---
_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: '5569'
abstract:
- lang: eng
text: "Nela Nikolic, Tobias Bergmiller, Alexandra Vandervelde, Tanino G. Albanese,
Lendert Gelens, and Isabella Moll (2018)\r\n“Autoregulation of mazEF expression
underlies growth heterogeneity in bacterial populations” Nucleic Acids Research,
doi: 10.15479/AT:ISTA:74;\r\nmicroscopy experiments by Tobias Bergmiller; image
and data analysis by Nela Nikolic."
article_processing_charge: No
author:
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Nela
full_name: Nikolic, Nela
id: 42D9CABC-F248-11E8-B48F-1D18A9856A87
last_name: Nikolic
orcid: 0000-0001-9068-6090
citation:
ama: Bergmiller T, Nikolic N. Time-lapse microscopy data. 2018. doi:10.15479/AT:ISTA:74
apa: Bergmiller, T., & Nikolic, N. (2018). Time-lapse microscopy data. Institute
of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:74
chicago: Bergmiller, Tobias, and Nela Nikolic. “Time-Lapse Microscopy Data.” Institute
of Science and Technology Austria, 2018. https://doi.org/10.15479/AT:ISTA:74.
ieee: T. Bergmiller and N. Nikolic, “Time-lapse microscopy data.” Institute of Science
and Technology Austria, 2018.
ista: Bergmiller T, Nikolic N. 2018. Time-lapse microscopy data, Institute of Science
and Technology Austria, 10.15479/AT:ISTA:74.
mla: Bergmiller, Tobias, and Nela Nikolic. Time-Lapse Microscopy Data. Institute
of Science and Technology Austria, 2018, doi:10.15479/AT:ISTA:74.
short: T. Bergmiller, N. Nikolic, (2018).
datarep_id: '74'
date_created: 2018-12-12T12:31:35Z
date_published: 2018-02-07T00:00:00Z
date_updated: 2024-02-21T13:44:45Z
day: '07'
ddc:
- '579'
department:
- _id: CaGu
doi: 10.15479/AT:ISTA:74
file:
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checksum: 61ebb92213cfffeba3ddbaff984b81af
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date_created: 2018-12-12T13:05:11Z
date_updated: 2020-07-14T12:47:04Z
file_id: '5639'
file_name: IST-2018-74-v1+4_Images_for_analysis.zip
file_size: 2140849248
relation: main_file
file_date_updated: 2020-07-14T12:47:04Z
has_accepted_license: '1'
keyword:
- microscopy
- microfluidics
license: https://creativecommons.org/publicdomain/zero/1.0/
month: '02'
oa: 1
oa_version: Published Version
publisher: Institute of Science and Technology Austria
publist_id: '7385'
related_material:
record:
- id: '438'
relation: research_paper
status: public
status: public
title: Time-lapse microscopy data
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
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
- first_name: Gasper
full_name: Tkacik, Gasper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkacik
orcid: 0000-0002-6699-1455
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).
date_created: 2018-12-11T11:44:57Z
date_published: 2018-07-30T00:00:00Z
date_updated: 2024-02-21T13:45:39Z
day: '30'
ddc:
- '570'
department:
- _id: GaTk
- _id: CaGu
doi: 10.1038/s41467-018-05417-9
ec_funded: 1
external_id:
isi:
- '000440149300021'
file:
- access_level: open_access
checksum: 3ba7ab27b27723c7dcf633e8fc1f8f18
content_type: application/pdf
creator: dernst
date_created: 2018-12-17T16:44:28Z
date_updated: 2020-07-14T12:45:06Z
file_id: '5728'
file_name: 2018_NatureComm_DeMartino.pdf
file_size: 1043205
relation: main_file
file_date_updated: 2020-07-14T12:45:06Z
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
issue: '1'
language:
- iso: eng
license: https://creativecommons.org/licenses/by/4.0/
month: '07'
oa: 1
oa_version: Published Version
project:
- _id: 254E9036-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P28844-B27
name: Biophysics of information processing in gene regulation
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
publication: Nature Communications
publication_status: published
publisher: Springer Nature
publist_id: '7760'
quality_controlled: '1'
related_material:
record:
- id: '5587'
relation: popular_science
status: public
scopus_import: '1'
status: public
title: Statistical mechanics for metabolic networks during steady state growth
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 9
year: '2018'
...
---
_id: '438'
abstract:
- lang: eng
text: The MazF toxin sequence-specifically cleaves single-stranded RNA upon various
stressful conditions, and it is activated as a part of the mazEF toxin–antitoxin
module in Escherichia coli. Although autoregulation of mazEF expression through
the MazE antitoxin-dependent transcriptional repression has been biochemically
characterized, less is known about post-transcriptional autoregulation, as well
as how both of these autoregulatory features affect growth of single cells during
conditions that promote MazF production. Here, we demonstrate post-transcriptional
autoregulation of mazF expression dynamics by MazF cleaving its own transcript.
Single-cell analyses of bacterial populations during ectopic MazF production indicated
that two-level autoregulation of mazEF expression influences cell-to-cell growth
rate heterogeneity. The increase in growth rate heterogeneity is governed by the
MazE antitoxin, and tuned by the MazF-dependent mazF mRNA cleavage. Also, both
autoregulatory features grant rapid exit from the stress caused by mazF overexpression.
Time-lapse microscopy revealed that MazF-mediated cleavage of mazF mRNA leads
to increased temporal variability in length of individual cells during ectopic
mazF overexpression, as explained by a stochastic model indicating that mazEF
mRNA cleavage underlies temporal fluctuations in MazF levels during stress.
article_processing_charge: Yes (in subscription journal)
author:
- first_name: Nela
full_name: Nikolic, Nela
id: 42D9CABC-F248-11E8-B48F-1D18A9856A87
last_name: Nikolic
orcid: 0000-0001-9068-6090
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Alexandra
full_name: Vandervelde, Alexandra
last_name: Vandervelde
- first_name: Tanino
full_name: Albanese, Tanino
last_name: Albanese
- first_name: Lendert
full_name: Gelens, Lendert
last_name: Gelens
- first_name: Isabella
full_name: Moll, Isabella
last_name: Moll
citation:
ama: Nikolic N, Bergmiller T, Vandervelde A, Albanese T, Gelens L, Moll I. Autoregulation
of mazEF expression underlies growth heterogeneity in bacterial populations. Nucleic
Acids Research. 2018;46(6):2918-2931. doi:10.1093/nar/gky079
apa: Nikolic, N., Bergmiller, T., Vandervelde, A., Albanese, T., Gelens, L., &
Moll, I. (2018). Autoregulation of mazEF expression underlies growth heterogeneity
in bacterial populations. Nucleic Acids Research. Oxford University Press.
https://doi.org/10.1093/nar/gky079
chicago: Nikolic, Nela, Tobias Bergmiller, Alexandra Vandervelde, Tanino Albanese,
Lendert Gelens, and Isabella Moll. “Autoregulation of MazEF Expression Underlies
Growth Heterogeneity in Bacterial Populations.” Nucleic Acids Research.
Oxford University Press, 2018. https://doi.org/10.1093/nar/gky079.
ieee: N. Nikolic, T. Bergmiller, A. Vandervelde, T. Albanese, L. Gelens, and I.
Moll, “Autoregulation of mazEF expression underlies growth heterogeneity in bacterial
populations,” Nucleic Acids Research, vol. 46, no. 6. Oxford University
Press, pp. 2918–2931, 2018.
ista: Nikolic N, Bergmiller T, Vandervelde A, Albanese T, Gelens L, Moll I. 2018.
Autoregulation of mazEF expression underlies growth heterogeneity in bacterial
populations. Nucleic Acids Research. 46(6), 2918–2931.
mla: Nikolic, Nela, et al. “Autoregulation of MazEF Expression Underlies Growth
Heterogeneity in Bacterial Populations.” Nucleic Acids Research, vol. 46,
no. 6, Oxford University Press, 2018, pp. 2918–31, doi:10.1093/nar/gky079.
short: N. Nikolic, T. Bergmiller, A. Vandervelde, T. Albanese, L. Gelens, I. Moll,
Nucleic Acids Research 46 (2018) 2918–2931.
date_created: 2018-12-11T11:46:29Z
date_published: 2018-04-06T00:00:00Z
date_updated: 2024-02-21T13:44:45Z
day: '06'
ddc:
- '576'
department:
- _id: CaGu
doi: 10.1093/nar/gky079
external_id:
isi:
- '000429009500021'
file:
- access_level: open_access
checksum: 3ff4f545c27e11a4cd20ccb30778793e
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:15:30Z
date_updated: 2020-07-14T12:46:27Z
file_id: '5151'
file_name: IST-2018-971-v1+1_2018_Nikoloc_Autoregulation_of.pdf
file_size: 5027978
relation: main_file
file_date_updated: 2020-07-14T12:46:27Z
has_accepted_license: '1'
intvolume: ' 46'
isi: 1
issue: '6'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 2918-2931
project:
- _id: 3AC91DDA-15DF-11EA-824D-93A3E7B544D1
call_identifier: FWF
name: FWF Open Access Fund
publication: Nucleic Acids Research
publication_status: published
publisher: Oxford University Press
pubrep_id: '971'
quality_controlled: '1'
related_material:
record:
- id: '5569'
relation: popular_science
status: public
scopus_import: '1'
status: public
title: Autoregulation of mazEF expression underlies growth heterogeneity in bacterial
populations
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 46
year: '2018'
...
