---
_id: '1619'
abstract:
- lang: eng
text: The emergence of drug resistant pathogens is a serious public health problem.
It is a long-standing goal to predict rates of resistance evolution and design
optimal treatment strategies accordingly. To this end, it is crucial to reveal
the underlying causes of drug-specific differences in the evolutionary dynamics
leading to resistance. However, it remains largely unknown why the rates of resistance
evolution via spontaneous mutations and the diversity of mutational paths vary
substantially between drugs. Here we comprehensively quantify the distribution
of fitness effects (DFE) of mutations, a key determinant of evolutionary dynamics,
in the presence of eight antibiotics representing the main modes of action. Using
precise high-throughput fitness measurements for genome-wide Escherichia coli
gene deletion strains, we find that the width of the DFE varies dramatically between
antibiotics and, contrary to conventional wisdom, for some drugs the DFE width
is lower than in the absence of stress. We show that this previously underappreciated
divergence in DFE width among antibiotics is largely caused by their distinct
drug-specific dose-response characteristics. Unlike the DFE, the magnitude of
the changes in tolerated drug concentration resulting from genome-wide mutations
is similar for most drugs but exceptionally small for the antibiotic nitrofurantoin,
i.e., mutations generally have considerably smaller resistance effects for nitrofurantoin
than for other drugs. A population genetics model predicts that resistance evolution
for drugs with this property is severely limited and confined to reproducible
mutational paths. We tested this prediction in laboratory evolution experiments
using the “morbidostat”, a device for evolving bacteria in well-controlled drug
environments. Nitrofurantoin resistance indeed evolved extremely slowly via reproducible
mutations—an almost paradoxical behavior since this drug causes DNA damage and
increases the mutation rate. Overall, we identified novel quantitative characteristics
of the evolutionary landscape that provide the conceptual foundation for predicting
the dynamics of drug resistance evolution.
article_number: e1002299
author:
- first_name: Guillaume
full_name: Chevereau, Guillaume
id: 424D78A0-F248-11E8-B48F-1D18A9856A87
last_name: Chevereau
- first_name: Marta
full_name: Dravecka, Marta
id: 4342E402-F248-11E8-B48F-1D18A9856A87
last_name: Dravecka
orcid: 0000-0002-2519-8004
- first_name: Tugce
full_name: Batur, Tugce
last_name: Batur
- first_name: Aysegul
full_name: Guvenek, Aysegul
last_name: Guvenek
- first_name: Dilay
full_name: Ayhan, Dilay
last_name: Ayhan
- first_name: Erdal
full_name: Toprak, Erdal
last_name: Toprak
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
citation:
ama: Chevereau G, Lukacisinova M, Batur T, et al. Quantifying the determinants of
evolutionary dynamics leading to drug resistance. PLoS Biology. 2015;13(11).
doi:10.1371/journal.pbio.1002299
apa: Chevereau, G., Lukacisinova, M., Batur, T., Guvenek, A., Ayhan, D., Toprak,
E., & Bollenbach, M. T. (2015). Quantifying the determinants of evolutionary
dynamics leading to drug resistance. PLoS Biology. Public Library of Science.
https://doi.org/10.1371/journal.pbio.1002299
chicago: Chevereau, Guillaume, Marta Lukacisinova, Tugce Batur, Aysegul Guvenek,
Dilay Ayhan, Erdal Toprak, and Mark Tobias Bollenbach. “Quantifying the Determinants
of Evolutionary Dynamics Leading to Drug Resistance.” PLoS Biology. Public
Library of Science, 2015. https://doi.org/10.1371/journal.pbio.1002299.
ieee: G. Chevereau et al., “Quantifying the determinants of evolutionary
dynamics leading to drug resistance,” PLoS Biology, vol. 13, no. 11. Public
Library of Science, 2015.
ista: Chevereau G, Lukacisinova M, Batur T, Guvenek A, Ayhan D, Toprak E, Bollenbach
MT. 2015. Quantifying the determinants of evolutionary dynamics leading to drug
resistance. PLoS Biology. 13(11), e1002299.
mla: Chevereau, Guillaume, et al. “Quantifying the Determinants of Evolutionary
Dynamics Leading to Drug Resistance.” PLoS Biology, vol. 13, no. 11, e1002299,
Public Library of Science, 2015, doi:10.1371/journal.pbio.1002299.
short: G. Chevereau, M. Lukacisinova, T. Batur, A. Guvenek, D. Ayhan, E. Toprak,
M.T. Bollenbach, PLoS Biology 13 (2015).
date_created: 2018-12-11T11:53:04Z
date_published: 2015-11-18T00:00:00Z
date_updated: 2024-03-25T23:30:14Z
day: '18'
ddc:
- '570'
department:
- _id: ToBo
doi: 10.1371/journal.pbio.1002299
ec_funded: 1
file:
- access_level: open_access
checksum: 0e82e3279f50b15c6c170c042627802b
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:09:00Z
date_updated: 2020-07-14T12:45:07Z
file_id: '4723'
file_name: IST-2016-468-v1+1_journal.pbio.1002299.pdf
file_size: 1387760
relation: main_file
file_date_updated: 2020-07-14T12:45:07Z
has_accepted_license: '1'
intvolume: ' 13'
issue: '11'
language:
- iso: eng
license: https://creativecommons.org/licenses/by/4.0/
month: '11'
oa: 1
oa_version: Published Version
project:
- _id: 25EB3A80-B435-11E9-9278-68D0E5697425
grant_number: RGP0042/2013
name: Revealing the fundamental limits of cell growth
- _id: 25E9AF9E-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P27201-B22
name: Revealing the mechanisms underlying drug interactions
- _id: 25E83C2C-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '303507'
name: Optimality principles in responses to antibiotics
publication: PLoS Biology
publication_status: published
publisher: Public Library of Science
publist_id: '5547'
pubrep_id: '468'
quality_controlled: '1'
related_material:
record:
- id: '9711'
relation: research_data
status: public
- id: '9765'
relation: research_data
status: public
- id: '6263'
relation: dissertation_contains
status: public
scopus_import: 1
status: public
title: Quantifying the determinants of evolutionary dynamics leading to drug resistance
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: '2015'
...
---
_id: '1623'
abstract:
- lang: eng
text: "Background\r\nPhotosynthetic cyanobacteria are attractive for a range of
biotechnological applications including biofuel production. However, due to slow
growth, screening of mutant libraries using microtiter plates is not feasible.\r\nResults\r\nWe
present a method for high-throughput, single-cell analysis and sorting of genetically
engineered l-lactate-producing strains of Synechocystis sp. PCC6803. A microfluidic
device is used to encapsulate single cells in picoliter droplets, assay the droplets
for l-lactate production, and sort strains with high productivity. We demonstrate
the separation of low- and high-producing reference strains, as well as enrichment
of a more productive l-lactate-synthesizing population after UV-induced mutagenesis.
The droplet platform also revealed population heterogeneity in photosynthetic
growth and lactate production, as well as the presence of metabolically stalled
cells.\r\nConclusions\r\nThe workflow will facilitate metabolic engineering and
directed evolution studies and will be useful in studies of cyanobacteria biochemistry
and physiology.\r\n"
article_number: '193'
author:
- first_name: Petter
full_name: Hammar, Petter
last_name: Hammar
- first_name: Andreas
full_name: Angermayr, Andreas
id: 4677C796-F248-11E8-B48F-1D18A9856A87
last_name: Angermayr
orcid: 0000-0001-8619-2223
- first_name: Staffan
full_name: Sjostrom, Staffan
last_name: Sjostrom
- first_name: Josefin
full_name: Van Der Meer, Josefin
last_name: Van Der Meer
- first_name: Klaas
full_name: Hellingwerf, Klaas
last_name: Hellingwerf
- first_name: Elton
full_name: Hudson, Elton
last_name: Hudson
- first_name: Hakaan
full_name: Joensson, Hakaan
last_name: Joensson
citation:
ama: Hammar P, Angermayr A, Sjostrom S, et al. Single-cell screening of photosynthetic
growth and lactate production by cyanobacteria. Biotechnology for Biofuels.
2015;8(1). doi:10.1186/s13068-015-0380-2
apa: Hammar, P., Angermayr, A., Sjostrom, S., Van Der Meer, J., Hellingwerf, K.,
Hudson, E., & Joensson, H. (2015). Single-cell screening of photosynthetic
growth and lactate production by cyanobacteria. Biotechnology for Biofuels.
BioMed Central. https://doi.org/10.1186/s13068-015-0380-2
chicago: Hammar, Petter, Andreas Angermayr, Staffan Sjostrom, Josefin Van Der Meer,
Klaas Hellingwerf, Elton Hudson, and Hakaan Joensson. “Single-Cell Screening of
Photosynthetic Growth and Lactate Production by Cyanobacteria.” Biotechnology
for Biofuels. BioMed Central, 2015. https://doi.org/10.1186/s13068-015-0380-2.
ieee: P. Hammar et al., “Single-cell screening of photosynthetic growth and
lactate production by cyanobacteria,” Biotechnology for Biofuels, vol.
