---
_id: '7569'
abstract:
- lang: eng
text: 'Genes differ in the frequency at which they are expressed and in the form
of regulation used to control their activity. In particular, positive or negative
regulation can lead to activation of a gene in response to an external signal.
Previous works proposed that the form of regulation of a gene correlates with
its frequency of usage: positive regulation when the gene is frequently expressed
and negative regulation when infrequently expressed. Such network design means
that, in the absence of their regulators, the genes are found in their least required
activity state, hence regulatory intervention is often necessary. Due to the multitude
of genes and regulators, spurious binding and unbinding events, called “crosstalk”,
could occur. To determine how the form of regulation affects the global crosstalk
in the network, we used a mathematical model that includes multiple regulators
and multiple target genes. We found that crosstalk depends non-monotonically on
the availability of regulators. Our analysis showed that excess use of regulation
entailed by the formerly suggested network design caused high crosstalk levels
in a large part of the parameter space. We therefore considered the opposite ‘idle’
design, where the default unregulated state of genes is their frequently required
activity state. We found, that ‘idle’ design minimized the use of regulation and
thus minimized crosstalk. In addition, we estimated global crosstalk of S. cerevisiae
using transcription factors binding data. We demonstrated that even partial network
data could suffice to estimate its global crosstalk, suggesting its applicability
to additional organisms. We found that S. cerevisiae estimated crosstalk is lower
than that of a random network, suggesting that natural selection reduces crosstalk.
In summary, our study highlights a new type of protein production cost which is
typically overlooked: that of regulatory interference caused by the presence of
excess regulators in the cell. It demonstrates the importance of whole-network
descriptions, which could show effects missed by single-gene models.'
article_number: e1007642
article_processing_charge: No
article_type: original
author:
- first_name: Rok
full_name: Grah, Rok
id: 483E70DE-F248-11E8-B48F-1D18A9856A87
last_name: Grah
orcid: 0000-0003-2539-3560
- first_name: Tamar
full_name: Friedlander, Tamar
last_name: Friedlander
citation:
ama: Grah R, Friedlander T. The relation between crosstalk and gene regulation form
revisited. PLOS Computational Biology. 2020;16(2). doi:10.1371/journal.pcbi.1007642
apa: Grah, R., & Friedlander, T. (2020). The relation between crosstalk and
gene regulation form revisited. PLOS Computational Biology. Public Library
of Science. https://doi.org/10.1371/journal.pcbi.1007642
chicago: Grah, Rok, and Tamar Friedlander. “The Relation between Crosstalk and Gene
Regulation Form Revisited.” PLOS Computational Biology. Public Library
of Science, 2020. https://doi.org/10.1371/journal.pcbi.1007642.
ieee: R. Grah and T. Friedlander, “The relation between crosstalk and gene regulation
form revisited,” PLOS Computational Biology, vol. 16, no. 2. Public Library
of Science, 2020.
ista: Grah R, Friedlander T. 2020. The relation between crosstalk and gene regulation
form revisited. PLOS Computational Biology. 16(2), e1007642.
mla: Grah, Rok, and Tamar Friedlander. “The Relation between Crosstalk and Gene
Regulation Form Revisited.” PLOS Computational Biology, vol. 16, no. 2,
e1007642, Public Library of Science, 2020, doi:10.1371/journal.pcbi.1007642.
short: R. Grah, T. Friedlander, PLOS Computational Biology 16 (2020).
date_created: 2020-03-06T07:39:38Z
date_published: 2020-02-25T00:00:00Z
date_updated: 2023-09-12T11:02:24Z
day: '25'
ddc:
- '000'
- '570'
department:
- _id: CaGu
- _id: GaTk
doi: 10.1371/journal.pcbi.1007642
external_id:
isi:
- '000526725200019'
file:
- access_level: open_access
checksum: 5239dd134dc6e1c71fe7b3ce2953da37
content_type: application/pdf
creator: dernst
date_created: 2020-03-09T15:12:21Z
date_updated: 2020-07-14T12:48:00Z
file_id: '7579'
file_name: 2020_PlosCompBio_Grah.pdf
file_size: 2209325
relation: main_file
file_date_updated: 2020-07-14T12:48:00Z
has_accepted_license: '1'
intvolume: ' 16'
isi: 1
issue: '2'
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
publication: PLOS Computational Biology
publication_identifier:
issn:
- 1553-7358
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
related_material:
record:
- id: '9716'
relation: research_data
status: deleted
- id: '9776'
relation: research_data
status: public
- id: '9779'
relation: used_in_publication
status: public
- id: '8155'
relation: dissertation_contains
status: public
- id: '9777'
relation: research_data
status: public
scopus_import: '1'
status: public
title: The relation between crosstalk and gene regulation form revisited
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 16
year: '2020'
...