---
_id: '665'
abstract:
- lang: eng
text: The molecular mechanisms underlying phenotypic variation in isogenic bacterial
populations remain poorly understood.We report that AcrAB-TolC, the main multidrug
efflux pump of Escherichia coli, exhibits a strong partitioning bias for old cell
poles by a segregation mechanism that is mediated by ternary AcrAB-TolC complex
formation. Mother cells inheriting old poles are phenotypically distinct and display
increased drug efflux activity relative to daughters. Consequently, we find systematic
and long-lived growth differences between mother and daughter cells in the presence
of subinhibitory drug concentrations. A simple model for biased partitioning predicts
a population structure of long-lived and highly heterogeneous phenotypes. This
straightforward mechanism of generating sustained growth rate differences at subinhibitory
antibiotic concentrations has implications for understanding the emergence of
multidrug resistance in bacteria.
article_processing_charge: No
article_type: original
author:
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Anna M
full_name: Andersson, Anna M
id: 2B8A40DA-F248-11E8-B48F-1D18A9856A87
last_name: Andersson
orcid: 0000-0003-2912-6769
- first_name: Kathrin
full_name: Tomasek, Kathrin
id: 3AEC8556-F248-11E8-B48F-1D18A9856A87
last_name: Tomasek
orcid: 0000-0003-3768-877X
- first_name: Enrique
full_name: Balleza, Enrique
last_name: Balleza
- first_name: Daniel
full_name: Kiviet, Daniel
last_name: Kiviet
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Gasper
full_name: Tkacik, Gasper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkacik
orcid: 0000-0002-6699-1455
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Bergmiller T, Andersson AM, Tomasek K, et al. Biased partitioning of the multidrug
efflux pump AcrAB TolC underlies long lived phenotypic heterogeneity. Science.
2017;356(6335):311-315. doi:10.1126/science.aaf4762
apa: Bergmiller, T., Andersson, A. M., Tomasek, K., Balleza, E., Kiviet, D., Hauschild,
R., … Guet, C. C. (2017). Biased partitioning of the multidrug efflux pump AcrAB
TolC underlies long lived phenotypic heterogeneity. Science. American Association
for the Advancement of Science. https://doi.org/10.1126/science.aaf4762
chicago: Bergmiller, Tobias, Anna M Andersson, Kathrin Tomasek, Enrique Balleza,
Daniel Kiviet, Robert Hauschild, Gašper Tkačik, and Calin C Guet. “Biased Partitioning
of the Multidrug Efflux Pump AcrAB TolC Underlies Long Lived Phenotypic Heterogeneity.”
Science. American Association for the Advancement of Science, 2017. https://doi.org/10.1126/science.aaf4762.
ieee: T. Bergmiller et al., “Biased partitioning of the multidrug efflux
pump AcrAB TolC underlies long lived phenotypic heterogeneity,” Science,
vol. 356, no. 6335. American Association for the Advancement of Science, pp. 311–315,
2017.
ista: Bergmiller T, Andersson AM, Tomasek K, Balleza E, Kiviet D, Hauschild R, Tkačik
G, Guet CC. 2017. Biased partitioning of the multidrug efflux pump AcrAB TolC
underlies long lived phenotypic heterogeneity. Science. 356(6335), 311–315.
mla: Bergmiller, Tobias, et al. “Biased Partitioning of the Multidrug Efflux Pump
AcrAB TolC Underlies Long Lived Phenotypic Heterogeneity.” Science, vol.
356, no. 6335, American Association for the Advancement of Science, 2017, pp.
311–15, doi:10.1126/science.aaf4762.
short: T. Bergmiller, A.M. Andersson, K. Tomasek, E. Balleza, D. Kiviet, R. Hauschild,
G. Tkačik, C.C. Guet, Science 356 (2017) 311–315.
date_created: 2018-12-11T11:47:48Z
date_published: 2017-04-21T00:00:00Z
date_updated: 2024-02-21T13:49:00Z
day: '21'
department:
- _id: CaGu
- _id: GaTk
- _id: Bio
doi: 10.1126/science.aaf4762
intvolume: ' 356'
issue: '6335'
language:
- iso: eng
month: '04'
oa_version: None
page: 311 - 315
project:
- _id: 254E9036-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P28844-B27
name: Biophysics of information processing in gene regulation
publication: Science
publication_identifier:
issn:
- '00368075'
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '7064'
quality_controlled: '1'
related_material:
record:
- id: '5560'
relation: popular_science
status: public
scopus_import: 1
status: public
title: Biased partitioning of the multidrug efflux pump AcrAB TolC underlies long
lived phenotypic heterogeneity
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 356
year: '2017'
...
---
_id: '541'
abstract:
- lang: eng
text: 'While we have good understanding of bacterial metabolism at the population
level, we know little about the metabolic behavior of individual cells: do single
cells in clonal populations sometimes specialize on different metabolic pathways?
Such metabolic specialization could be driven by stochastic gene expression and
could provide individual cells with growth benefits of specialization. We measured
the degree of phenotypic specialization in two parallel metabolic pathways, the
assimilation of glucose and arabinose. We grew Escherichia coli in chemostats,
and used isotope-labeled sugars in combination with nanometer-scale secondary
ion mass spectrometry and mathematical modeling to quantify sugar assimilation
at the single-cell level. We found large variation in metabolic activities between
single cells, both in absolute assimilation and in the degree to which individual
cells specialize in the assimilation of different sugars. Analysis of transcriptional
reporters indicated that this variation was at least partially based on cell-to-cell
variation in gene expression. Metabolic differences between cells in clonal populations
could potentially reduce metabolic incompatibilities between different pathways,
and increase the rate at which parallel reactions can be performed.'
article_number: e1007122
author:
- first_name: Nela
full_name: Nikolic, Nela
id: 42D9CABC-F248-11E8-B48F-1D18A9856A87
last_name: Nikolic
orcid: 0000-0001-9068-6090
- first_name: Frank
full_name: Schreiber, Frank
last_name: Schreiber
- first_name: Alma
full_name: Dal Co, Alma
last_name: Dal Co
- first_name: Daniel
full_name: Kiviet, Daniel
last_name: Kiviet
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Sten
full_name: Littmann, Sten
last_name: Littmann
- first_name: Marcel
full_name: Kuypers, Marcel
last_name: Kuypers
- first_name: Martin
full_name: Ackermann, Martin
last_name: Ackermann
citation:
ama: Nikolic N, Schreiber F, Dal Co A, et al. Cell-to-cell variation and specialization
in sugar metabolism in clonal bacterial populations. PLoS Genetics. 2017;13(12).
doi:10.1371/journal.pgen.1007122
apa: Nikolic, N., Schreiber, F., Dal Co, A., Kiviet, D., Bergmiller, T., Littmann,
S., … Ackermann, M. (2017). Cell-to-cell variation and specialization in sugar
metabolism in clonal bacterial populations. PLoS Genetics. Public Library
of Science. https://doi.org/10.1371/journal.pgen.1007122
chicago: Nikolic, Nela, Frank Schreiber, Alma Dal Co, Daniel Kiviet, Tobias Bergmiller,
Sten Littmann, Marcel Kuypers, and Martin Ackermann. “Cell-to-Cell Variation and
Specialization in Sugar Metabolism in Clonal Bacterial Populations.” PLoS Genetics.
Public Library of Science, 2017. https://doi.org/10.1371/journal.pgen.1007122.
ieee: N. Nikolic et al., “Cell-to-cell variation and specialization in sugar
metabolism in clonal bacterial populations,” PLoS Genetics, vol. 13, no.
12. Public Library of Science, 2017.
ista: Nikolic N, Schreiber F, Dal Co A, Kiviet D, Bergmiller T, Littmann S, Kuypers
M, Ackermann M. 2017. Cell-to-cell variation and specialization in sugar metabolism
in clonal bacterial populations. PLoS Genetics. 13(12), e1007122.
mla: Nikolic, Nela, et al. “Cell-to-Cell Variation and Specialization in Sugar Metabolism
in Clonal Bacterial Populations.” PLoS Genetics, vol. 13, no. 12, e1007122,
Public Library of Science, 2017, doi:10.1371/journal.pgen.1007122.
short: N. Nikolic, F. Schreiber, A. Dal Co, D. Kiviet, T. Bergmiller, S. Littmann,
M. Kuypers, M. Ackermann, PLoS Genetics 13 (2017).
date_created: 2018-12-11T11:47:04Z
date_published: 2017-12-18T00:00:00Z
date_updated: 2023-02-23T14:10:34Z
day: '18'
ddc:
- '576'
- '579'
department:
- _id: CaGu
doi: 10.1371/journal.pgen.1007122
ec_funded: 1
file:
- access_level: open_access
checksum: 22426d9382f21554bad5fa5967afcfd0
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:35Z
date_updated: 2020-07-14T12:46:46Z
file_id: '5088'
file_name: IST-2018-959-v1+1_2017_Nikolic_Cell-to-cell.pdf
file_size: 1308475
relation: main_file
file_date_updated: 2020-07-14T12:46:46Z
has_accepted_license: '1'
intvolume: ' 13'
issue: '12'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
publication: PLoS Genetics
publication_identifier:
issn:
- '15537390'
publication_status: published
publisher: Public Library of Science
publist_id: '7275'
pubrep_id: '959'
quality_controlled: '1'
related_material:
record:
- id: '9844'
relation: research_data
status: public
- id: '9845'
relation: research_data
status: public
- id: '9846'
relation: research_data
status: public
scopus_import: 1
status: public
title: Cell-to-cell variation and specialization in sugar metabolism in clonal bacterial
populations
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 13
year: '2017'
...