8, no. 1. BioMed Central, 2015.
ista: Hammar P, Angermayr A, Sjostrom S, Van Der Meer J, Hellingwerf K, Hudson E,
Joensson H. 2015. Single-cell screening of photosynthetic growth and lactate production
by cyanobacteria. Biotechnology for Biofuels. 8(1), 193.
mla: Hammar, Petter, et al. “Single-Cell Screening of Photosynthetic Growth and
Lactate Production by Cyanobacteria.” Biotechnology for Biofuels, vol.
8, no. 1, 193, BioMed Central, 2015, doi:10.1186/s13068-015-0380-2.
short: P. Hammar, A. Angermayr, S. Sjostrom, J. Van Der Meer, K. Hellingwerf, E.
Hudson, H. Joensson, Biotechnology for Biofuels 8 (2015).
date_created: 2018-12-11T11:53:05Z
date_published: 2015-11-25T00:00:00Z
date_updated: 2021-01-12T06:52:04Z
day: '25'
ddc:
- '570'
department:
- _id: ToBo
doi: 10.1186/s13068-015-0380-2
file:
- access_level: open_access
checksum: 172b0b6f4eb2e5c22b7cec1d57dc0107
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:10:11Z
date_updated: 2020-07-14T12:45:07Z
file_id: '4796'
file_name: IST-2016-467-v1+1_s13068-015-0380-2.pdf
file_size: 2914089
relation: main_file
file_date_updated: 2020-07-14T12:45:07Z
has_accepted_license: '1'
intvolume: ' 8'
issue: '1'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
publication: Biotechnology for Biofuels
publication_status: published
publisher: BioMed Central
publist_id: '5537'
pubrep_id: '467'
quality_controlled: '1'
scopus_import: 1
status: public
title: Single-cell screening of photosynthetic growth and lactate production by cyanobacteria
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: 8
year: '2015'
...
---
_id: '1810'
abstract:
- lang: eng
text: Combining antibiotics is a promising strategy for increasing treatment efficacy
and for controlling resistance evolution. When drugs are combined, their effects
on cells may be amplified or weakened, that is the drugs may show synergistic
or antagonistic interactions. Recent work revealed the underlying mechanisms of
such drug interactions by elucidating the drugs'; joint effects on cell physiology.
Moreover, new treatment strategies that use drug combinations to exploit evolutionary
tradeoffs were shown to affect the rate of resistance evolution in predictable
ways. High throughput studies have further identified drug candidates based on
their interactions with established antibiotics and general principles that enable
the prediction of drug interactions were suggested. Overall, the conceptual and
technical foundation for the rational design of potent drug combinations is rapidly
developing.
author:
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
citation:
ama: 'Bollenbach MT. Antimicrobial interactions: Mechanisms and implications for
drug discovery and resistance evolution. Current Opinion in Microbiology.
2015;27:1-9. doi:10.1016/j.mib.2015.05.008'
apa: 'Bollenbach, M. T. (2015). Antimicrobial interactions: Mechanisms and implications
for drug discovery and resistance evolution. Current Opinion in Microbiology.
Elsevier. https://doi.org/10.1016/j.mib.2015.05.008'
chicago: 'Bollenbach, Mark Tobias. “Antimicrobial Interactions: Mechanisms and Implications
for Drug Discovery and Resistance Evolution.” Current Opinion in Microbiology.
Elsevier, 2015. https://doi.org/10.1016/j.mib.2015.05.008.'
ieee: 'M. T. Bollenbach, “Antimicrobial interactions: Mechanisms and implications
for drug discovery and resistance evolution,” Current Opinion in Microbiology,
vol. 27. Elsevier, pp. 1–9, 2015.'
ista: 'Bollenbach MT. 2015. Antimicrobial interactions: Mechanisms and implications
for drug discovery and resistance evolution. Current Opinion in Microbiology.
27, 1–9.'
mla: 'Bollenbach, Mark Tobias. “Antimicrobial Interactions: Mechanisms and Implications
for Drug Discovery and Resistance Evolution.” Current Opinion in Microbiology,
vol. 27, Elsevier, 2015, pp. 1–9, doi:10.1016/j.mib.2015.05.008.'
short: M.T. Bollenbach, Current Opinion in Microbiology 27 (2015) 1–9.
date_created: 2018-12-11T11:54:08Z
date_published: 2015-06-01T00:00:00Z
date_updated: 2021-01-12T06:53:21Z
day: '01'
ddc:
- '570'
department:
- _id: ToBo
doi: 10.1016/j.mib.2015.05.008
ec_funded: 1
file:
- access_level: open_access
checksum: 1683bb0f42ef892a5b3b71a050d65d25
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:17:23Z
date_updated: 2020-07-14T12:45:17Z
file_id: '5277'
file_name: IST-2016-493-v1+1_1-s2.0-S1369527415000594-main.pdf
file_size: 1047255
relation: main_file
file_date_updated: 2020-07-14T12:45:17Z
has_accepted_license: '1'
intvolume: ' 27'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: 1 - 9
project:
- _id: 25E9AF9E-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P27201-B22
name: Revealing the mechanisms underlying drug interactions
- _id: 25E83C2C-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '303507'
name: Optimality principles in responses to antibiotics
- _id: 25EB3A80-B435-11E9-9278-68D0E5697425
grant_number: RGP0042/2013
name: Revealing the fundamental limits of cell growth
publication: Current Opinion in Microbiology
publication_status: published
publisher: Elsevier
publist_id: '5298'
pubrep_id: '493'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'Antimicrobial interactions: Mechanisms and implications for drug discovery
and resistance evolution'
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: 27
year: '2015'
...
---
_id: '1823'
abstract:
- lang: eng
text: Abstract Drug combinations are increasingly important in disease treatments,
for combating drug resistance, and for elucidating fundamental relationships in
cell physiology. When drugs are combined, their individual effects on cells may
be amplified or weakened. Such drug interactions are crucial for treatment efficacy,
but their underlying mechanisms remain largely unknown. To uncover the causes
of drug interactions, we developed a systematic approach based on precise quantification
of the individual and joint effects of antibiotics on growth of genome-wide Escherichia
coli gene deletion strains. We found that drug interactions between antibiotics
representing the main modes of action are highly robust to genetic perturbation.
This robustness is encapsulated in a general principle of bacterial growth, which
enables the quantitative prediction of mutant growth rates under drug combinations.
Rare violations of this principle exposed recurring cellular functions controlling
drug interactions. In particular, we found that polysaccharide and ATP synthesis
control multiple drug interactions with previously unexplained mechanisms, and
small molecule adjuvants targeting these functions synthetically reshape drug
interactions in predictable ways. These results provide a new conceptual framework
for the design of multidrug combinations and suggest that there are universal
mechanisms at the heart of most drug interactions. Synopsis A general principle
of bacterial growth enables the prediction of mutant growth rates under drug combinations.
Rare violations of this principle expose cellular functions that control drug
interactions and can be targeted by small molecules to alter drug interactions
in predictable ways. Drug interactions between antibiotics are highly robust to
genetic perturbations. A general principle of bacterial growth enables the prediction
of mutant growth rates under drug combinations. Rare violations of this principle
expose cellular functions that control drug interactions. Diverse drug interactions
are controlled by recurring cellular functions, including LPS synthesis and ATP
synthesis. A general principle of bacterial growth enables the prediction of mutant
growth rates under drug combinations. Rare violations of this principle expose
cellular functions that control drug interactions and can be targeted by small
molecules to alter drug interactions in predictable ways.
article_number: '807'
author:
- first_name: Guillaume
full_name: Chevereau, Guillaume
id: 424D78A0-F248-11E8-B48F-1D18A9856A87
last_name: Chevereau
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
citation:
ama: Chevereau G, Bollenbach MT. Systematic discovery of drug interaction mechanisms.