---
_id: '8951'
abstract:
- lang: eng
text: Gene expression levels are influenced by multiple coexisting molecular mechanisms.
Some of these interactions, such as those of transcription factors and promoters
have been studied extensively. However, predicting phenotypes of gene regulatory
networks remains a major challenge. Here, we use a well-defined synthetic gene
regulatory network to study how network phenotypes depend on local genetic context,
i.e. the genetic neighborhood of a transcription factor and its relative position.
We show that one gene regulatory network with fixed topology can display not only
quantitatively but also qualitatively different phenotypes, depending solely on
the local genetic context of its components. Our results demonstrate that changes
in local genetic context can place a single transcriptional unit within two separate
regulons without the need for complex regulatory sequences. We propose that relative
order of individual transcriptional units, with its potential for combinatorial
complexity, plays an important role in shaping phenotypes of gene regulatory networks.
article_processing_charge: No
author:
- first_name: Anna A
full_name: Nagy-Staron, Anna A
id: 3ABC5BA6-F248-11E8-B48F-1D18A9856A87
last_name: Nagy-Staron
orcid: 0000-0002-1391-8377
citation:
ama: Nagy-Staron AA. Sequences of gene regulatory network permutations for the article
“Local genetic context shapes the function of a gene regulatory network.” 2020.
doi:10.15479/AT:ISTA:8951
apa: Nagy-Staron, A. A. (2020). Sequences of gene regulatory network permutations
for the article “Local genetic context shapes the function of a gene regulatory
network.” Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:8951
chicago: Nagy-Staron, Anna A. “Sequences of Gene Regulatory Network Permutations
for the Article ‘Local Genetic Context Shapes the Function of a Gene Regulatory
Network.’” Institute of Science and Technology Austria, 2020. https://doi.org/10.15479/AT:ISTA:8951.
ieee: A. A. Nagy-Staron, “Sequences of gene regulatory network permutations for
the article ‘Local genetic context shapes the function of a gene regulatory network.’”
Institute of Science and Technology Austria, 2020.
ista: Nagy-Staron AA. 2020. Sequences of gene regulatory network permutations for
the article ‘Local genetic context shapes the function of a gene regulatory network’,
Institute of Science and Technology Austria, 10.15479/AT:ISTA:8951.
mla: Nagy-Staron, Anna A. Sequences of Gene Regulatory Network Permutations for
the Article “Local Genetic Context Shapes the Function of a Gene Regulatory Network.”
Institute of Science and Technology Austria, 2020, doi:10.15479/AT:ISTA:8951.
short: A.A. Nagy-Staron, (2020).
contributor:
- contributor_type: project_member
first_name: Anna A
id: 3ABC5BA6-F248-11E8-B48F-1D18A9856A87
last_name: Nagy-Staron
- contributor_type: project_member
first_name: Kathrin
id: 3AEC8556-F248-11E8-B48F-1D18A9856A87
last_name: Tomasek
- contributor_type: project_member
first_name: Caroline
last_name: Caruso Carter
- contributor_type: project_member
first_name: Elisabeth
last_name: Sonnleitner
- contributor_type: project_member
first_name: Bor
id: 350F91D2-F248-11E8-B48F-1D18A9856A87
last_name: Kavcic
orcid: 0000-0001-6041-254X
- contributor_type: project_member
first_name: Tiago
last_name: Paixão
- contributor_type: project_manager
first_name: Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
date_created: 2020-12-20T10:00:26Z
date_published: 2020-12-21T00:00:00Z
date_updated: 2024-02-21T12:41:57Z
day: '21'
ddc:
- '570'
department:
- _id: CaGu
doi: 10.15479/AT:ISTA:8951
file:
- access_level: open_access
checksum: f57862aeee1690c7effd2b1117d40ed1
content_type: text/plain
creator: bkavcic
date_created: 2020-12-20T09:52:52Z
date_updated: 2020-12-20T09:52:52Z
file_id: '8952'
file_name: readme.txt
file_size: 523
relation: main_file
success: 1
- access_level: open_access
checksum: f2c6d5232ec6d551b6993991e8689e9f
content_type: application/octet-stream
creator: bkavcic
date_created: 2020-12-20T22:01:44Z
date_updated: 2020-12-20T22:01:44Z
file_id: '8954'
file_name: GRNs Research depository.gb
file_size: 379228
relation: main_file
success: 1
file_date_updated: 2020-12-20T22:01:44Z
has_accepted_license: '1'
keyword:
- Gene regulatory networks
- Gene expression
- Escherichia coli
- Synthetic Biology
month: '12'
oa: 1
oa_version: Published Version
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '9283'
relation: used_in_publication
status: public
status: public
title: Sequences of gene regulatory network permutations for the article "Local genetic
context shapes the function of a gene regulatory network"
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: research_data
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2020'
...