---
_id: '5560'
abstract:
- lang: eng
text: "This repository contains the data collected for the manuscript \"Biased partitioning
of the multi-drug efflux pump AcrAB-TolC underlies long-lived phenotypic heterogeneity\".\r\nThe
data is compressed into a single archive. Within the archive, different folders
correspond to figures of the main text and the SI of the related publication.\r\nData
is saved as plain text, with each folder containing a separate readme file describing
the format. Typically, the data is from fluorescence microscopy measurements of
single cells growing in a microfluidic \"mother machine\" device, and consists
of relevant values (primarily arbitrary unit or normalized fluorescence measurements,
and division times / growth rates) after raw microscopy images have been processed,
segmented, and their features extracted, as described in the methods section of
the related publication."
article_processing_charge: No
author:
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Anna M
full_name: Andersson, Anna M
id: 2B8A40DA-F248-11E8-B48F-1D18A9856A87
last_name: Andersson
orcid: 0000-0003-2912-6769
- first_name: Kathrin
full_name: Tomasek, Kathrin
id: 3AEC8556-F248-11E8-B48F-1D18A9856A87
last_name: Tomasek
orcid: 0000-0003-3768-877X
- first_name: Enrique
full_name: Balleza, Enrique
last_name: Balleza
- first_name: Daniel
full_name: Kiviet, Daniel
last_name: Kiviet
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Gasper
full_name: Tkacik, Gasper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkacik
orcid: 0000-0002-6699-1455
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Bergmiller T, Andersson AM, Tomasek K, et al. Biased partitioning of the multi-drug
efflux pump AcrAB-TolC underlies long-lived phenotypic heterogeneity. 2017. doi:10.15479/AT:ISTA:53
apa: Bergmiller, T., Andersson, A. M., Tomasek, K., Balleza, E., Kiviet, D., Hauschild,
R., … Guet, C. C. (2017). Biased partitioning of the multi-drug efflux pump AcrAB-TolC
underlies long-lived phenotypic heterogeneity. Institute of Science and Technology
Austria. https://doi.org/10.15479/AT:ISTA:53
chicago: Bergmiller, Tobias, Anna M Andersson, Kathrin Tomasek, Enrique Balleza,
Daniel Kiviet, Robert Hauschild, Gašper Tkačik, and Calin C Guet. “Biased Partitioning
of the Multi-Drug Efflux Pump AcrAB-TolC Underlies Long-Lived Phenotypic Heterogeneity.”
Institute of Science and Technology Austria, 2017. https://doi.org/10.15479/AT:ISTA:53.
ieee: T. Bergmiller et al., “Biased partitioning of the multi-drug efflux
pump AcrAB-TolC underlies long-lived phenotypic heterogeneity.” Institute of Science
and Technology Austria, 2017.
ista: Bergmiller T, Andersson AM, Tomasek K, Balleza E, Kiviet D, Hauschild R, Tkačik
G, Guet CC. 2017. Biased partitioning of the multi-drug efflux pump AcrAB-TolC
underlies long-lived phenotypic heterogeneity, Institute of Science and Technology
Austria, 10.15479/AT:ISTA:53.
mla: Bergmiller, Tobias, et al. Biased Partitioning of the Multi-Drug Efflux
Pump AcrAB-TolC Underlies Long-Lived Phenotypic Heterogeneity. Institute of
Science and Technology Austria, 2017, doi:10.15479/AT:ISTA:53.
short: T. Bergmiller, A.M. Andersson, K. Tomasek, E. Balleza, D. Kiviet, R. Hauschild,
G. Tkačik, C.C. Guet, (2017).
datarep_id: '53'
date_created: 2018-12-12T12:31:32Z
date_published: 2017-03-10T00:00:00Z
date_updated: 2024-02-21T13:49:00Z
day: '10'
ddc:
- '571'
department:
- _id: CaGu
- _id: GaTk
- _id: Bio
doi: 10.15479/AT:ISTA:53
file:
- access_level: open_access
checksum: d77859af757ac8025c50c7b12b52eaf3
content_type: application/zip
creator: system
date_created: 2018-12-12T13:02:38Z
date_updated: 2020-07-14T12:47:03Z
file_id: '5603'
file_name: IST-2017-53-v1+1_Data_MDE.zip
file_size: 6773204
relation: main_file
file_date_updated: 2020-07-14T12:47:03Z
has_accepted_license: '1'
keyword:
- single cell microscopy
- mother machine microfluidic device
- AcrAB-TolC pump
- multi-drug efflux
- Escherichia coli
month: '03'
oa: 1
oa_version: Published Version
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '665'
relation: research_paper
status: public
status: public
title: Biased partitioning of the multi-drug efflux pump AcrAB-TolC underlies long-lived
phenotypic heterogeneity
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: '2017'
...
---
_id: '613'
abstract:
- lang: eng
text: 'Bacteria in groups vary individually, and interact with other bacteria and
the environment to produce population-level patterns of gene expression. Investigating
such behavior in detail requires measuring and controlling populations at the
single-cell level alongside precisely specified interactions and environmental
characteristics. Here we present an automated, programmable platform that combines
image-based gene expression and growth measurements with on-line optogenetic expression
control for hundreds of individual Escherichia coli cells over days, in a dynamically
adjustable environment. This integrated platform broadly enables experiments that
bridge individual and population behaviors. We demonstrate: (i) population structuring
by independent closed-loop control of gene expression in many individual cells,
(ii) cell-cell variation control during antibiotic perturbation, (iii) hybrid
bio-digital circuits in single cells, and freely specifiable digital communication
between individual bacteria. These examples showcase the potential for real-time
integration of theoretical models with measurement and control of many individual
cells to investigate and engineer microbial population behavior.'
acknowledgement: We are grateful to M. Lang, H. Janovjak, M. Khammash, A. Milias-Argeitis,
M. Rullan, G. Batt, A. Bosma-Moody, Aryan, S. Leibler, and members of the Guet and
Tkačik groups for helpful discussion, comments, and suggestions. We thank A. Moglich,
T. Mathes, J. Tabor, and S. Schmidl for kind gifts of strains, and R. Hauschild,
B. Knep, M. Lang, T. Asenov, E. Papusheva, T. Menner, T. Adletzberger, and J. Merrin
for technical assistance. The research leading to these results has received funding
from the People Programme (Marie Curie Actions) of the European Union’s Seventh
Framework Programme (FP7/2007–2013) under REA grant agreement no. [291734]. (to
R.C. and J.R.), Austrian Science Fund grant FWF P28844 (to G.T.), and internal IST
Austria Interdisciplinary Project Support. J.R. acknowledges support from the Agence
Nationale de la Recherche (ANR) under Grant Nos. ANR-16-CE33-0018 (MEMIP), ANR-16-CE12-0025
(COGEX) and ANR-10-BINF-06-01 (ICEBERG).
article_number: '1535'
article_processing_charge: Yes (in subscription journal)
author:
- first_name: Remy P
full_name: Chait, Remy P
id: 3464AE84-F248-11E8-B48F-1D18A9856A87
last_name: Chait
orcid: 0000-0003-0876-3187
- first_name: Jakob
full_name: Ruess, Jakob
id: 4A245D00-F248-11E8-B48F-1D18A9856A87
last_name: Ruess
orcid: 0000-0003-1615-3282
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Gasper
full_name: Tkacik, Gasper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkacik
orcid: 0000-0002-6699-1455
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Chait RP, Ruess J, Bergmiller T, Tkačik G, Guet CC. Shaping bacterial population
behavior through computer interfaced control of individual cells. Nature Communications.
2017;8(1). doi:10.1038/s41467-017-01683-1
apa: Chait, R. P., Ruess, J., Bergmiller, T., Tkačik, G., & Guet, C. C. (2017).
Shaping bacterial population behavior through computer interfaced control of individual
cells. Nature Communications. Nature Publishing Group. https://doi.org/10.1038/s41467-017-01683-1
chicago: Chait, Remy P, Jakob Ruess, Tobias Bergmiller, Gašper Tkačik, and Calin
C Guet. “Shaping Bacterial Population Behavior through Computer Interfaced Control
of Individual Cells.” Nature Communications. Nature Publishing Group, 2017.
https://doi.org/10.1038/s41467-017-01683-1.
ieee: R. P. Chait, J. Ruess, T. Bergmiller, G. Tkačik, and C. C. Guet, “Shaping
bacterial population behavior through computer interfaced control of individual
cells,” Nature Communications, vol. 8, no. 1. Nature Publishing Group,
2017.
ista: Chait RP, Ruess J, Bergmiller T, Tkačik G, Guet CC. 2017. Shaping bacterial
population behavior through computer interfaced control of individual cells. Nature
Communications. 8(1), 1535.
mla: Chait, Remy P., et al. “Shaping Bacterial Population Behavior through Computer
Interfaced Control of Individual Cells.” Nature Communications, vol. 8,
no. 1, 1535, Nature Publishing Group, 2017, doi:10.1038/s41467-017-01683-1.
short: R.P. Chait, J. Ruess, T. Bergmiller, G. Tkačik, C.C. Guet, Nature Communications
8 (2017).
date_created: 2018-12-11T11:47:30Z
date_published: 2017-12-01T00:00:00Z
date_updated: 2021-01-12T08:06:15Z
day: '01'
ddc:
- '576'
- '579'
department:
- _id: CaGu
- _id: GaTk
doi: 10.1038/s41467-017-01683-1
ec_funded: 1
file:
- access_level: open_access
checksum: 44bb5d0229926c23a9955d9fe0f9723f
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:16:05Z
date_updated: 2020-07-14T12:47:20Z
file_id: '5190'
file_name: IST-2017-911-v1+1_s41467-017-01683-1.pdf
file_size: 1951699
relation: main_file
file_date_updated: 2020-07-14T12:47:20Z
has_accepted_license: '1'
intvolume: ' 8'
issue: '1'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 254E9036-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P28844-B27
name: Biophysics of information processing in gene regulation
publication: Nature Communications
publication_identifier:
issn:
- '20411723'
publication_status: published
publisher: Nature Publishing Group
publist_id: '7191'
pubrep_id: '911'
quality_controlled: '1'
scopus_import: 1
status: public
title: Shaping bacterial population behavior through computer interfaced control of
individual cells
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 8
year: '2017'
...