Molecular Systems Biology. 2015;11(4). doi:10.15252/msb.20156098
apa: Chevereau, G., & Bollenbach, M. T. (2015). Systematic discovery of drug
interaction mechanisms. Molecular Systems Biology. Nature Publishing Group.
https://doi.org/10.15252/msb.20156098
chicago: Chevereau, Guillaume, and Mark Tobias Bollenbach. “Systematic Discovery
of Drug Interaction Mechanisms.” Molecular Systems Biology. Nature Publishing
Group, 2015. https://doi.org/10.15252/msb.20156098.
ieee: G. Chevereau and M. T. Bollenbach, “Systematic discovery of drug interaction
mechanisms,” Molecular Systems Biology, vol. 11, no. 4. Nature Publishing
Group, 2015.
ista: Chevereau G, Bollenbach MT. 2015. Systematic discovery of drug interaction
mechanisms. Molecular Systems Biology. 11(4), 807.
mla: Chevereau, Guillaume, and Mark Tobias Bollenbach. “Systematic Discovery of
Drug Interaction Mechanisms.” Molecular Systems Biology, vol. 11, no. 4,
807, Nature Publishing Group, 2015, doi:10.15252/msb.20156098.
short: G. Chevereau, M.T. Bollenbach, Molecular Systems Biology 11 (2015).
date_created: 2018-12-11T11:54:12Z
date_published: 2015-04-01T00:00:00Z
date_updated: 2021-01-12T06:53:26Z
day: '01'
ddc:
- '570'
department:
- _id: ToBo
doi: 10.15252/msb.20156098
ec_funded: 1
file:
- access_level: open_access
checksum: 4289b518fbe2166682fb1a1ef9b405f3
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:34Z
date_updated: 2020-07-14T12:45:17Z
file_id: '5087'
file_name: IST-2015-395-v1+1_807.full.pdf
file_size: 1273573
relation: main_file
file_date_updated: 2020-07-14T12:45:17Z
has_accepted_license: '1'
intvolume: ' 11'
issue: '4'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
project:
- _id: 25E9AF9E-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P27201-B22
name: Revealing the mechanisms underlying drug interactions
- _id: 25EB3A80-B435-11E9-9278-68D0E5697425
grant_number: RGP0042/2013
name: Revealing the fundamental limits of cell growth
- _id: 25E83C2C-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '303507'
name: Optimality principles in responses to antibiotics
publication: Molecular Systems Biology
publication_status: published
publisher: Nature Publishing Group
publist_id: '5283'
pubrep_id: '395'
quality_controlled: '1'
scopus_import: 1
status: public
title: Systematic discovery of drug interaction mechanisms
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: 11
year: '2015'
...
---
_id: '1509'
abstract:
- lang: eng
text: The Auxin Binding Protein1 (ABP1) has been identified based on its ability
to bind auxin with high affinity and studied for a long time as a prime candidate
for the extracellular auxin receptor responsible for mediating in particular the
fast non-transcriptional auxin responses. However, the contradiction between the
embryo-lethal phenotypes of the originally described Arabidopsis T-DNA insertional
knock-out alleles (abp1-1 and abp1-1s) and the wild type-like phenotypes of other
recently described loss-of-function alleles (abp1-c1 and abp1-TD1) questions the
biological importance of ABP1 and relevance of the previous genetic studies. Here
we show that there is no hidden copy of the ABP1 gene in the Arabidopsis genome
but the embryo-lethal phenotypes of abp1-1 and abp1-1s alleles are very similar
to the knock-out phenotypes of the neighboring gene, BELAYA SMERT (BSM). Furthermore,
the allelic complementation test between bsm and abp1 alleles shows that the embryo-lethality
in the abp1-1 and abp1-1s alleles is caused by the off-target disruption of the
BSM locus by the T-DNA insertions. This clarifies the controversy of different
phenotypes among published abp1 knock-out alleles and asks for reflections on
the developmental role of ABP1.
acknowledgement: "This work was supported by ERC Independent Research grant (ERC-2011-StG-20101109-PSDP
to JF). JM internship was supported by the grant “Action Austria – Slovakia”.\r\nData
associated with the article are available under the terms of the Creative Commons
Zero \"No rights reserved\" data waiver (CC0 1.0 Public domain dedication). \r\n\r\nData
availability: \r\nF1000Research: Dataset 1. Dataset 1, 10.5256/f1000research.7143.d104552\r\n\r\nF1000Research:
Dataset 2. Dataset 2, 10.5256/f1000research.7143.d104553\r\n\r\nF1000Research: Dataset
3. Dataset 3, 10.5256/f1000research.7143.d104554"
article_processing_charge: No
author:
- first_name: Jaroslav
full_name: Michalko, Jaroslav
id: 483727CA-F248-11E8-B48F-1D18A9856A87
last_name: Michalko
- first_name: Marta
full_name: Dravecka, Marta
id: 4342E402-F248-11E8-B48F-1D18A9856A87
last_name: Dravecka
orcid: 0000-0002-2519-8004
- first_name: Tobias
full_name: Bollenbach, Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
- first_name: Jirí
full_name: Friml, Jirí
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
citation:
ama: Michalko J, Lukacisinova M, Bollenbach MT, Friml J. Embryo-lethal phenotypes
in early abp1 mutants are due to disruption of the neighboring BSM gene. F1000
Research . 2015;4. doi:10.12688/f1000research.7143.1
apa: Michalko, J., Lukacisinova, M., Bollenbach, M. T., & Friml, J. (2015).
Embryo-lethal phenotypes in early abp1 mutants are due to disruption of the neighboring
BSM gene. F1000 Research . F1000 Research. https://doi.org/10.12688/f1000research.7143.1
chicago: Michalko, Jaroslav, Marta Lukacisinova, Mark Tobias Bollenbach, and Jiří
Friml. “Embryo-Lethal Phenotypes in Early Abp1 Mutants Are Due to Disruption of
the Neighboring BSM Gene.” F1000 Research . F1000 Research, 2015. https://doi.org/10.12688/f1000research.7143.1.
ieee: J. Michalko, M. Lukacisinova, M. T. Bollenbach, and J. Friml, “Embryo-lethal
phenotypes in early abp1 mutants are due to disruption of the neighboring BSM
gene,” F1000 Research , vol. 4. F1000 Research, 2015.
ista: Michalko J, Lukacisinova M, Bollenbach MT, Friml J. 2015. Embryo-lethal phenotypes
in early abp1 mutants are due to disruption of the neighboring BSM gene. F1000
Research . 4.
mla: Michalko, Jaroslav, et al. “Embryo-Lethal Phenotypes in Early Abp1 Mutants
Are Due to Disruption of the Neighboring BSM Gene.” F1000 Research , vol.
4, F1000 Research, 2015, doi:10.12688/f1000research.7143.1.
short: J. Michalko, M. Lukacisinova, M.T. Bollenbach, J. Friml, F1000 Research 4
(2015).
date_created: 2018-12-11T11:52:26Z
date_published: 2015-10-01T00:00:00Z
date_updated: 2025-05-07T11:12:30Z
day: '01'
ddc:
- '570'
department:
- _id: JiFr
- _id: ToBo
doi: 10.12688/f1000research.7143.1
ec_funded: 1
file:
- access_level: open_access
checksum: 8beae5cbe988e1060265ae7de2ee8306
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:16:12Z
date_updated: 2020-07-14T12:44:59Z
file_id: '5198'
file_name: IST-2016-497-v1+1_10.12688_f1000research.7143.1_20151102.pdf
file_size: 4414248
relation: main_file
file_date_updated: 2020-07-14T12:44:59Z
has_accepted_license: '1'
intvolume: ' 4'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
project:
- _id: 25716A02-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '282300'
name: Polarity and subcellular dynamics in plants
publication: 'F1000 Research '
publication_status: published
publisher: F1000 Research
publist_id: '5668'
pubrep_id: '497'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Embryo-lethal phenotypes in early abp1 mutants are due to disruption of the
neighboring BSM gene
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: 4
year: '2015'
...
---
_id: '1571'
abstract:
- lang: eng
text: Epistatic interactions can frustrate and shape evolutionary change. Indeed,
phenotypes may fail to evolve when essential mutations are only accessible through
positive selection if they are fixed simultaneously. How environmental variability
affects such constraints is poorly understood. Here, we studied genetic constraints
in fixed and fluctuating environments using the Escherichia coli lac operon as
a model system for genotype-environment interactions. We found that, in different
fixed environments, all trajectories that were reconstructed by applying point
mutations within the transcription factor-operator interface became trapped at
suboptima, where no additional improvements were possible. Paradoxically, repeated
switching between these same environments allows unconstrained adaptation by continuous
improvements. This evolutionary mode is explained by pervasive cross-environmental
tradeoffs that reposition the peaks in such a way that trapped genotypes can repeatedly
climb ascending slopes and hence, escape adaptive stasis. Using a Markov approach,
we developed a mathematical framework to quantify the landscape-crossing rates
and show that this ratchet-like adaptive mechanism is robust in a wide spectrum
of fluctuating environments. Overall, this study shows that genetic constraints
can be overcome by environmental change and that crossenvironmental tradeoffs
do not necessarily impede but also, can facilitate adaptive evolution. Because
tradeoffs and environmental variability are ubiquitous in nature, we speculate
this evolutionary mode to be of general relevance.
acknowledgement: This work is part of the research program of the Foundation for Fundamental
Research on Matter, which is part of the Netherlands Organization for Scientific
Research (NWO). M.G.J.d.V. was (partially) funded by NWO Earth and Life Sciences
(ALW), project 863.14.015. We thank D. M. Weinreich, J. A. G. M. de Visser, T. Paixão,
J. Polechová, T. Friedlander, and A. E. Mayo for reading and commenting on earlier
versions of the manuscript and B. Houchmandzadeh, O. Rivoire, and M. Hemery for
discussions and suggestions on the Markov computation. Furthermore, we thank F.
