacteria.
Unless able to discriminate lytic from lysogenic infections, mechanisms of immunity
to bacteriophages are expected to act as a double-edged sword and increase the
odds of survival at the cost of depriving bacteria of potentially beneficial prophages.
We show that although restriction-modification systems as mechanisms of innate
immunity prevent both lytic and lysogenic infections indiscriminately in individual
bacteria, they increase the number of prophage-acquiring individuals at the population
level. We find that this counterintuitive result is a consequence of phage-host
population dynamics, in which restriction-modification systems delay infection
onset until bacteria reach densities at which the probability of lysogeny increases.
These results underscore the importance of population-level dynamics as a key
factor modulating costs and benefits of immunity to temperate bacteriophages
article_processing_charge: No
author:
- first_name: Maros
full_name: Pleska, Maros
id: 4569785E-F248-11E8-B48F-1D18A9856A87
last_name: Pleska
orcid: 0000-0001-7460-7479
- first_name: Moritz
full_name: Lang, Moritz
id: 29E0800A-F248-11E8-B48F-1D18A9856A87
last_name: Lang
- first_name: Dominik
full_name: Refardt, Dominik
last_name: Refardt
- first_name: Bruce
full_name: Levin, Bruce
last_name: Levin
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Pleska M, Lang M, Refardt D, Levin B, Guet CC. Phage-host population dynamics
promotes prophage acquisition in bacteria with innate immunity. Nature Ecology
and Evolution. 2018;2(2):359-366. doi:10.1038/s41559-017-0424-z
apa: Pleska, M., Lang, M., Refardt, D., Levin, B., & Guet, C. C. (2018). Phage-host
population dynamics promotes prophage acquisition in bacteria with innate immunity.
Nature Ecology and Evolution. Springer Nature. https://doi.org/10.1038/s41559-017-0424-z
chicago: Pleska, Maros, Moritz Lang, Dominik Refardt, Bruce Levin, and Calin C Guet.
“Phage-Host Population Dynamics Promotes Prophage Acquisition in Bacteria with
Innate Immunity.” Nature Ecology and Evolution. Springer Nature, 2018.
https://doi.org/10.1038/s41559-017-0424-z.
ieee: M. Pleska, M. Lang, D. Refardt, B. Levin, and C. C. Guet, “Phage-host population
dynamics promotes prophage acquisition in bacteria with innate immunity,” Nature
Ecology and Evolution, vol. 2, no. 2. Springer Nature, pp. 359–366, 2018.
ista: Pleska M, Lang M, Refardt D, Levin B, Guet CC. 2018. Phage-host population
dynamics promotes prophage acquisition in bacteria with innate immunity. Nature
Ecology and Evolution. 2(2), 359–366.
mla: Pleska, Maros, et al. “Phage-Host Population Dynamics Promotes Prophage Acquisition
in Bacteria with Innate Immunity.” Nature Ecology and Evolution, vol. 2,
no. 2, Springer Nature, 2018, pp. 359–66, doi:10.1038/s41559-017-0424-z.
short: M. Pleska, M. Lang, D. Refardt, B. Levin, C.C. Guet, Nature Ecology and Evolution
2 (2018) 359–366.
date_created: 2018-12-11T11:46:35Z
date_published: 2018-02-01T00:00:00Z
date_updated: 2023-09-15T12:04:57Z
day: '01'
department:
- _id: CaGu
- _id: GaTk
doi: 10.1038/s41559-017-0424-z
ec_funded: 1
external_id:
isi:
- '000426516400027'
intvolume: ' 2'
isi: 1
issue: '2'
language:
- iso: eng
month: '02'
oa_version: None
page: 359 - 366
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 251BCBEC-B435-11E9-9278-68D0E5697425
grant_number: RGY0079/2011
name: Multi-Level Conflicts in Evolutionary Dynamics of Restriction-Modification
Systems (HFSP Young investigators' grant)
- _id: 251D65D8-B435-11E9-9278-68D0E5697425
grant_number: '24210'
name: Effects of Stochasticity on the Function of Restriction-Modi cation Systems
at the Single-Cell Level (DOC Fellowship)
publication: Nature Ecology and Evolution
publication_status: published
publisher: Springer Nature
publist_id: '7364'
quality_controlled: '1'
related_material:
record:
- id: '202'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Phage-host population dynamics promotes prophage acquisition in bacteria with
innate immunity
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 2
year: '2018'
...