---
_id: '655'
abstract:
- lang: eng
text: 'The bacterial flagellum is a self-assembling nanomachine. The external flagellar
filament, several times longer than a bacterial cell body, is made of a few tens
of thousands subunits of a single protein: flagellin. A fundamental problem concerns
the molecular mechanism of how the flagellum grows outside the cell, where no
discernible energy source is available. Here, we monitored the dynamic assembly
of individual flagella using in situ labelling and real-time immunostaining of
elongating flagellar filaments. We report that the rate of flagellum growth, initially
~1,700 amino acids per second, decreases with length and that the previously proposed
chain mechanism does not contribute to the filament elongation dynamics. Inhibition
of the proton motive force-dependent export apparatus revealed a major contribution
of substrate injection in driving filament elongation. The combination of experimental
and mathematical evidence demonstrates that a simple, injection-diffusion mechanism
controls bacterial flagella growth outside the cell.'
article_number: e23136
author:
- first_name: Thibaud
full_name: Renault, Thibaud
last_name: Renault
- first_name: Anthony
full_name: Abraham, Anthony
last_name: Abraham
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Guillaume
full_name: Paradis, Guillaume
last_name: Paradis
- first_name: Simon
full_name: Rainville, Simon
last_name: Rainville
- first_name: Emmanuelle
full_name: Charpentier, Emmanuelle
last_name: Charpentier
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
- first_name: Yuhai
full_name: Tu, Yuhai
last_name: Tu
- first_name: Keiichi
full_name: Namba, Keiichi
last_name: Namba
- first_name: James
full_name: Keener, James
last_name: Keener
- first_name: Tohru
full_name: Minamino, Tohru
last_name: Minamino
- first_name: Marc
full_name: Erhardt, Marc
last_name: Erhardt
citation:
ama: Renault T, Abraham A, Bergmiller T, et al. Bacterial flagella grow through
an injection diffusion mechanism. eLife. 2017;6. doi:10.7554/eLife.23136
apa: Renault, T., Abraham, A., Bergmiller, T., Paradis, G., Rainville, S., Charpentier,
E., … Erhardt, M. (2017). Bacterial flagella grow through an injection diffusion
mechanism. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.23136
chicago: Renault, Thibaud, Anthony Abraham, Tobias Bergmiller, Guillaume Paradis,
Simon Rainville, Emmanuelle Charpentier, Calin C Guet, et al. “Bacterial Flagella
Grow through an Injection Diffusion Mechanism.” ELife. eLife Sciences Publications,
2017. https://doi.org/10.7554/eLife.23136.
ieee: T. Renault et al., “Bacterial flagella grow through an injection diffusion
mechanism,” eLife, vol. 6. eLife Sciences Publications, 2017.
ista: Renault T, Abraham A, Bergmiller T, Paradis G, Rainville S, Charpentier E,
Guet CC, Tu Y, Namba K, Keener J, Minamino T, Erhardt M. 2017. Bacterial flagella
grow through an injection diffusion mechanism. eLife. 6, e23136.
mla: Renault, Thibaud, et al. “Bacterial Flagella Grow through an Injection Diffusion
Mechanism.” ELife, vol. 6, e23136, eLife Sciences Publications, 2017, doi:10.7554/eLife.23136.
short: T. Renault, A. Abraham, T. Bergmiller, G. Paradis, S. Rainville, E. Charpentier,
C.C. Guet, Y. Tu, K. Namba, J. Keener, T. Minamino, M. Erhardt, ELife 6 (2017).
date_created: 2018-12-11T11:47:44Z
date_published: 2017-03-06T00:00:00Z
date_updated: 2021-01-12T08:07:55Z
day: '06'
ddc:
- '579'
department:
- _id: CaGu
doi: 10.7554/eLife.23136
file:
- access_level: open_access
checksum: 39e1c3e82ddac83a30422fa72fa1a383
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:08:53Z
date_updated: 2020-07-14T12:47:33Z
file_id: '4716'
file_name: IST-2017-904-v1+1_elife-23136-v2.pdf
file_size: 5520359
relation: main_file
- access_level: open_access
checksum: a6d542253028f52e00aa29739ddffe8f
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:08:54Z
date_updated: 2020-07-14T12:47:33Z
file_id: '4717'
file_name: IST-2017-904-v1+2_elife-23136-figures-v2.pdf
file_size: 11242920
relation: main_file
file_date_updated: 2020-07-14T12:47:33Z
has_accepted_license: '1'
intvolume: ' 6'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
issn:
- 2050084X
publication_status: published
publisher: eLife Sciences Publications
publist_id: '7082'
pubrep_id: '904'
quality_controlled: '1'
scopus_import: 1
status: public
title: Bacterial flagella grow through an injection diffusion mechanism
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 6
year: '2017'
...
---
_id: '9844'
article_processing_charge: No
author:
- first_name: Nela
full_name: Nikolic, Nela
id: 42D9CABC-F248-11E8-B48F-1D18A9856A87
last_name: Nikolic
orcid: 0000-0001-9068-6090
- first_name: Frank
full_name: Schreiber, Frank
last_name: Schreiber
- first_name: Alma
full_name: Dal Co, Alma
last_name: Dal Co
- first_name: Daniel
full_name: Kiviet, Daniel
last_name: Kiviet
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Sten
full_name: Littmann, Sten
last_name: Littmann
- first_name: Marcel
full_name: Kuypers, Marcel
last_name: Kuypers
- first_name: Martin
full_name: Ackermann, Martin
last_name: Ackermann
citation:
ama: Nikolic N, Schreiber F, Dal Co A, et al. Source data for figures and tables.
2017. doi:10.1371/journal.pgen.1007122.s018
apa: Nikolic, N., Schreiber, F., Dal Co, A., Kiviet, D., Bergmiller, T., Littmann,
S., … Ackermann, M. (2017). Source data for figures and tables. Public Library
of Science. https://doi.org/10.1371/journal.pgen.1007122.s018
chicago: Nikolic, Nela, Frank Schreiber, Alma Dal Co, Daniel Kiviet, Tobias Bergmiller,
Sten Littmann, Marcel Kuypers, and Martin Ackermann. “Source Data for Figures
and Tables.” Public Library of Science, 2017. https://doi.org/10.1371/journal.pgen.1007122.s018.
ieee: N. Nikolic et al., “Source data for figures and tables.” Public Library
of Science, 2017.
ista: Nikolic N, Schreiber F, Dal Co A, Kiviet D, Bergmiller T, Littmann S, Kuypers
M, Ackermann M. 2017. Source data for figures and tables, Public Library of Science,
10.1371/journal.pgen.1007122.s018.
mla: Nikolic, Nela, et al. Source Data for Figures and Tables. Public Library
of Science, 2017, doi:10.1371/journal.pgen.1007122.s018.
short: N. Nikolic, F. Schreiber, A. Dal Co, D. Kiviet, T. Bergmiller, S. Littmann,
M. Kuypers, M. Ackermann, (2017).
date_created: 2021-08-09T13:27:16Z
date_published: 2017-12-18T00:00:00Z
date_updated: 2023-02-23T12:25:04Z
day: '18'
department:
- _id: CaGu
doi: 10.1371/journal.pgen.1007122.s018
month: '12'
oa_version: Published Version
publisher: Public Library of Science
related_material:
record:
- id: '541'
relation: used_in_publication
status: public
status: public
title: Source data for figures and tables
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2017'
...
---
_id: '9845'
abstract:
- lang: eng
text: "Estimates of 13 C-arabinose and 2 H-glucose uptake from the fractions of
heavy isotopes measured\tin single cells"
article_processing_charge: No
author:
- first_name: Nela
full_name: Nikolic, Nela
id: 42D9CABC-F248-11E8-B48F-1D18A9856A87
last_name: Nikolic
orcid: 0000-0001-9068-6090
- first_name: Frank
full_name: Schreiber, Frank
last_name: Schreiber
- first_name: Alma
full_name: Dal Co, Alma
last_name: Dal Co
- first_name: Daniel
full_name: Kiviet, Daniel
last_name: Kiviet
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Sten
full_name: Littmann, Sten
last_name: Littmann
- first_name: Marcel
full_name: Kuypers, Marcel
last_name: Kuypers
- first_name: Martin
full_name: Ackermann, Martin
last_name: Ackermann
citation:
ama: Nikolic N, Schreiber F, Dal Co A, et al. Mathematical model. 2017. doi:10.1371/journal.pgen.1007122.s017
apa: Nikolic, N., Schreiber, F., Dal Co, A., Kiviet, D., Bergmiller, T., Littmann,
S., … Ackermann, M. (2017). Mathematical model. Public Library of Science. https://doi.org/10.1371/journal.pgen.1007122.s017
chicago: Nikolic, Nela, Frank Schreiber, Alma Dal Co, Daniel Kiviet, Tobias Bergmiller,
Sten Littmann, Marcel Kuypers, and Martin Ackermann. “Mathematical Model.” Public
Library of Science, 2017. https://doi.org/10.1371/journal.pgen.1007122.s017.
ieee: N. Nikolic et al., “Mathematical model.” Public Library of Science,
2017.
ista: Nikolic N, Schreiber F, Dal Co A, Kiviet D, Bergmiller T, Littmann S, Kuypers
M, Ackermann M. 2017. Mathematical model, Public Library of Science, 10.1371/journal.pgen.1007122.s017.
mla: Nikolic, Nela, et al. Mathematical Model. Public Library of Science,
2017, doi:10.1371/journal.pgen.1007122.s017.
short: N. Nikolic, F. Schreiber, A. Dal Co, D. Kiviet, T. Bergmiller, S. Littmann,
M. Kuypers, M. Ackermann, (2017).
date_created: 2021-08-09T13:31:51Z
date_published: 2017-12-18T00:00:00Z
date_updated: 2023-02-23T12:25:04Z
day: '18'
department:
- _id: CaGu
doi: 10.1371/journal.pgen.1007122.s017
month: '12'
oa_version: None
publisher: Public Library of Science
related_material:
record:
- id: '541'
relation: used_in_publication
status: public
status: public
title: Mathematical model
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2017'
...