J. Poelwijk for sharing plasmid pCascade5 and pRD007 and Y. Yokobayashi for sharing
plasmid pINV-110. We also thank the anonymous reviewers for remarks on the initial
version of the manuscript.
author:
- first_name: Marjon
full_name: De Vos, Marjon
id: 3111FFAC-F248-11E8-B48F-1D18A9856A87
last_name: De Vos
- first_name: Alexandre
full_name: Dawid, Alexandre
last_name: Dawid
- first_name: Vanda
full_name: Šunderlíková, Vanda
last_name: Šunderlíková
- first_name: Sander
full_name: Tans, Sander
last_name: Tans
citation:
ama: de Vos M, Dawid A, Šunderlíková V, Tans S. Breaking evolutionary constraint
with a tradeoff ratchet. PNAS. 2015;112(48):14906-14911. doi:10.1073/pnas.1510282112
apa: de Vos, M., Dawid, A., Šunderlíková, V., & Tans, S. (2015). Breaking evolutionary
constraint with a tradeoff ratchet. PNAS. National Academy of Sciences.
https://doi.org/10.1073/pnas.1510282112
chicago: Vos, Marjon de, Alexandre Dawid, Vanda Šunderlíková, and Sander Tans. “Breaking
Evolutionary Constraint with a Tradeoff Ratchet.” PNAS. National Academy
of Sciences, 2015. https://doi.org/10.1073/pnas.1510282112.
ieee: M. de Vos, A. Dawid, V. Šunderlíková, and S. Tans, “Breaking evolutionary
constraint with a tradeoff ratchet,” PNAS, vol. 112, no. 48. National Academy
of Sciences, pp. 14906–14911, 2015.
ista: de Vos M, Dawid A, Šunderlíková V, Tans S. 2015. Breaking evolutionary constraint
with a tradeoff ratchet. PNAS. 112(48), 14906–14911.
mla: de Vos, Marjon, et al. “Breaking Evolutionary Constraint with a Tradeoff Ratchet.”
PNAS, vol. 112, no. 48, National Academy of Sciences, 2015, pp. 14906–11,
doi:10.1073/pnas.1510282112.
short: M. de Vos, A. Dawid, V. Šunderlíková, S. Tans, PNAS 112 (2015) 14906–14911.
date_created: 2018-12-11T11:52:47Z
date_published: 2015-12-01T00:00:00Z
date_updated: 2021-01-12T06:51:40Z
day: '01'
department:
- _id: ToBo
doi: 10.1073/pnas.1510282112
intvolume: ' 112'
issue: '48'
language:
- iso: eng
month: '12'
oa_version: None
page: 14906 - 14911
publication: PNAS
publication_status: published
publisher: National Academy of Sciences
publist_id: '5600'
quality_controlled: '1'
scopus_import: 1
status: public
title: Breaking evolutionary constraint with a tradeoff ratchet
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 112
year: '2015'
...
---
_id: '1581'
abstract:
- lang: eng
text: In animal embryos, morphogen gradients determine tissue patterning and morphogenesis.
Shyer et al. provide evidence that, during vertebrate gut formation, tissue folding
generates graded activity of signals required for subsequent steps of gut growth
and differentiation, thereby revealing an intriguing link between tissue morphogenesis
and morphogen gradient formation.
article_processing_charge: No
author:
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
citation:
ama: Bollenbach MT, Heisenberg C-PJ. Gradients are shaping up. Cell. 2015;161(3):431-432.
doi:10.1016/j.cell.2015.04.009
apa: Bollenbach, M. T., & Heisenberg, C.-P. J. (2015). Gradients are shaping
up. Cell. Cell Press. https://doi.org/10.1016/j.cell.2015.04.009
chicago: Bollenbach, Mark Tobias, and Carl-Philipp J Heisenberg. “Gradients Are
Shaping Up.” Cell. Cell Press, 2015. https://doi.org/10.1016/j.cell.2015.04.009.
ieee: M. T. Bollenbach and C.-P. J. Heisenberg, “Gradients are shaping up,” Cell,
vol. 161, no. 3. Cell Press, pp. 431–432, 2015.
ista: Bollenbach MT, Heisenberg C-PJ. 2015. Gradients are shaping up. Cell. 161(3),
431–432.
mla: Bollenbach, Mark Tobias, and Carl-Philipp J. Heisenberg. “Gradients Are Shaping
Up.” Cell, vol. 161, no. 3, Cell Press, 2015, pp. 431–32, doi:10.1016/j.cell.2015.04.009.
short: M.T. Bollenbach, C.-P.J. Heisenberg, Cell 161 (2015) 431–432.
date_created: 2018-12-11T11:52:50Z
date_published: 2015-04-23T00:00:00Z
date_updated: 2022-08-25T13:56:10Z
day: '23'
department:
- _id: ToBo
- _id: CaHe
doi: 10.1016/j.cell.2015.04.009
intvolume: ' 161'
issue: '3'
language:
- iso: eng
month: '04'
oa_version: None
page: 431 - 432
publication: Cell
publication_status: published
publisher: Cell Press
publist_id: '5590'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Gradients are shaping up
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 161
year: '2015'
...
---
_id: '1586'
abstract:
- lang: eng
text: Through metabolic engineering cyanobacteria can be employed in biotechnology.
Combining the capacity for oxygenic photosynthesis and carbon fixation with an
engineered metabolic pathway allows carbon-based product formation from CO2, light,
and water directly. Such cyanobacterial 'cell factories' are constructed to produce
biofuels, bioplastics, and commodity chemicals. Efforts of metabolic engineers
and synthetic biologists allow the modification of the intermediary metabolism
at various branching points, expanding the product range. The new biosynthesis
routes 'tap' the metabolism ever more efficiently, particularly through the engineering
of driving forces and utilization of cofactors generated during the light reactions
of photosynthesis, resulting in higher product titers. High rates of carbon rechanneling
ultimately allow an almost-complete allocation of fixed carbon to product above
biomass.
author:
- first_name: Andreas
full_name: Angermayr, Andreas
id: 4677C796-F248-11E8-B48F-1D18A9856A87
last_name: Angermayr
orcid: 0000-0001-8619-2223
- first_name: Aleix
full_name: Gorchs, Aleix
last_name: Gorchs
- first_name: Klaas
full_name: Hellingwerf, Klaas
last_name: Hellingwerf
citation:
ama: Angermayr A, Gorchs A, Hellingwerf K. Metabolic engineering of cyanobacteria
for the synthesis of commodity products. Trends in Biotechnology. 2015;33(6):352-361.
doi:10.1016/j.tibtech.2015.03.009
apa: Angermayr, A., Gorchs, A., & Hellingwerf, K. (2015). Metabolic engineering
of cyanobacteria for the synthesis of commodity products. Trends in Biotechnology.
Elsevier. https://doi.org/10.1016/j.tibtech.2015.03.009
chicago: Angermayr, Andreas, Aleix Gorchs, and Klaas Hellingwerf. “Metabolic Engineering
of Cyanobacteria for the Synthesis of Commodity Products.” Trends in Biotechnology.
Elsevier, 2015. https://doi.org/10.1016/j.tibtech.2015.03.009.
ieee: A. Angermayr, A. Gorchs, and K. Hellingwerf, “Metabolic engineering of cyanobacteria
for the synthesis of commodity products,” Trends in Biotechnology, vol.
33, no. 6. Elsevier, pp. 352–361, 2015.
ista: Angermayr A, Gorchs A, Hellingwerf K. 2015. Metabolic engineering of cyanobacteria
for the synthesis of commodity products. Trends in Biotechnology. 33(6), 352–361.
mla: Angermayr, Andreas, et al. “Metabolic Engineering of Cyanobacteria for the
Synthesis of Commodity Products.” Trends in Biotechnology, vol. 33, no.
6, Elsevier, 2015, pp. 352–61, doi:10.1016/j.tibtech.2015.03.009.
short: A. Angermayr, A. Gorchs, K. Hellingwerf, Trends in Biotechnology 33 (2015)
352–361.
date_created: 2018-12-11T11:52:52Z
date_published: 2015-06-01T00:00:00Z
date_updated: 2021-01-12T06:51:46Z
day: '01'
department:
- _id: ToBo
doi: 10.1016/j.tibtech.2015.03.009
intvolume: ' 33'
issue: '6'
language:
- iso: eng
month: '06'
oa_version: None
page: 352 - 361
publication: Trends in Biotechnology
publication_status: published
publisher: Elsevier
publist_id: '5585'
quality_controlled: '1'
scopus_import: 1
status: public
title: Metabolic engineering of cyanobacteria for the synthesis of commodity products
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 33
year: '2015'
...