---
_id: '503'
abstract:
- lang: eng
text: Buffers are essential for diluting bacterial cultures for flow cytometry analysis
in order to study bacterial physiology and gene expression parameters based on
fluorescence signals. Using a variety of constitutively expressed fluorescent
proteins in Escherichia coli K-12 strain MG1655, we found strong artifactual changes
in fluorescence levels after dilution into the commonly used flow cytometry buffer
phosphate-buffered saline (PBS) and two other buffer solutions, Tris-HCl and M9
salts. These changes appeared very rapidly after dilution, and were linked to
increased membrane permeability and loss in cell viability. We observed buffer-related
effects in several different E. coli strains, K-12, C and W, but not E. coli B,
which can be partially explained by differences in lipopolysaccharide (LPS) and
outer membrane composition. Supplementing the buffers with divalent cations responsible
for outer membrane stability, Mg2+ and Ca2+, preserved fluorescence signals, membrane
integrity and viability of E. coli. Thus, stabilizing the bacterial outer membrane
is essential for precise and unbiased measurements of fluorescence parameters
using flow cytometry.
acknowledged_ssus:
- _id: Bio
acknowledgement: "We thank R Chait and M Lagator for sharing Bacillus subtilis CR_Y1
and pZS*_2R-cIPtet-Venus-Prm, respectively. We are grateful to T Pilizota and all
members of the Guet lab for critically reading the manuscript. We also thank the
Bioimaging facility at IST Austria for assistance using the FACSAria III system.\r\n\r\n"
article_processing_charge: No
author:
- first_name: Kathrin
full_name: Tomasek, Kathrin
id: 3AEC8556-F248-11E8-B48F-1D18A9856A87
last_name: Tomasek
orcid: 0000-0003-3768-877X
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Tomasek K, Bergmiller T, Guet CC. Lack of cations in flow cytometry buffers
affect fluorescence signals by reducing membrane stability and viability of Escherichia
coli strains. Journal of Biotechnology. 2018;268:40-52. doi:10.1016/j.jbiotec.2018.01.008
apa: Tomasek, K., Bergmiller, T., & Guet, C. C. (2018). Lack of cations in flow
cytometry buffers affect fluorescence signals by reducing membrane stability and
viability of Escherichia coli strains. Journal of Biotechnology. Elsevier.
https://doi.org/10.1016/j.jbiotec.2018.01.008
chicago: Tomasek, Kathrin, Tobias Bergmiller, and Calin C Guet. “Lack of Cations
in Flow Cytometry Buffers Affect Fluorescence Signals by Reducing Membrane Stability
and Viability of Escherichia Coli Strains.” Journal of Biotechnology. Elsevier,
2018. https://doi.org/10.1016/j.jbiotec.2018.01.008.
ieee: K. Tomasek, T. Bergmiller, and C. C. Guet, “Lack of cations in flow cytometry
buffers affect fluorescence signals by reducing membrane stability and viability
of Escherichia coli strains,” Journal of Biotechnology, vol. 268. Elsevier,
pp. 40–52, 2018.
ista: Tomasek K, Bergmiller T, Guet CC. 2018. Lack of cations in flow cytometry
buffers affect fluorescence signals by reducing membrane stability and viability
of Escherichia coli strains. Journal of Biotechnology. 268, 40–52.
mla: Tomasek, Kathrin, et al. “Lack of Cations in Flow Cytometry Buffers Affect
Fluorescence Signals by Reducing Membrane Stability and Viability of Escherichia
Coli Strains.” Journal of Biotechnology, vol. 268, Elsevier, 2018, pp.