---
_id: '9846'
article_processing_charge: No
author:
- first_name: Nela
full_name: Nikolic, Nela
id: 42D9CABC-F248-11E8-B48F-1D18A9856A87
last_name: Nikolic
orcid: 0000-0001-9068-6090
- first_name: Frank
full_name: Schreiber, Frank
last_name: Schreiber
- first_name: Alma
full_name: Dal Co, Alma
last_name: Dal Co
- first_name: Daniel
full_name: Kiviet, Daniel
last_name: Kiviet
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Sten
full_name: Littmann, Sten
last_name: Littmann
- first_name: Marcel
full_name: Kuypers, Marcel
last_name: Kuypers
- first_name: Martin
full_name: Ackermann, Martin
last_name: Ackermann
citation:
ama: Nikolic N, Schreiber F, Dal Co A, et al. Supplementary methods. 2017. doi:10.1371/journal.pgen.1007122.s016
apa: Nikolic, N., Schreiber, F., Dal Co, A., Kiviet, D., Bergmiller, T., Littmann,
S., … Ackermann, M. (2017). Supplementary methods. Public Library of Science.
https://doi.org/10.1371/journal.pgen.1007122.s016
chicago: Nikolic, Nela, Frank Schreiber, Alma Dal Co, Daniel Kiviet, Tobias Bergmiller,
Sten Littmann, Marcel Kuypers, and Martin Ackermann. “Supplementary Methods.”
Public Library of Science, 2017. https://doi.org/10.1371/journal.pgen.1007122.s016.
ieee: N. Nikolic et al., “Supplementary methods.” Public Library of Science,
2017.
ista: Nikolic N, Schreiber F, Dal Co A, Kiviet D, Bergmiller T, Littmann S, Kuypers
M, Ackermann M. 2017. Supplementary methods, Public Library of Science, 10.1371/journal.pgen.1007122.s016.
mla: Nikolic, Nela, et al. Supplementary Methods. Public Library of Science,
2017, doi:10.1371/journal.pgen.1007122.s016.
short: N. Nikolic, F. Schreiber, A. Dal Co, D. Kiviet, T. Bergmiller, S. Littmann,
M. Kuypers, M. Ackermann, (2017).
date_created: 2021-08-09T13:35:17Z
date_published: 2017-12-18T00:00:00Z
date_updated: 2023-02-23T12:25:04Z
day: '18'
department:
- _id: CaGu
doi: 10.1371/journal.pgen.1007122.s016
month: '12'
oa_version: Published Version
publisher: Public Library of Science
related_material:
record:
- id: '541'
relation: used_in_publication
status: public
status: public
title: Supplementary methods
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2017'
...
---
_id: '5749'
abstract:
- lang: eng
text: Parasitism creates selection for resistance mechanisms in host populations
and is hypothesized to promote increased host evolvability. However, the influence
of these traits on host evolution when parasites are no longer present is unclear.
We used experimental evolution and whole-genome sequencing of Escherichia coli
to determine the effects of past and present exposure to parasitic viruses (phages)
on the spread of mutator alleles, resistance, and bacterial competitive fitness.
We found that mutator alleles spread rapidly during adaptation to any of four
different phage species, and this pattern was even more pronounced with multiple
phages present simultaneously. However, hypermutability did not detectably accelerate
adaptation in the absence of phages and recovery of fitness costs associated with
resistance. Several lineages evolved phage resistance through elevated mucoidy,
and during subsequent evolution in phage-free conditions they rapidly reverted
to nonmucoid, phage-susceptible phenotypes. Genome sequencing revealed that this
phenotypic reversion was achieved by additional genetic changes rather than by
genotypic reversion of the initial resistance mutations. Insertion sequence (IS)
elements played a key role in both the acquisition of resistance and adaptation
in the absence of parasites; unlike single nucleotide polymorphisms, IS insertions
were not more frequent in mutator lineages. Our results provide a genetic explanation
for rapid reversion of mucoidy, a phenotype observed in other bacterial species
including human pathogens. Moreover, this demonstrates that the types of genetic
change underlying adaptation to fitness costs, and consequently the impact of
evolvability mechanisms such as increased point-mutation rates, depend critically
on the mechanism of resistance.
acknowledgement: The authors thank three anonymous reviewers and the editor for helpful
comments on the manuscript, as well as Dominique Schneider for feedback on an earlier
draft, Jenna Gallie for lytic λ and Julien Capelle for T5 and T6. This work was
supported by the Swiss National Science Foundation (PZ00P3_148255 to A.H.) and an
EU Marie Curie PEOPLE Postdoctoral Fellowship for Career Development (FP7-PEOPLE-2012-IEF-331824
to S.W.).
article_processing_charge: No
author:
- first_name: Sébastien
full_name: Wielgoss, Sébastien
last_name: Wielgoss
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Anna M.
full_name: Bischofberger, Anna M.
last_name: Bischofberger
- first_name: Alex R.
full_name: Hall, Alex R.
last_name: Hall
citation:
ama: Wielgoss S, Bergmiller T, Bischofberger AM, Hall AR. Adaptation to parasites
and costs of parasite resistance in mutator and nonmutator bacteria. Molecular
Biology and Evolution. 2016;33(3):770-782. doi:10.1093/molbev/msv270
apa: Wielgoss, S., Bergmiller, T., Bischofberger, A. M., & Hall, A. R. (2016).
Adaptation to parasites and costs of parasite resistance in mutator and nonmutator
bacteria. Molecular Biology and Evolution. Oxford University Press. https://doi.org/10.1093/molbev/msv270
chicago: Wielgoss, Sébastien, Tobias Bergmiller, Anna M. Bischofberger, and Alex
R. Hall. “Adaptation to Parasites and Costs of Parasite Resistance in Mutator
and Nonmutator Bacteria.” Molecular Biology and Evolution. Oxford University
Press, 2016. https://doi.org/10.1093/molbev/msv270.
ieee: S. Wielgoss, T. Bergmiller, A. M. Bischofberger, and A. R. Hall, “Adaptation
to parasites and costs of parasite resistance in mutator and nonmutator bacteria,”
Molecular Biology and Evolution, vol. 33, no. 3. Oxford University Press,
pp. 770–782, 2016.
ista: Wielgoss S, Bergmiller T, Bischofberger AM, Hall AR. 2016. Adaptation to parasites
and costs of parasite resistance in mutator and nonmutator bacteria. Molecular
Biology and Evolution. 33(3), 770–782.
mla: Wielgoss, Sébastien, et al. “Adaptation to Parasites and Costs of Parasite
Resistance in Mutator and Nonmutator Bacteria.” Molecular Biology and Evolution,
vol. 33, no. 3, Oxford University Press, 2016, pp. 770–82, doi:10.1093/molbev/msv270.
short: S. Wielgoss, T. Bergmiller, A.M. Bischofberger, A.R. Hall, Molecular Biology
and Evolution 33 (2016) 770–782.
date_created: 2018-12-18T13:18:10Z
date_published: 2016-03-01T00:00:00Z
date_updated: 2023-09-05T13:46:05Z
day: '01'
ddc:
- '576'
department:
- _id: CaGu
doi: 10.1093/molbev/msv270
external_id:
pmid:
- '26609077'
file:
- access_level: open_access
checksum: 47d9010690b6c5c17f2ac830cc63ac5c
content_type: application/pdf
creator: dernst
date_created: 2018-12-18T13:21:45Z
date_updated: 2020-07-14T12:47:10Z
file_id: '5750'
file_name: 2016_MolBiolEvol_Wielgoss.pdf
file_size: 634037
relation: main_file
file_date_updated: 2020-07-14T12:47:10Z
has_accepted_license: '1'
intvolume: ' 33'
issue: '3'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc/4.0/
month: '03'
oa: 1
oa_version: Published Version
page: 770-782
pmid: 1
publication: Molecular Biology and Evolution
publication_identifier:
eissn:
- 1537-1719
issn:
- 0737-4038
publication_status: published
publisher: Oxford University Press
pubrep_id: '587'
quality_controlled: '1'
related_material:
record:
- id: '9719'
relation: research_data
status: public
scopus_import: '1'
status: public
title: Adaptation to parasites and costs of parasite resistance in mutator and nonmutator
bacteria
tmp:
image: /images/cc_by_nc.png
legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode
name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
short: CC BY-NC (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 33
year: '2016'
...