---
_id: '9711'
article_processing_charge: No
author:
- first_name: Guillaume
full_name: Chevereau, Guillaume
id: 424D78A0-F248-11E8-B48F-1D18A9856A87
last_name: Chevereau
- first_name: Marta
full_name: Lukacisinova, Marta
id: 4342E402-F248-11E8-B48F-1D18A9856A87
last_name: Lukacisinova
orcid: 0000-0002-2519-8004
- first_name: Tugce
full_name: Batur, Tugce
last_name: Batur
- first_name: Aysegul
full_name: Guvenek, Aysegul
last_name: Guvenek
- first_name: Dilay Hazal
full_name: Ayhan, Dilay Hazal
last_name: Ayhan
- first_name: Erdal
full_name: Toprak, Erdal
last_name: Toprak
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
citation:
ama: Chevereau G, Lukacisinova M, Batur T, et al. Excel file containing the raw
data for all figures. 2015. doi:10.1371/journal.pbio.1002299.s001
apa: Chevereau, G., Lukacisinova, M., Batur, T., Guvenek, A., Ayhan, D. H., Toprak,
E., & Bollenbach, M. T. (2015). Excel file containing the raw data for all
figures. Public Library of Science. https://doi.org/10.1371/journal.pbio.1002299.s001
chicago: Chevereau, Guillaume, Marta Lukacisinova, Tugce Batur, Aysegul Guvenek,
Dilay Hazal Ayhan, Erdal Toprak, and Mark Tobias Bollenbach. “Excel File Containing
the Raw Data for All Figures.” Public Library of Science, 2015. https://doi.org/10.1371/journal.pbio.1002299.s001.
ieee: G. Chevereau et al., “Excel file containing the raw data for all figures.”
Public Library of Science, 2015.
ista: Chevereau G, Lukacisinova M, Batur T, Guvenek A, Ayhan DH, Toprak E, Bollenbach
MT. 2015. Excel file containing the raw data for all figures, Public Library of
Science, 10.1371/journal.pbio.1002299.s001.
mla: Chevereau, Guillaume, et al. Excel File Containing the Raw Data for All
Figures. Public Library of Science, 2015, doi:10.1371/journal.pbio.1002299.s001.
short: G. Chevereau, M. Lukacisinova, T. Batur, A. Guvenek, D.H. Ayhan, E. Toprak,
M.T. Bollenbach, (2015).
date_created: 2021-07-23T11:53:50Z
date_published: 2015-11-18T00:00:00Z
date_updated: 2023-02-23T10:07:02Z
day: '18'
department:
- _id: ToBo
doi: 10.1371/journal.pbio.1002299.s001
month: '11'
oa_version: Published Version
publisher: Public Library of Science
related_material:
record:
- id: '1619'
relation: used_in_publication
status: public
status: public
title: Excel file containing the raw data for all figures
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2015'
...
---
_id: '9765'
article_processing_charge: No
author:
- first_name: Guillaume
full_name: Chevereau, Guillaume
id: 424D78A0-F248-11E8-B48F-1D18A9856A87
last_name: Chevereau
- first_name: Marta
full_name: Lukacisinova, Marta
id: 4342E402-F248-11E8-B48F-1D18A9856A87
last_name: Lukacisinova
orcid: 0000-0002-2519-8004
- first_name: Tugce
full_name: Batur, Tugce
last_name: Batur
- first_name: Aysegul
full_name: Guvenek, Aysegul
last_name: Guvenek
- first_name: Dilay Hazal
full_name: Ayhan, Dilay Hazal
last_name: Ayhan
- first_name: Erdal
full_name: Toprak, Erdal
last_name: Toprak
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
citation:
ama: Chevereau G, Lukacisinova M, Batur T, et al. Gene ontology enrichment analysis
for the most sensitive gene deletion strains for all drugs. 2015. doi:10.1371/journal.pbio.1002299.s008
apa: Chevereau, G., Lukacisinova, M., Batur, T., Guvenek, A., Ayhan, D. H., Toprak,
E., & Bollenbach, M. T. (2015). Gene ontology enrichment analysis for the
most sensitive gene deletion strains for all drugs. Public Library of Science.
https://doi.org/10.1371/journal.pbio.1002299.s008
chicago: Chevereau, Guillaume, Marta Lukacisinova, Tugce Batur, Aysegul Guvenek,
Dilay Hazal Ayhan, Erdal Toprak, and Mark Tobias Bollenbach. “Gene Ontology Enrichment
Analysis for the Most Sensitive Gene Deletion Strains for All Drugs.” Public Library
of Science, 2015. https://doi.org/10.1371/journal.pbio.1002299.s008.
ieee: G. Chevereau et al., “Gene ontology enrichment analysis for the most
sensitive gene deletion strains for all drugs.” Public Library of Science, 2015.
ista: Chevereau G, Lukacisinova M, Batur T, Guvenek A, Ayhan DH, Toprak E, Bollenbach
MT. 2015. Gene ontology enrichment analysis for the most sensitive gene deletion
strains for all drugs, Public Library of Science, 10.1371/journal.pbio.1002299.s008.
mla: Chevereau, Guillaume, et al. Gene Ontology Enrichment Analysis for the Most
Sensitive Gene Deletion Strains for All Drugs. Public Library of Science,
2015, doi:10.1371/journal.pbio.1002299.s008.
short: G. Chevereau, M. Lukacisinova, T. Batur, A. Guvenek, D.H. Ayhan, E. Toprak,
M.T. Bollenbach, (2015).
date_created: 2021-08-03T07:05:16Z
date_published: 2015-11-18T00:00:00Z
date_updated: 2023-02-23T10:07:02Z
day: '18'
department:
- _id: ToBo
doi: 10.1371/journal.pbio.1002299.s008
month: '11'
oa_version: Published Version
publisher: Public Library of Science
related_material:
record:
- id: '1619'
relation: used_in_publication
status: public
status: public
title: Gene ontology enrichment analysis for the most sensitive gene deletion strains
for all drugs
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2015'
...
---
_id: '2001'
abstract:
- lang: eng
text: Antibiotics affect bacterial cell physiology at many levels. Rather than just
compensating for the direct cellular defects caused by the drug, bacteria respond
to antibiotics by changing their morphology, macromolecular composition, metabolism,
gene expression and possibly even their mutation rate. Inevitably, these processes
affect each other, resulting in a complex response with changes in the expression
of numerous genes. Genome‐wide approaches can thus help in gaining a comprehensive
understanding of bacterial responses to antibiotics. In addition, a combination
of experimental and theoretical approaches is needed for identifying general principles
that underlie these responses. Here, we review recent progress in our understanding
of bacterial responses to antibiotics and their combinations, focusing on effects
at the levels of growth rate and gene expression. We concentrate on studies performed
in controlled laboratory conditions, which combine promising experimental techniques
with quantitative data analysis and mathematical modeling. While these basic research
approaches are not immediately applicable in the clinic, uncovering the principles
and mechanisms underlying bacterial responses to antibiotics may, in the long
term, contribute to the development of new treatment strategies to cope with and
prevent the rise of resistant pathogenic bacteria.
author:
- first_name: Karin
full_name: Mitosch, Karin
id: 39B66846-F248-11E8-B48F-1D18A9856A87
last_name: Mitosch
- first_name: Tobias
full_name: Bollenbach, Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
citation:
ama: Mitosch K, Bollenbach MT. Bacterial responses to antibiotics and their combinations.
Environmental Microbiology Reports. 2014;6(6):545-557. doi:10.1111/1758-2229.12190
apa: Mitosch, K., & Bollenbach, M. T. (2014). Bacterial responses to antibiotics
and their combinations. Environmental Microbiology Reports. Wiley. https://doi.org/10.1111/1758-2229.12190
chicago: Mitosch, Karin, and Mark Tobias Bollenbach. “Bacterial Responses to Antibiotics
and Their Combinations.” Environmental Microbiology Reports. Wiley, 2014.
https://doi.org/10.1111/1758-2229.12190.
ieee: K. Mitosch and M. T. Bollenbach, “Bacterial responses to antibiotics and their
combinations,” Environmental Microbiology Reports, vol. 6, no. 6. Wiley,
pp. 545–557, 2014.
ista: Mitosch K, Bollenbach MT. 2014. Bacterial responses to antibiotics and their
combinations. Environmental Microbiology Reports. 6(6), 545–557.
mla: Mitosch, Karin, and Mark Tobias Bollenbach. “Bacterial Responses to Antibiotics
and Their Combinations.” Environmental Microbiology Reports, vol. 6, no.