40–52, doi:10.1016/j.jbiotec.2018.01.008.
short: K. Tomasek, T. Bergmiller, C.C. Guet, Journal of Biotechnology 268 (2018)
40–52.
date_created: 2018-12-11T11:46:50Z
date_published: 2018-02-20T00:00:00Z
date_updated: 2023-09-13T08:24:51Z
day: '20'
department:
- _id: CaGu
doi: 10.1016/j.jbiotec.2018.01.008
external_id:
isi:
- '000425715100006'
intvolume: ' 268'
isi: 1
language:
- iso: eng
month: '02'
oa_version: None
page: 40 - 52
publication: Journal of Biotechnology
publication_status: published
publisher: Elsevier
publist_id: '7317'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Lack of cations in flow cytometry buffers affect fluorescence signals by reducing
membrane stability and viability of Escherichia coli strains
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 268
year: '2018'
...
---
_id: '5585'
abstract:
- lang: eng
text: Mean repression values and standard error of the mean are given for all operator
mutant libraries.
article_processing_charge: No
author:
- first_name: Claudia
full_name: Igler, Claudia
id: 46613666-F248-11E8-B48F-1D18A9856A87
last_name: Igler
- first_name: Mato
full_name: Lagator, Mato
id: 345D25EC-F248-11E8-B48F-1D18A9856A87
last_name: Lagator
- first_name: Gasper
full_name: Tkacik, Gasper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkacik
orcid: 0000-0002-6699-1455
- 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: Igler C, Lagator M, Tkačik G, Bollback JP, Guet CC. Data for the paper Evolutionary
potential of transcription factors for gene regulatory rewiring. 2018. doi:10.15479/AT:ISTA:108
apa: Igler, C., Lagator, M., Tkačik, G., Bollback, J. P., & Guet, C. C. (2018).
Data for the paper Evolutionary potential of transcription factors for gene regulatory
rewiring. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:108
chicago: Igler, Claudia, Mato Lagator, Gašper Tkačik, Jonathan P Bollback, and Calin
C Guet. “Data for the Paper Evolutionary Potential of Transcription Factors for
Gene Regulatory Rewiring.” Institute of Science and Technology Austria, 2018.
https://doi.org/10.15479/AT:ISTA:108.
ieee: C. Igler, M. Lagator, G. Tkačik, J. P. Bollback, and C. C. Guet, “Data for
the paper Evolutionary potential of transcription factors for gene regulatory
rewiring.” Institute of Science and Technology Austria, 2018.
ista: Igler C, Lagator M, Tkačik G, Bollback JP, Guet CC. 2018. Data for the paper
Evolutionary potential of transcription factors for gene regulatory rewiring,
Institute of Science and Technology Austria, 10.15479/AT:ISTA:108.
mla: Igler, Claudia, et al. Data for the Paper Evolutionary Potential of Transcription
Factors for Gene Regulatory Rewiring. Institute of Science and Technology
Austria, 2018, doi:10.15479/AT:ISTA:108.
short: C. Igler, M. Lagator, G. Tkačik, J.P. Bollback, C.C. Guet, (2018).