---
_id: '1243'
abstract:
- lang: eng
text: Restriction-modification (RM) systems represent a minimal and ubiquitous biological
system of self/non-self discrimination in prokaryotes [1], which protects hosts
from exogenous DNA [2]. The mechanism is based on the balance between methyltransferase
(M) and cognate restriction endonuclease (R). M tags endogenous DNA as self by
methylating short specific DNA sequences called restriction sites, whereas R recognizes
unmethylated restriction sites as non-self and introduces a double-stranded DNA
break [3]. Restriction sites are significantly underrepresented in prokaryotic
genomes [4-7], suggesting that the discrimination mechanism is imperfect and occasionally
leads to autoimmunity due to self-DNA cleavage (self-restriction) [8]. Furthermore,
RM systems can promote DNA recombination [9] and contribute to genetic variation
in microbial populations, thus facilitating adaptive evolution [10]. However,
cleavage of self-DNA by RM systems as elements shaping prokaryotic genomes has
not been directly detected, and its cause, frequency, and outcome are unknown.
We quantify self-restriction caused by two RM systems of Escherichia coli and
find that, in agreement with levels of restriction site avoidance, EcoRI, but
not EcoRV, cleaves self-DNA at a measurable rate. Self-restriction is a stochastic
process, which temporarily induces the SOS response, and is followed by DNA repair,
maintaining cell viability. We find that RM systems with higher restriction efficiency
against bacteriophage infections exhibit a higher rate of self-restriction, and
that this rate can be further increased by stochastic imbalance between R and
M. Our results identify molecular noise in RM systems as a factor shaping prokaryotic
genomes.
acknowledgement: This work was funded by an HFSP Young Investigators’ grant. M.P.
is a recipient of a DOC Fellowship of the Austrian Academy of Science at the Institute
of Science and Technology Austria. R.O. and Y.W. were supported by the Platform
for Dynamic Approaches to Living System from MEXT, Japan. We wish to thank I. Kobayashi
for providing us with the EcoRI and EcoRV plasmids, and A. Campbell for providing
us with the λ vir phage. We thank D. Siekhaus and C. Uhler and members of the C.C.G.
and J.P. Bollback laboratories for in-depth discussions. We thank B. Stern for comments
on an earlier version of the manuscript. We especially thank B.R. Levin for advice
and comments, and the anonymous reviewers for significantly improving the manuscript.
author:
- first_name: Maros
full_name: Pleska, Maros
id: 4569785E-F248-11E8-B48F-1D18A9856A87
last_name: Pleska
orcid: 0000-0001-7460-7479
- first_name: Long
full_name: Qian, Long
last_name: Qian
- first_name: Reiko
full_name: Okura, Reiko
last_name: Okura
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Yuichi
full_name: Wakamoto, Yuichi
last_name: Wakamoto
- first_name: Edo
full_name: Kussell, Edo
last_name: Kussell
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Pleska M, Qian L, Okura R, et al. Bacterial autoimmunity due to a restriction-modification
system. Current Biology. 2016;26(3):404-409. doi:10.1016/j.cub.2015.12.041
apa: Pleska, M., Qian, L., Okura, R., Bergmiller, T., Wakamoto, Y., Kussell, E.,
& Guet, C. C. (2016). Bacterial autoimmunity due to a restriction-modification
system. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2015.12.041
chicago: Pleska, Maros, Long Qian, Reiko Okura, Tobias Bergmiller, Yuichi Wakamoto,
Edo Kussell, and Calin C Guet. “Bacterial Autoimmunity Due to a Restriction-Modification
System.” Current Biology. Cell Press, 2016. https://doi.org/10.1016/j.cub.2015.12.041.
ieee: M. Pleska et al., “Bacterial autoimmunity due to a restriction-modification
system,” Current Biology, vol. 26, no. 3. Cell Press, pp. 404–409, 2016.
ista: Pleska M, Qian L, Okura R, Bergmiller T, Wakamoto Y, Kussell E, Guet CC. 2016.
Bacterial autoimmunity due to a restriction-modification system. Current Biology.
26(3), 404–409.
mla: Pleska, Maros, et al. “Bacterial Autoimmunity Due to a Restriction-Modification
System.” Current Biology, vol. 26, no. 3, Cell Press, 2016, pp. 404–09,
doi:10.1016/j.cub.2015.12.041.
short: M. Pleska, L. Qian, R. Okura, T. Bergmiller, Y. Wakamoto, E. Kussell, C.C.
Guet, Current Biology 26 (2016) 404–409.
date_created: 2018-12-11T11:50:54Z
date_published: 2016-02-08T00:00:00Z
date_updated: 2023-09-07T11:59:32Z
day: '08'
department:
- _id: CaGu
doi: 10.1016/j.cub.2015.12.041
intvolume: ' 26'
issue: '3'
language:
- iso: eng
month: '02'
oa_version: None
page: 404 - 409
project:
- _id: 251D65D8-B435-11E9-9278-68D0E5697425
grant_number: '24210'
name: Effects of Stochasticity on the Function of Restriction-Modi cation Systems
at the Single-Cell Level (DOC Fellowship)
publication: Current Biology
publication_status: published
publisher: Cell Press
publist_id: '6087'
quality_controlled: '1'
related_material:
record:
- id: '202'
relation: dissertation_contains
status: public
scopus_import: 1
status: public
title: Bacterial autoimmunity due to a restriction-modification system
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 26
year: '2016'
...
---
_id: '1250'
abstract:
- lang: eng
text: In bacteria, replicative aging manifests as a difference in growth or survival
between the two cells emerging from division. One cell can be regarded as an aging
mother with a decreased potential for future survival and division, the other
as a rejuvenated daughter. Here, we aimed at investigating some of the processes
involved in aging in the bacterium Escherichia coli, where the two types of cells
can be distinguished by the age of their cell poles. We found that certain changes
in the regulation of the carbohydrate metabolism can affect aging. A mutation
in the carbon storage regulator gene, csrA, leads to a dramatically shorter replicative
lifespan; csrA mutants stop dividing once their pole exceeds an age of about five
divisions. These old-pole cells accumulate glycogen at their old cell poles; after
their last division, they do not contain a chromosome, presumably because of spatial
exclusion by the glycogen aggregates. The new-pole daughters produced by these
aging mothers are born young; they only express the deleterious phenotype once
their pole is old. These results demonstrate how manipulations of nutrient allocation
can lead to the exclusion of the chromosome and limit replicative lifespan in
E. coli, and illustrate how mutations can have phenotypic effects that are specific
for cells with old poles. This raises the question how bacteria can avoid the
accumulation of such mutations in their genomes over evolutionary times, and how
they can achieve the long replicative lifespans that have recently been reported.
acknowledgement: This manuscript is dedicated to the memory of Alex Böhm, who was
a great friend and a passionate biologist. Alex passed away after the initial submission
of this manuscript. We thank Vesna Olivera and Ursula Sauder from the Zentrum für
Mikroskopie Uni Basel for excellent service, and Olin Silander, Nikki Freed, and
Nela Nikolic for helpful discussions. This work was supported by the Swiss National
Science Foundation grants to M. Ackermann and Urs Jenal (supporting AB).
article_number: e1005974
author:
- first_name: Alex
full_name: Boehm, Alex
last_name: Boehm
- first_name: Markus
full_name: Arnoldini, Markus
last_name: Arnoldini
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Thomas
full_name: Röösli, Thomas
last_name: Röösli
- first_name: Colette
full_name: Bigosch, Colette
last_name: Bigosch
- first_name: Martin
full_name: Ackermann, Martin
last_name: Ackermann
citation:
ama: Boehm A, Arnoldini M, Bergmiller T, Röösli T, Bigosch C, Ackermann M. Genetic
manipulation of glycogen allocation affects replicative lifespan in E coli. PLoS
Genetics. 2016;12(4). doi:10.1371/journal.pgen.1005974
apa: Boehm, A., Arnoldini, M., Bergmiller, T., Röösli, T., Bigosch, C., & Ackermann,
M. (2016). Genetic manipulation of glycogen allocation affects replicative lifespan
in E coli. PLoS Genetics. Public Library of Science. https://doi.org/10.1371/journal.pgen.1005974
chicago: Boehm, Alex, Markus Arnoldini, Tobias Bergmiller, Thomas Röösli, Colette
Bigosch, and Martin Ackermann. “Genetic Manipulation of Glycogen Allocation Affects
Replicative Lifespan in E Coli.” PLoS Genetics. Public Library of Science,
2016. https://doi.org/10.1371/journal.pgen.1005974.
ieee: A. Boehm, M. Arnoldini, T. Bergmiller, T. Röösli, C. Bigosch, and M. Ackermann,
“Genetic manipulation of glycogen allocation affects replicative lifespan in E
coli,” PLoS Genetics, vol. 12, no. 4. Public Library of Science, 2016.
ista: Boehm A, Arnoldini M, Bergmiller T, Röösli T, Bigosch C, Ackermann M. 2016.
Genetic manipulation of glycogen allocation affects replicative lifespan in E
coli. PLoS Genetics. 12(4), e1005974.
mla: Boehm, Alex, et al. “Genetic Manipulation of Glycogen Allocation Affects Replicative
Lifespan in E Coli.” PLoS Genetics, vol. 12, no. 4, e1005974, Public Library
of Science, 2016, doi:10.1371/journal.pgen.1005974.
short: A. Boehm, M. Arnoldini, T. Bergmiller, T. Röösli, C. Bigosch, M. Ackermann,
PLoS Genetics 12 (2016).
date_created: 2018-12-11T11:50:56Z
date_published: 2016-04-19T00:00:00Z
date_updated: 2023-02-23T14:11:39Z
day: '19'
ddc:
- '576'
- '579'
department:
- _id: CaGu
doi: 10.1371/journal.pgen.1005974
file:
- access_level: open_access
checksum: 53d22b2b39e5adc243d34f18b2615a85
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:17Z
date_updated: 2020-07-14T12:44:41Z
file_id: '5067'
file_name: IST-2016-705-v1+1_journal.pgen.1005974.PDF
file_size: 6273249
relation: main_file
file_date_updated: 2020-07-14T12:44:41Z
has_accepted_license: '1'
intvolume: ' 12'
issue: '4'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
publication: PLoS Genetics
publication_status: published
publisher: Public Library of Science
publist_id: '6077'
pubrep_id: '705'
quality_controlled: '1'
related_material:
record:
- id: '9873'
relation: research_data
status: public
scopus_import: 1
status: public
title: Genetic manipulation of glycogen allocation affects replicative lifespan in
E coli
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: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 12
year: '2016'
...