6, Wiley, 2014, pp. 545–57, doi:10.1111/1758-2229.12190.
short: K. Mitosch, M.T. Bollenbach, Environmental Microbiology Reports 6 (2014)
545–557.
date_created: 2018-12-11T11:55:08Z
date_published: 2014-06-22T00:00:00Z
date_updated: 2023-09-07T12:00:25Z
day: '22'
department:
- _id: ToBo
doi: 10.1111/1758-2229.12190
ec_funded: 1
intvolume: ' 6'
issue: '6'
language:
- iso: eng
month: '06'
oa_version: None
page: 545 - 557
project:
- _id: 25EB3A80-B435-11E9-9278-68D0E5697425
grant_number: RGP0042/2013
name: Revealing the fundamental limits of cell growth
- _id: 25E83C2C-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '303507'
name: Optimality principles in responses to antibiotics
publication: Environmental Microbiology Reports
publication_status: published
publisher: Wiley
publist_id: '5076'
quality_controlled: '1'
related_material:
record:
- id: '818'
relation: dissertation_contains
status: public
scopus_import: 1
status: public
title: Bacterial responses to antibiotics and their combinations
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 6
year: '2014'
...
---
_id: '2040'
abstract:
- lang: eng
text: 'Development requires tissue growth as well as cell diversification. To address
how these processes are coordinated, we analyzed the development of molecularly
distinct domains of neural progenitors in the mouse and chick neural tube. We
show that during development, these domains undergo changes in size that do not
scale with changes in overall tissue size. Our data show that domain proportions
are first established by opposing morphogen gradients and subsequently controlled
by domain-specific regulation of differentiation rate but not differences in proliferation
rate. Regulation of differentiation rate is key to maintaining domain proportions
while accommodating both intra- and interspecies variations in size. Thus, the
sequential control of progenitor specification and differentiation elaborates
pattern without requiring that signaling gradients grow as tissues expand. '
article_number: '1254927'
author:
- first_name: Anna
full_name: Kicheva, Anna
last_name: Kicheva
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
- first_name: Ana
full_name: Ribeiro, Ana
last_name: Ribeiro
- first_name: Helena
full_name: Pérez Valle, Helena
last_name: Pérez Valle
- first_name: Robin
full_name: Lovell Badge, Robin
last_name: Lovell Badge
- first_name: Vasso
full_name: Episkopou, Vasso
last_name: Episkopou
- first_name: James
full_name: Briscoe, James
last_name: Briscoe
citation:
ama: Kicheva A, Bollenbach MT, Ribeiro A, et al. Coordination of progenitor specification
and growth in mouse and chick spinal cord. Science. 2014;345(6204). doi:10.1126/science.1254927
apa: Kicheva, A., Bollenbach, M. T., Ribeiro, A., Pérez Valle, H., Lovell Badge,
R., Episkopou, V., & Briscoe, J. (2014). Coordination of progenitor specification
and growth in mouse and chick spinal cord. Science. American Association
for the Advancement of Science. https://doi.org/10.1126/science.1254927
chicago: Kicheva, Anna, Mark Tobias Bollenbach, Ana Ribeiro, Helena Pérez Valle,
Robin Lovell Badge, Vasso Episkopou, and James Briscoe. “Coordination of Progenitor
Specification and Growth in Mouse and Chick Spinal Cord.” Science. American
Association for the Advancement of Science, 2014. https://doi.org/10.1126/science.1254927.
ieee: A. Kicheva et al., “Coordination of progenitor specification and growth
in mouse and chick spinal cord,” Science, vol. 345, no. 6204. American
Association for the Advancement of Science, 2014.
ista: Kicheva A, Bollenbach MT, Ribeiro A, Pérez Valle H, Lovell Badge R, Episkopou
V, Briscoe J. 2014. Coordination of progenitor specification and growth in mouse
and chick spinal cord. Science. 345(6204), 1254927.
mla: Kicheva, Anna, et al. “Coordination of Progenitor Specification and Growth
in Mouse and Chick Spinal Cord.” Science, vol. 345, no. 6204, 1254927,
American Association for the Advancement of Science, 2014, doi:10.1126/science.1254927.
short: A. Kicheva, M.T. Bollenbach, A. Ribeiro, H. Pérez Valle, R. Lovell Badge,
V. Episkopou, J. Briscoe, Science 345 (2014).
date_created: 2018-12-11T11:55:22Z
date_published: 2014-09-26T00:00:00Z
date_updated: 2021-01-12T06:54:55Z
day: '26'
department:
- _id: ToBo
doi: 10.1126/science.1254927
intvolume: ' 345'
issue: '6204'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4228193/
month: '09'
oa: 1
oa_version: Submitted Version
publication: Science
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '5011'
quality_controlled: '1'
scopus_import: 1
status: public
title: Coordination of progenitor specification and growth in mouse and chick spinal
cord
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 345
year: '2014'
...
---
_id: '2220'
abstract:
- lang: eng
text: In this issue of Chemistry & Biology, Cokol and colleagues report a systematic
study of drug interactions between antifungal compounds. Suppressive drug interactions
occur more frequently than previously realized and come in different flavors with
interesting implications.
author:
- first_name: Marjon
full_name: De Vos, Marjon
id: 3111FFAC-F248-11E8-B48F-1D18A9856A87
last_name: De Vos
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
citation:
ama: de Vos M, Bollenbach MT. Suppressive drug interactions between antifungals.
Chemistry and Biology. 2014;21(4):439-440. doi:10.1016/j.chembiol.2014.04.004
apa: de Vos, M., & Bollenbach, M. T. (2014). Suppressive drug interactions between
antifungals. Chemistry and Biology. Cell Press. https://doi.org/10.1016/j.chembiol.2014.04.004
chicago: Vos, Marjon de, and Mark Tobias Bollenbach. “Suppressive Drug Interactions
between Antifungals.” Chemistry and Biology. Cell Press, 2014. https://doi.org/10.1016/j.chembiol.2014.04.004.
ieee: M. de Vos and M. T. Bollenbach, “Suppressive drug interactions between antifungals,”
Chemistry and Biology, vol. 21, no. 4. Cell Press, pp. 439–440, 2014.
ista: de Vos M, Bollenbach MT. 2014. Suppressive drug interactions between antifungals.
Chemistry and Biology. 21(4), 439–440.
mla: de Vos, Marjon, and Mark Tobias Bollenbach. “Suppressive Drug Interactions
between Antifungals.” Chemistry and Biology, vol. 21, no. 4, Cell Press,
2014, pp. 439–40, doi:10.1016/j.chembiol.2014.04.004.
short: M. de Vos, M.T. Bollenbach, Chemistry and Biology 21 (2014) 439–440.
date_created: 2018-12-11T11:56:24Z
date_published: 2014-04-24T00:00:00Z
date_updated: 2021-01-12T06:56:06Z
day: '24'
department:
- _id: ToBo
doi: 10.1016/j.chembiol.2014.04.004
external_id:
pmid:
- '24766845'
intvolume: ' 21'
issue: '4'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pubmed/24766845
month: '04'
oa: 1
oa_version: Published Version
page: 439 - 440
pmid: 1
publication: Chemistry and Biology
publication_identifier:
issn:
- '10745521'
publication_status: published
publisher: Cell Press
publist_id: '4747'
quality_controlled: '1'
scopus_import: 1
status: public
title: Suppressive drug interactions between antifungals
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 21
year: '2014'
...
---
_id: '2810'
abstract:
- lang: eng
text: The epistatic interactions that underlie evolutionary constraint have mainly
been studied for constant external conditions. However, environmental changes
may modulate epistasis and hence affect genetic constraints. Here we investigate
genetic constraints in the adaptive evolution of a novel regulatory function in
variable environments, using the lac repressor, LacI, as a model system. We have
systematically reconstructed mutational trajectories from wild type LacI to three
different variants that each exhibit an inverse response to the inducing ligand
IPTG, and analyzed the higher-order interactions between genetic and environmental
changes. We find epistasis to depend strongly on the environment. As a result,
mutational steps essential to inversion but inaccessible by positive selection
in one environment, become accessible in another. We present a graphical method
to analyze the observed complex higher-order interactions between multiple mutations
and environmental change, and show how the interactions can be explained by a
combination of mutational effects on allostery and thermodynamic stability. This
dependency of genetic constraint on the environment should fundamentally affect
evolutionary dynamics and affects the interpretation of phylogenetic data.
article_number: e1003580
author:
- first_name: Marjon
full_name: De Vos, Marjon
id: 3111FFAC-F248-11E8-B48F-1D18A9856A87
last_name: De Vos
- first_name: Frank
full_name: Poelwijk, Frank
last_name: Poelwijk
- first_name: Nico
full_name: Battich, Nico
last_name: Battich
- first_name: Joseph
full_name: Ndika, Joseph
last_name: Ndika
- first_name: Sander
full_name: Tans, Sander
last_name: Tans
citation:
ama: de Vos M, Poelwijk F, Battich N, Ndika J, Tans S. Environmental dependence
of genetic constraint. PLoS Genetics. 2013;9(6). doi:10.1371/journal.pgen.1003580
apa: de Vos, M., Poelwijk, F., Battich, N., Ndika, J., & Tans, S. (2013). Environmental
dependence of genetic constraint. PLoS Genetics. Public Library of Science.
https://doi.org/10.1371/journal.pgen.1003580
chicago: Vos, Marjon de, Frank Poelwijk, Nico Battich, Joseph Ndika, and Sander
Tans. “Environmental Dependence of Genetic Constraint.” PLoS Genetics.