datarep_id: '108'
date_created: 2018-12-12T12:31:40Z
date_published: 2018-07-20T00:00:00Z
date_updated: 2024-03-25T23:30:27Z
day: '20'
ddc:
- '576'
department:
- _id: CaGu
- _id: GaTk
doi: 10.15479/AT:ISTA:108
ec_funded: 1
file:
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creator: system
date_created: 2018-12-12T13:02:45Z
date_updated: 2020-07-14T12:47:07Z
file_id: '5611'
file_name: IST-2018-108-v1+1_data_figures.xlsx
file_size: 16507
relation: main_file
file_date_updated: 2020-07-14T12:47:07Z
has_accepted_license: '1'
license: https://creativecommons.org/publicdomain/zero/1.0/
month: '07'
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
- _id: 251EE76E-B435-11E9-9278-68D0E5697425
grant_number: '24573'
name: Design principles underlying genetic switch architecture (DOC Fellowship)
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '67'
relation: research_paper
status: public
- id: '6371'
relation: research_paper
status: public
status: public
title: Data for the paper Evolutionary potential of transcription factors for gene
regulatory rewiring
tmp:
image: /images/cc_0.png
legal_code_url: https://creativecommons.org/publicdomain/zero/1.0/legalcode
name: Creative Commons Public Domain Dedication (CC0 1.0)
short: CC0 (1.0)
type: research_data
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2018'
...
---
_id: '161'
abstract:
- lang: eng
text: 'Which properties of metabolic networks can be derived solely from stoichiometry?
Predictive results have been obtained by flux balance analysis (FBA), by postulating
that cells set metabolic fluxes to maximize growth rate. Here we consider a generalization
of FBA to single-cell level using maximum entropy modeling, which we extend and
test experimentally. Specifically, we define for Escherichia coli metabolism a
flux distribution that yields the experimental growth rate: the model, containing
FBA as a limit, provides a better match to measured fluxes and it makes a wide
range of predictions: on flux variability, regulation, and correlations; on the
relative importance of stoichiometry vs. optimization; on scaling relations for
growth rate distributions. We validate the latter here with single-cell data at
different sub-inhibitory antibiotic concentrations. The model quantifies growth
optimization as emerging from the interplay of competitive dynamics in the population
and regulation of metabolism at the level of single cells.'
article_number: '2988'
article_processing_charge: No
author:
- first_name: Daniele
full_name: De Martino, Daniele
id: 3FF5848A-F248-11E8-B48F-1D18A9856A87
last_name: De Martino
orcid: 0000-0002-5214-4706
- first_name: Andersson Anna
full_name: Mc, Andersson Anna
last_name: Mc
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
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citation:
ama: De Martino D, Mc AA, Bergmiller T, Guet CC, Tkačik G. Statistical mechanics
for metabolic networks during steady state growth. Nature Communications.
2018;9(1). doi:10.1038/s41467-018-05417-9
apa: De Martino, D., Mc, A. A., Bergmiller, T., Guet, C. C., & Tkačik, G. (2018).
Statistical mechanics for metabolic networks during steady state growth. Nature
Communications. Springer Nature. https://doi.org/10.1038/s41467-018-05417-9
chicago: De Martino, Daniele, Andersson Anna Mc, Tobias Bergmiller, Calin C Guet,
and Gašper Tkačik. “Statistical Mechanics for Metabolic Networks during Steady
State Growth.” Nature Communications. Springer Nature, 2018. https://doi.org/10.1038/s41467-018-05417-9.
ieee: D. De Martino, A. A. Mc, T. Bergmiller, C. C. Guet, and G. Tkačik, “Statistical
mechanics for metabolic networks during steady state growth,” Nature Communications,
vol. 9, no. 1. Springer Nature, 2018.
ista: De Martino D, Mc AA, Bergmiller T, Guet CC, Tkačik G. 2018. Statistical mechanics
for metabolic networks during steady state growth. Nature Communications. 9(1),
2988.
mla: De Martino, Daniele, et al. “Statistical Mechanics for Metabolic Networks during
Steady State Growth.” Nature Communications, vol. 9, no. 1, 2988, Springer
Nature, 2018, doi:10.1038/s41467-018-05417-9.
short: D. De Martino, A.A. Mc, T. Bergmiller, C.C. Guet, G. Tkačik, Nature Communications
9 (2018).
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chicago: Chaudhry, Waqas, Maros Pleska, Nilang Shah, Howard Weiss, Ingrid Mccall,
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in Figures.” Public Library of Science, 2018. https://doi.org/10.1371/journal.pbio.2005971.s008.
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