---
_id: '9873'
article_processing_charge: No
author:
- first_name: Alex
full_name: Boehm, Alex
last_name: Boehm
- first_name: Markus
full_name: Arnoldini, Markus
last_name: Arnoldini
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Thomas
full_name: Röösli, Thomas
last_name: Röösli
- first_name: Colette
full_name: Bigosch, Colette
last_name: Bigosch
- first_name: Martin
full_name: Ackermann, Martin
last_name: Ackermann
citation:
ama: Boehm A, Arnoldini M, Bergmiller T, Röösli T, Bigosch C, Ackermann M. Quantification
of the growth rate reduction as a consequence of age-specific mortality. 2016.
doi:10.1371/journal.pgen.1005974.s015
apa: Boehm, A., Arnoldini, M., Bergmiller, T., Röösli, T., Bigosch, C., & Ackermann,
M. (2016). Quantification of the growth rate reduction as a consequence of age-specific
mortality. Public Library of Science. https://doi.org/10.1371/journal.pgen.1005974.s015
chicago: Boehm, Alex, Markus Arnoldini, Tobias Bergmiller, Thomas Röösli, Colette
Bigosch, and Martin Ackermann. “Quantification of the Growth Rate Reduction as
a Consequence of Age-Specific Mortality.” Public Library of Science, 2016. https://doi.org/10.1371/journal.pgen.1005974.s015.
ieee: A. Boehm, M. Arnoldini, T. Bergmiller, T. Röösli, C. Bigosch, and M. Ackermann,
“Quantification of the growth rate reduction as a consequence of age-specific
mortality.” Public Library of Science, 2016.
ista: Boehm A, Arnoldini M, Bergmiller T, Röösli T, Bigosch C, Ackermann M. 2016.
Quantification of the growth rate reduction as a consequence of age-specific mortality,
Public Library of Science, 10.1371/journal.pgen.1005974.s015.
mla: Boehm, Alex, et al. Quantification of the Growth Rate Reduction as a Consequence
of Age-Specific Mortality. Public Library of Science, 2016, doi:10.1371/journal.pgen.1005974.s015.
short: A. Boehm, M. Arnoldini, T. Bergmiller, T. Röösli, C. Bigosch, M. Ackermann,
(2016).
date_created: 2021-08-10T09:42:34Z
date_updated: 2023-02-21T16:50:13Z
day: '19'
department:
- _id: CaGu
doi: 10.1371/journal.pgen.1005974.s015
month: '04'
oa_version: Published Version
publisher: Public Library of Science
related_material:
record:
- id: '1250'
relation: used_in_publication
status: public
status: public
title: Quantification of the growth rate reduction as a consequence of age-specific
mortality
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2016'
...
---
_id: '9719'
abstract:
- lang: eng
text: Parasitism creates selection for resistance mechanisms in host populations
and is hypothesized to promote increased host evolvability. However, the influence
of these traits on host evolution when parasites are no longer present is unclear.
We used experimental evolution and whole-genome sequencing of Escherichia coli
to determine the effects of past and present exposure to parasitic viruses (phages)
on the spread of mutator alleles, resistance, and bacterial competitive fitness.
We found that mutator alleles spread rapidly during adaptation to any of four
different phage species, and this pattern was even more pronounced with multiple
phages present simultaneously. However, hypermutability did not detectably accelerate
adaptation in the absence of phages and recovery of fitness costs associated with
resistance. Several lineages evolved phage resistance through elevated mucoidy,
and during subsequent evolution in phage-free conditions they rapidly reverted
to nonmucoid, phage-susceptible phenotypes. Genome sequencing revealed that this
phenotypic reversion was achieved by additional genetic changes rather than by
genotypic reversion of the initial resistance mutations. Insertion sequence (IS)
elements played a key role in both the acquisition of resistance and adaptation
in the absence of parasites; unlike single nucleotide polymorphisms, IS insertions
were not more frequent in mutator lineages. Our results provide a genetic explanation
for rapid reversion of mucoidy, a phenotype observed in other bacterial species
including human pathogens. Moreover, this demonstrates that the types of genetic
change underlying adaptation to fitness costs, and consequently the impact of
evolvability mechanisms such as increased point-mutation rates, depend critically
on the mechanism of resistance.
article_processing_charge: No
author:
- first_name: Sébastien
full_name: Wielgoss, Sébastien
last_name: Wielgoss
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Anna M.
full_name: Bischofberger, Anna M.
last_name: Bischofberger
- first_name: Alex R.
full_name: Hall, Alex R.
last_name: Hall
citation:
ama: 'Wielgoss S, Bergmiller T, Bischofberger AM, Hall AR. Data from: Adaptation
to parasites and costs of parasite resistance in mutator and non-mutator bacteria.
2015. doi:10.5061/dryad.cj910'
apa: 'Wielgoss, S., Bergmiller, T., Bischofberger, A. M., & Hall, A. R. (2015).
Data from: Adaptation to parasites and costs of parasite resistance in mutator
and non-mutator bacteria. Dryad. https://doi.org/10.5061/dryad.cj910'
chicago: 'Wielgoss, Sébastien, Tobias Bergmiller, Anna M. Bischofberger, and Alex
R. Hall. “Data from: Adaptation to Parasites and Costs of Parasite Resistance
in Mutator and Non-Mutator Bacteria.” Dryad, 2015. https://doi.org/10.5061/dryad.cj910.'
ieee: 'S. Wielgoss, T. Bergmiller, A. M. Bischofberger, and A. R. Hall, “Data from:
Adaptation to parasites and costs of parasite resistance in mutator and non-mutator
bacteria.” Dryad, 2015.'
ista: 'Wielgoss S, Bergmiller T, Bischofberger AM, Hall AR. 2015. Data from: Adaptation
to parasites and costs of parasite resistance in mutator and non-mutator bacteria,
Dryad, 10.5061/dryad.cj910.'
mla: 'Wielgoss, Sébastien, et al. Data from: Adaptation to Parasites and Costs
of Parasite Resistance in Mutator and Non-Mutator Bacteria. Dryad, 2015, doi:10.5061/dryad.cj910.'
short: S. Wielgoss, T. Bergmiller, A.M. Bischofberger, A.R. Hall, (2015).
date_created: 2021-07-26T08:44:04Z
date_published: 2015-12-21T00:00:00Z
date_updated: 2023-09-05T13:46:04Z
day: '21'
department:
- _id: CaGu
doi: 10.5061/dryad.cj910
main_file_link:
- open_access: '1'
url: https://doi.org/10.5061/dryad.cj910
month: '12'
oa: 1
oa_version: Published Version
publisher: Dryad
related_material:
record:
- id: '5749'
relation: used_in_publication
status: public
status: public
title: 'Data from: Adaptation to parasites and costs of parasite resistance in mutator
and non-mutator bacteria'
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2015'
...
---
_id: '9931'
abstract:
- lang: eng
text: Gene duplication is important in evolution, because it provides new raw material
for evolutionary adaptations. Several existing hypotheses about the causes of
duplicate retention and diversification differ in their emphasis on gene dosage,
subfunctionalization, and neofunctionalization. Little experimental data exist
on the relative importance of gene expression changes and changes in coding regions
for the evolution of duplicate genes. Furthermore, we do not know how strongly
the environment could affect this importance. To address these questions, we performed
evolution experiments with the TEM-1 beta lactamase gene in Escherichia coli to
study the initial stages of duplicate gene evolution in the laboratory. We mimicked
tandem duplication by inserting two copies of the TEM-1 gene on the same plasmid.
We then subjected these copies to repeated cycles of mutagenesis and selection
in various environments that contained antibiotics in different combinations and
concentrations. Our experiments showed that gene dosage is the most important
factor in the initial stages of duplicate gene evolution, and overshadows the
importance of point mutations in the coding region.
acknowledgement: We thank the Functional Genomics Center Zurich for its service in
generating sequencing data, M. Ackermann and E. Hayden for helpful discussions,
A. de Visser for comments on earlier versions of this manuscript, and M. Moser for
help with quantitative PCR. This work was supported by Swiss National Science Foundation
(grant 315230–129708), as well as through the YeastX project of SystemsX.ch, and
the University Priority Research Program in Systems Biology at the University of
Zurich. RD acknowledges support from the Forschungskredit program of the University
of Zurich. The authors declare no conflict of interest.
article_processing_charge: No
article_type: original
author:
- first_name: Riddhiman
full_name: Dhar, Riddhiman
last_name: Dhar
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Andreas
full_name: Wagner, Andreas
last_name: Wagner
citation:
ama: Dhar R, Bergmiller T, Wagner A. Increased gene dosage plays a predominant role
in the initial stages of evolution of duplicate TEM-1 beta lactamase genes. Evolution.