Public Library of Science, 2013. https://doi.org/10.1371/journal.pgen.1003580.
ieee: M. de Vos, F. Poelwijk, N. Battich, J. Ndika, and S. Tans, “Environmental
dependence of genetic constraint,” PLoS Genetics, vol. 9, no. 6. Public
Library of Science, 2013.
ista: de Vos M, Poelwijk F, Battich N, Ndika J, Tans S. 2013. Environmental dependence
of genetic constraint. PLoS Genetics. 9(6), e1003580.
mla: de Vos, Marjon, et al. “Environmental Dependence of Genetic Constraint.” PLoS
Genetics, vol. 9, no. 6, e1003580, Public Library of Science, 2013, doi:10.1371/journal.pgen.1003580.
short: M. de Vos, F. Poelwijk, N. Battich, J. Ndika, S. Tans, PLoS Genetics 9 (2013).
date_created: 2018-12-11T11:59:43Z
date_published: 2013-06-27T00:00:00Z
date_updated: 2021-01-12T06:59:52Z
day: '27'
ddc:
- '570'
department:
- _id: ToBo
doi: 10.1371/journal.pgen.1003580
file:
- access_level: open_access
checksum: 7a4736dd80496d29ff6908b6f2329b4e
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:08:51Z
date_updated: 2020-07-14T12:45:48Z
file_id: '4713'
file_name: IST-2016-412-v1+1_journal.pgen.1003580.pdf
file_size: 474655
relation: main_file
file_date_updated: 2020-07-14T12:45:48Z
has_accepted_license: '1'
intvolume: ' 9'
issue: '6'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
publication: PLoS Genetics
publication_status: published
publisher: Public Library of Science
publist_id: '4075'
pubrep_id: '412'
quality_controlled: '1'
scopus_import: 1
status: public
title: Environmental dependence of genetic constraint
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: 9
year: '2013'
...
---
_id: '2970'
abstract:
- lang: eng
text: Morphogen gradients regulate the patterning and growth of many tissues, hence
a key question is how they are established and maintained during development.
Theoretical descriptions have helped to explain how gradient shape is controlled
by the rates of morphogen production, spreading and degradation. These effective
rates have been measured using fluorescence recovery after photobleaching (FRAP)
and photoactivation. To unravel which molecular events determine the effective
rates, such tissue-level assays have been combined with genetic analysis, high-resolution
assays, and models that take into account interactions with receptors, extracellular
components and trafficking. Nevertheless, because of the natural and experimental
data variability, and the underlying assumptions of transport models, it remains
challenging to conclusively distinguish between cellular mechanisms.
acknowledgement: AK is currently supported by an MRC CDF. MGG and OW were supported
by the Swiss National Science Foundation, grants from the Swiss SystemsX.ch initiative,
LipidX-2008/011, an ERC advanced investigator grant and the Polish-Swiss research
program.
author:
- first_name: Anna
full_name: Kicheva, Anna
id: 3959A2A0-F248-11E8-B48F-1D18A9856A87
last_name: Kicheva
orcid: 0000-0003-4509-4998
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
- first_name: Ortrud
full_name: Wartlick, Ortrud
last_name: Wartlick
- first_name: Frank
full_name: Julicher, Frank
last_name: Julicher
- first_name: Marcos
full_name: Gonzalez Gaitan, Marcos
last_name: Gonzalez Gaitan
citation:
ama: 'Kicheva A, Bollenbach MT, Wartlick O, Julicher F, Gonzalez Gaitan M. Investigating
the principles of morphogen gradient formation: from tissues to cells. Current
Opinion in Genetics & Development. 2012;22(6):527-532. doi:10.1016/j.gde.2012.08.004'
apa: 'Kicheva, A., Bollenbach, M. T., Wartlick, O., Julicher, F., & Gonzalez
Gaitan, M. (2012). Investigating the principles of morphogen gradient formation:
from tissues to cells. Current Opinion in Genetics & Development. Elsevier.
https://doi.org/10.1016/j.gde.2012.08.004'
chicago: 'Kicheva, Anna, Mark Tobias Bollenbach, Ortrud Wartlick, Frank Julicher,
and Marcos Gonzalez Gaitan. “Investigating the Principles of Morphogen Gradient
Formation: From Tissues to Cells.” Current Opinion in Genetics & Development.
Elsevier, 2012. https://doi.org/10.1016/j.gde.2012.08.004.'
ieee: 'A. Kicheva, M. T. Bollenbach, O. Wartlick, F. Julicher, and M. Gonzalez Gaitan,
“Investigating the principles of morphogen gradient formation: from tissues to
cells,” Current Opinion in Genetics & Development, vol. 22, no. 6.
Elsevier, pp. 527–532, 2012.'
ista: 'Kicheva A, Bollenbach MT, Wartlick O, Julicher F, Gonzalez Gaitan M. 2012.
Investigating the principles of morphogen gradient formation: from tissues to
cells. Current Opinion in Genetics & Development. 22(6), 527–532.'
mla: 'Kicheva, Anna, et al. “Investigating the Principles of Morphogen Gradient
Formation: From Tissues to Cells.” Current Opinion in Genetics & Development,
vol. 22, no. 6, Elsevier, 2012, pp. 527–32, doi:10.1016/j.gde.2012.08.004.'
short: A. Kicheva, M.T. Bollenbach, O. Wartlick, F. Julicher, M. Gonzalez Gaitan,
Current Opinion in Genetics & Development 22 (2012) 527–532.
date_created: 2018-12-11T12:00:37Z
date_published: 2012-12-01T00:00:00Z
date_updated: 2021-01-12T07:40:09Z
day: '01'
department:
- _id: ToBo
doi: 10.1016/j.gde.2012.08.004
intvolume: ' 22'
issue: '6'
language:
- iso: eng
month: '12'
oa_version: None
page: 527 - 532
publication: Current Opinion in Genetics & Development
publication_status: published
publisher: Elsevier
publist_id: '3739'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'Investigating the principles of morphogen gradient formation: from tissues
to cells'
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 22
year: '2012'
...
---
_id: '3160'
abstract:
- lang: eng
text: There is a long-running controversy about how early cell fate decisions are
made in the developing mammalian embryo. 1,2 In particular, it is controversial
when the first events that can predict the establishment of the pluripotent and
extra-embryonic lineages in the blastocyst of the pre-implantation embryo occur.
It has long been proposed that the position and polarity of cells at the 16- to
32-cell stage embryo influence their decision to either give rise to the pluripotent
cell lineage that eventually contributes to the inner cell mass (ICM), comprising
the primitive endoderm (PE) and the epiblast (EPI), or the extra-embryonic trophectoderm
(TE) surrounding the blastocoel. The positioning of cells in the embryo at this
developmental stage could largely be the result of random events, making this
a stochastic model of cell lineage allocation. Contrary to such a stochastic model,
some studies have detected putative differences in the lineage potential of individual
blastomeres before compaction, indicating that the first cell fate decisions may
occur as early as at the 4-cell stage. Using a non-invasive, quantitative in vivo
imaging assay to study the kinetic behavior of Oct4 (also known as POU5F1), a
key transcription factor (TF) controlling pre-implantation development in the
mouse embryo, 3-5 a recent study identifies Oct4 kinetics as a predictive measure
of cell lineage patterning in the early mouse embryo. 6 Here, we discuss the implications
of such molecular heterogeneities in early development and offer potential avenues
toward a mechanistic understanding of these observations, contributing to the
resolution of the controversy of developmental cell lineage allocation.
author:
- first_name: Periklis
full_name: Pantazis, Periklis
last_name: Pantazis
- first_name: Tobias
full_name: Bollenbach, Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
citation:
ama: Pantazis P, Bollenbach MT. Transcription factor kinetics and the emerging asymmetry
in the early mammalian embryo. Cell Cycle. 2012;11(11):2055-2058. doi:10.4161/cc.20118
apa: Pantazis, P., & Bollenbach, M. T. (2012). Transcription factor kinetics
and the emerging asymmetry in the early mammalian embryo. Cell Cycle. Taylor
and Francis. https://doi.org/10.4161/cc.20118
chicago: Pantazis, Periklis, and Mark Tobias Bollenbach. “Transcription Factor Kinetics
and the Emerging Asymmetry in the Early Mammalian Embryo.” Cell Cycle.
Taylor and Francis, 2012. https://doi.org/10.4161/cc.20118.
ieee: P. Pantazis and M. T. Bollenbach, “Transcription factor kinetics and the emerging
asymmetry in the early mammalian embryo,” Cell Cycle, vol. 11, no. 11.