2014;68(6):1775-1791. doi:10.1111/evo.12373
apa: Dhar, R., Bergmiller, T., & Wagner, A. (2014). Increased gene dosage plays
a predominant role in the initial stages of evolution of duplicate TEM-1 beta
lactamase genes. Evolution. Wiley. https://doi.org/10.1111/evo.12373
chicago: Dhar, Riddhiman, Tobias Bergmiller, and Andreas Wagner. “Increased Gene
Dosage Plays a Predominant Role in the Initial Stages of Evolution of Duplicate
TEM-1 Beta Lactamase Genes.” Evolution. Wiley, 2014. https://doi.org/10.1111/evo.12373.
ieee: R. Dhar, T. Bergmiller, and A. Wagner, “Increased gene dosage plays a predominant
role in the initial stages of evolution of duplicate TEM-1 beta lactamase genes,”
Evolution, vol. 68, no. 6. Wiley, pp. 1775–1791, 2014.
ista: Dhar R, Bergmiller T, Wagner A. 2014. Increased gene dosage plays a predominant
role in the initial stages of evolution of duplicate TEM-1 beta lactamase genes.
Evolution. 68(6), 1775–1791.
mla: Dhar, Riddhiman, et al. “Increased Gene Dosage Plays a Predominant Role in
the Initial Stages of Evolution of Duplicate TEM-1 Beta Lactamase Genes.” Evolution,
vol. 68, no. 6, Wiley, 2014, pp. 1775–91, doi:10.1111/evo.12373.
short: R. Dhar, T. Bergmiller, A. Wagner, Evolution 68 (2014) 1775–1791.
date_created: 2021-08-17T09:03:09Z
date_published: 2014-06-03T00:00:00Z
date_updated: 2023-02-23T14:13:27Z
day: '03'
department:
- _id: CaGu
doi: 10.1111/evo.12373
external_id:
pmid:
- '24495000'
intvolume: ' 68'
issue: '6'
language:
- iso: eng
month: '06'
oa_version: None
page: 1775-1791
pmid: 1
publication: Evolution
publication_identifier:
eissn:
- 1558-5646
issn:
- 0014-3820
publication_status: published
publisher: Wiley
quality_controlled: '1'
related_material:
record:
- id: '9932'
relation: research_data
status: public
scopus_import: '1'
status: public
title: Increased gene dosage plays a predominant role in the initial stages of evolution
of duplicate TEM-1 beta lactamase genes
type: journal_article
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
volume: 68
year: '2014'
...
---
_id: '9932'
abstract:
- lang: eng
text: Gene duplication is important in evolution, because it provides new raw material
for evolutionary adaptations. Several existing hypotheses about the causes of
duplicate retention and diversification differ in their emphasis on gene dosage,
sub-functionalization, and neo-functionalization. Little experimental data exists
on the relative importance of gene expression changes and changes in coding regions
for the evolution of duplicate genes. Furthermore, we do not know how strongly
the environment could affect this importance. To address these questions, we performed
evolution experiments with the TEM-1 beta lactamase gene in E. coli to study the
initial stages of duplicate gene evolution in the laboratory. We mimicked tandem
duplication by inserting two copies of the TEM-1 gene on the same plasmid. We
then subjected these copies to repeated cycles of mutagenesis and selection in
various environments that contained antibiotics in different combinations and
concentrations. Our experiments showed that gene dosage is the most important
factor in the initial stages of duplicate gene evolution, and overshadows the
importance of point mutations in the coding region.
article_processing_charge: No
author:
- first_name: Riddhiman
full_name: Dhar, Riddhiman
last_name: Dhar
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Andreas
full_name: Wagner, Andreas
last_name: Wagner
citation:
ama: 'Dhar R, Bergmiller T, Wagner A. Data from: Increased gene dosage plays a predominant
role in the initial stages of evolution of duplicate TEM-1 beta lactamase genes.
2014. doi:10.5061/dryad.jc402'
apa: 'Dhar, R., Bergmiller, T., & Wagner, A. (2014). Data from: Increased gene
dosage plays a predominant role in the initial stages of evolution of duplicate
TEM-1 beta lactamase genes. Dryad. https://doi.org/10.5061/dryad.jc402'
chicago: 'Dhar, Riddhiman, Tobias Bergmiller, and Andreas Wagner. “Data from: Increased
Gene Dosage Plays a Predominant Role in the Initial Stages of Evolution of Duplicate
TEM-1 Beta Lactamase Genes.” Dryad, 2014. https://doi.org/10.5061/dryad.jc402.'
ieee: 'R. Dhar, T. Bergmiller, and A. Wagner, “Data from: Increased gene dosage
plays a predominant role in the initial stages of evolution of duplicate TEM-1
beta lactamase genes.” Dryad, 2014.'
ista: 'Dhar R, Bergmiller T, Wagner A. 2014. Data from: Increased gene dosage plays
a predominant role in the initial stages of evolution of duplicate TEM-1 beta
lactamase genes, Dryad, 10.5061/dryad.jc402.'
mla: 'Dhar, Riddhiman, et al. Data from: Increased Gene Dosage Plays a Predominant
Role in the Initial Stages of Evolution of Duplicate TEM-1 Beta Lactamase Genes.
Dryad, 2014, doi:10.5061/dryad.jc402.'
short: R. Dhar, T. Bergmiller, A. Wagner, (2014).
date_created: 2021-08-17T09:11:40Z
date_published: 2014-01-27T00:00:00Z
date_updated: 2023-02-23T14:13:24Z
day: '27'
department:
- _id: CaGu
doi: 10.5061/dryad.jc402
main_file_link:
- open_access: '1'
url: https://doi.org/10.5061/dryad.jc402
month: '01'
oa: 1
oa_version: Published Version
publisher: Dryad
related_material:
record:
- id: '9931'
relation: used_in_publication
status: public
status: public
title: 'Data from: Increased gene dosage plays a predominant role in the initial stages
of evolution of duplicate TEM-1 beta lactamase genes'
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2014'
...
---
_id: '2853'
abstract:
- lang: eng
text: High relatedness among interacting individuals has generally been considered
a precondition for the evolution of altruism. However, kin-selection theory also
predicts the evolution of altruism when relatedness is low, as long as the cost
of the altruistic act is minor compared with its benefit. Here, we demonstrate
evidence for a low-cost altruistic act in bacteria. We investigated Escherichia
coli responding to the attack of an obligately lytic phage by committing suicide
in order to prevent parasite transmission to nearby relatives. We found that bacterial
suicide provides large benefits to survivors at marginal costs to committers.
The cost of suicide was low, because infected cells are moribund, rapidly dying
upon phage infection, such that no more opportunity for reproduction remains.
As a consequence of its marginal cost, host suicide was selectively favoured even
when relatedness between committers and survivors approached zero. Altogether,
our findings demonstrate that low-cost suicide can evolve with ease, represents
an effective host-defence strategy, and seems to be widespread among microbes.
Moreover, low-cost suicide might also occur in higher organisms as exemplified
by infected social insect workers leaving the colony to die in isolation.
article_processing_charge: No
article_type: original
author:
- first_name: Dominik
full_name: Refardt, Dominik
last_name: Refardt
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Rolf
full_name: Kümmerli, Rolf
last_name: Kümmerli
citation:
ama: 'Refardt D, Bergmiller T, Kümmerli R. Altruism can evolve when relatedness
is low: Evidence from bacteria committing suicide upon phage infection. Proceedings
of the Royal Society of London Series B Biological Sciences. 2013;280(1759).
doi:10.1098/rspb.2012.3035'
apa: 'Refardt, D., Bergmiller, T., & Kümmerli, R. (2013). Altruism can evolve
when relatedness is low: Evidence from bacteria committing suicide upon phage
infection. Proceedings of the Royal Society of London Series B Biological Sciences.
The Royal Society. https://doi.org/10.1098/rspb.2012.3035'
chicago: 'Refardt, Dominik, Tobias Bergmiller, and Rolf Kümmerli. “Altruism Can
Evolve When Relatedness Is Low: Evidence from Bacteria Committing Suicide upon
Phage Infection.” Proceedings of the Royal Society of London Series B Biological
Sciences. The Royal Society, 2013. https://doi.org/10.1098/rspb.2012.3035.'
ieee: 'D. Refardt, T. Bergmiller, and R. Kümmerli, “Altruism can evolve when relatedness
is low: Evidence from bacteria committing suicide upon phage infection,” Proceedings
of the Royal Society of London Series B Biological Sciences, vol. 280, no.
1759. The Royal Society, 2013.'
ista: 'Refardt D, Bergmiller T, Kümmerli R. 2013. Altruism can evolve when relatedness
is low: Evidence from bacteria committing suicide upon phage infection. Proceedings
of the Royal Society of London Series B Biological Sciences. 280(1759).'
mla: 'Refardt, Dominik, et al. “Altruism Can Evolve When Relatedness Is Low: Evidence
from Bacteria Committing Suicide upon Phage Infection.” Proceedings of the
Royal Society of London Series B Biological Sciences, vol. 280, no. 1759,
The Royal Society, 2013, doi:10.1098/rspb.2012.3035.'
short: D. Refardt, T. Bergmiller, R. Kümmerli, Proceedings of the Royal Society
of London Series B Biological Sciences 280 (2013).
date_created: 2018-12-11T11:59:56Z
date_published: 2013-05-22T00:00:00Z
date_updated: 2023-10-18T06:43:23Z
day: '22'
department:
- _id: CaGu
doi: 10.1098/rspb.2012.3035
external_id:
pmid:
- '23516238'
intvolume: ' 280'
issue: '1759'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3619501/
month: '05'
oa: 1
oa_version: Submitted Version
pmid: 1
publication: Proceedings of the Royal Society of London Series B Biological Sciences
publication_identifier:
eissn:
- 1471-2954
publication_status: published
publisher: The Royal Society
publist_id: '3939'
quality_controlled: '1'
related_material:
record:
- id: '9751'
relation: research_data
status: public
scopus_import: '1'
status: public
title: 'Altruism can evolve when relatedness is low: Evidence from bacteria committing
suicide upon phage infection'
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 280
year: '2013'
...