Taylor and Francis, pp. 2055–2058, 2012.
ista: Pantazis P, Bollenbach MT. 2012. Transcription factor kinetics and the emerging
asymmetry in the early mammalian embryo. Cell Cycle. 11(11), 2055–2058.
mla: Pantazis, Periklis, and Mark Tobias Bollenbach. “Transcription Factor Kinetics
and the Emerging Asymmetry in the Early Mammalian Embryo.” Cell Cycle,
vol. 11, no. 11, Taylor and Francis, 2012, pp. 2055–58, doi:10.4161/cc.20118.
short: P. Pantazis, M.T. Bollenbach, Cell Cycle 11 (2012) 2055–2058.
date_created: 2018-12-11T12:01:44Z
date_published: 2012-06-01T00:00:00Z
date_updated: 2021-01-12T07:41:28Z
day: '01'
department:
- _id: ToBo
doi: 10.4161/cc.20118
intvolume: ' 11'
issue: '11'
language:
- iso: eng
month: '06'
oa_version: None
page: 2055 - 2058
publication: Cell Cycle
publication_status: published
publisher: Taylor and Francis
publist_id: '3531'
quality_controlled: '1'
scopus_import: 1
status: public
title: Transcription factor kinetics and the emerging asymmetry in the early mammalian
embryo
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 11
year: '2012'
...
---
_id: '3376'
abstract:
- lang: eng
text: Regulatory conflicts occur when two signals that individually trigger opposite
cellular responses are present simultaneously. Here, we investigate regulatory
conflicts in the bacterial response to antibiotic combinations. We use an Escherichia
coli promoter-GFP library to study the transcriptional response of many promoters
to either additive or antagonistic drug pairs at fine two-dimensional (2D) resolution
of drug concentration. Surprisingly, we find that this data set can be characterized
as a linear sum of only two principal components. Component one, accounting for
over 70% of the response, represents the response to growth inhibition by the
drugs. Component two describes how regulatory conflicts are resolved. For the
additive drug pair, conflicts are resolved by linearly interpolating the single
drug responses, while for the antagonistic drug pair, the growth-limiting drug
dominates the response. Importantly, for a given drug pair, the same conflict
resolution strategy applies to almost all genes. These results provide a recipe
for predicting gene expression responses to antibiotic combinations.
acknowledgement: This work was supported by a Feodor Lynen Fellowship of the Alexander
von Humboldt Foundation (to T.B.).
author:
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
- first_name: Roy
full_name: Kishony, Roy
last_name: Kishony
citation:
ama: Bollenbach MT, Kishony R. Resolution of gene regulatory conflicts caused by
combinations of antibiotics. Molecular Cell. 2011;42(4):413-425. doi:10.1016/j.molcel.2011.04.016
apa: Bollenbach, M. T., & Kishony, R. (2011). Resolution of gene regulatory
conflicts caused by combinations of antibiotics. Molecular Cell. Cell Press.
https://doi.org/10.1016/j.molcel.2011.04.016
chicago: Bollenbach, Mark Tobias, and Roy Kishony. “Resolution of Gene Regulatory
Conflicts Caused by Combinations of Antibiotics.” Molecular Cell. Cell
Press, 2011. https://doi.org/10.1016/j.molcel.2011.04.016.
ieee: M. T. Bollenbach and R. Kishony, “Resolution of gene regulatory conflicts
caused by combinations of antibiotics,” Molecular Cell, vol. 42, no. 4.
Cell Press, pp. 413–425, 2011.
ista: Bollenbach MT, Kishony R. 2011. Resolution of gene regulatory conflicts caused
by combinations of antibiotics. Molecular Cell. 42(4), 413–425.
mla: Bollenbach, Mark Tobias, and Roy Kishony. “Resolution of Gene Regulatory Conflicts
Caused by Combinations of Antibiotics.” Molecular Cell, vol. 42, no. 4,
Cell Press, 2011, pp. 413–25, doi:10.1016/j.molcel.2011.04.016.
short: M.T. Bollenbach, R. Kishony, Molecular Cell 42 (2011) 413–425.
date_created: 2018-12-11T12:02:59Z
date_published: 2011-05-20T00:00:00Z
date_updated: 2021-01-12T07:43:03Z
day: '20'
department:
- _id: ToBo
doi: 10.1016/j.molcel.2011.04.016
intvolume: ' 42'
issue: '4'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3143497/
month: '05'
oa: 1
oa_version: Submitted Version
page: 413 - 425
publication: Molecular Cell
publication_status: published
publisher: Cell Press
publist_id: '3231'
quality_controlled: '1'
scopus_import: 1
status: public
title: Resolution of gene regulatory conflicts caused by combinations of antibiotics
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 42
year: '2011'
...
---
_id: '3429'
abstract:
- lang: eng
text: Transcription factors are central to sustaining pluripotency, yet little is
known about transcription factor dynamics in defining pluripotency in the early
mammalian embryo. Here, we establish a fluorescence decay after photoactivation
(FDAP) assay to quantitatively study the kinetic behaviour of Oct4, a key transcription
factor controlling pre-implantation development in the mouse embryo. FDAP measurements
reveal that each cell in a developing embryo shows one of two distinct Oct4 kinetics,
before there are any morphologically distinguishable differences or outward signs
of lineage patterning. The differences revealed by FDAP are due to differences
in the accessibility of Oct4 to its DNA binding sites in the nucleus. Lineage
tracing of the cells in the two distinct sub-populations demonstrates that the
Oct4 kinetics predict lineages of the early embryo. Cells with slower Oct4 kinetics
are more likely to give rise to the pluripotent cell lineage that contributes
to the inner cell mass. Those with faster Oct4 kinetics contribute mostly to the
extra-embryonic lineage. Our findings identify Oct4 kinetics, rather than differences
in total transcription factor expression levels, as a predictive measure of developmental
cell lineage patterning in the early mouse embryo.
acknowledgement: This work was supported by the Beckman Institute and Biological Imaging
Center at the California Institute of Technology and by the NHGRI Center of Excellence
in Genomic Science grant P50HG004071.
author:
- first_name: Nicolas
full_name: Plachta, Nicolas
last_name: Plachta
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
- first_name: Shirley
full_name: Pease, Shirley
last_name: Pease
- first_name: Scott
full_name: Fraser, Scott
last_name: Fraser
- first_name: Periklis
full_name: Pantazis, Periklis
last_name: Pantazis
citation:
ama: Plachta N, Bollenbach MT, Pease S, Fraser S, Pantazis P. Oct4 kinetics predict
cell lineage patterning in the early mammalian embryo. Nature Cell Biology.
2011;13(2):117-123. doi:10.1038/ncb2154
apa: Plachta, N., Bollenbach, M. T., Pease, S., Fraser, S., & Pantazis, P. (2011).
Oct4 kinetics predict cell lineage patterning in the early mammalian embryo. Nature
Cell Biology. Nature Publishing Group. https://doi.org/10.1038/ncb2154
chicago: Plachta, Nicolas, Mark Tobias Bollenbach, Shirley Pease, Scott Fraser,
and Periklis Pantazis. “Oct4 Kinetics Predict Cell Lineage Patterning in the Early
Mammalian Embryo.” Nature Cell Biology. Nature Publishing Group, 2011.
https://doi.org/10.1038/ncb2154.
ieee: N. Plachta, M. T. Bollenbach, S. Pease, S. Fraser, and P. Pantazis, “Oct4
kinetics predict cell lineage patterning in the early mammalian embryo,” Nature
Cell Biology, vol. 13, no. 2. Nature Publishing Group, pp. 117–123, 2011.
ista: Plachta N, Bollenbach MT, Pease S, Fraser S, Pantazis P. 2011. Oct4 kinetics
predict cell lineage patterning in the early mammalian embryo. Nature Cell Biology.
13(2), 117–123.
mla: Plachta, Nicolas, et al. “Oct4 Kinetics Predict Cell Lineage Patterning in
the Early Mammalian Embryo.” Nature Cell Biology, vol. 13, no. 2, Nature
Publishing Group, 2011, pp. 117–23, doi:10.1038/ncb2154.
short: N. Plachta, M.T. Bollenbach, S. Pease, S. Fraser, P. Pantazis, Nature Cell
Biology 13 (2011) 117–123.
date_created: 2018-12-11T12:03:17Z
date_published: 2011-01-23T00:00:00Z
date_updated: 2021-01-12T07:43:24Z
day: '23'
department:
- _id: ToBo
doi: 10.1038/ncb2154
intvolume: ' 13'
issue: '2'
language:
- iso: eng
month: '01'
oa_version: None
page: 117 - 123
publication: Nature Cell Biology
publication_status: published
publisher: Nature Publishing Group
publist_id: '2971'
scopus_import: 1
status: public
title: Oct4 kinetics predict cell lineage patterning in the early mammalian embryo
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 13
year: '2011'
...