---
_id: '7383'
abstract:
- lang: eng
text: Organisms cope with change by employing transcriptional regulators. However,
when faced with rare environments, the evolution of transcriptional regulators
and their promoters may be too slow. We ask whether the intrinsic instability
of gene duplication and amplification provides a generic alternative to canonical
gene regulation. By real-time monitoring of gene copy number mutations in E. coli,
we show that gene duplications and amplifications enable adaptation to fluctuating
environments by rapidly generating copy number, and hence expression level, polymorphism.
This ‘amplification-mediated gene expression tuning’ occurs on timescales similar
to canonical gene regulation and can deal with rapid environmental changes. Mathematical
modeling shows that amplifications also tune gene expression in stochastic environments
where transcription factor-based schemes are hard to evolve or maintain. The fleeting
nature of gene amplifications gives rise to a generic population-level mechanism
that relies on genetic heterogeneity to rapidly tune expression of any gene, without
leaving any genomic signature.
article_processing_charge: No
author:
- first_name: Rok
full_name: Grah, Rok
id: 483E70DE-F248-11E8-B48F-1D18A9856A87
last_name: Grah
orcid: 0000-0003-2539-3560
citation:
ama: 'Grah R. Matlab scripts for the Paper: Gene Amplification as a Form of Population-Level
Gene Expression regulation. 2020. doi:10.15479/AT:ISTA:7383'
apa: 'Grah, R. (2020). Matlab scripts for the Paper: Gene Amplification as a Form
of Population-Level Gene Expression regulation. Institute of Science and Technology
Austria. https://doi.org/10.15479/AT:ISTA:7383'
chicago: 'Grah, Rok. “Matlab Scripts for the Paper: Gene Amplification as a Form
of Population-Level Gene Expression Regulation.” Institute of Science and Technology
Austria, 2020. https://doi.org/10.15479/AT:ISTA:7383.'
ieee: 'R. Grah, “Matlab scripts for the Paper: Gene Amplification as a Form of Population-Level
Gene Expression regulation.” Institute of Science and Technology Austria, 2020.'
ista: 'Grah R. 2020. Matlab scripts for the Paper: Gene Amplification as a Form
of Population-Level Gene Expression regulation, Institute of Science and Technology
Austria, 10.15479/AT:ISTA:7383.'
mla: 'Grah, Rok. Matlab Scripts for the Paper: Gene Amplification as a Form of
Population-Level Gene Expression Regulation. Institute of Science and Technology
Austria, 2020, doi:10.15479/AT:ISTA:7383.'
short: R. Grah, (2020).
contributor:
- contributor_type: project_leader
first_name: Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
date_created: 2020-01-28T10:41:49Z
date_published: 2020-01-28T00:00:00Z
date_updated: 2024-02-21T12:42:31Z
day: '28'
department:
- _id: CaGu
- _id: GaTk
doi: 10.15479/AT:ISTA:7383
file:
- access_level: open_access
checksum: 9d292cf5207b3829225f44c044cdb3fd
content_type: application/zip
creator: rgrah
date_created: 2020-01-28T10:39:40Z
date_updated: 2020-07-14T12:47:57Z
file_id: '7384'
file_name: Scripts.zip
file_size: 73363365
relation: main_file
- access_level: open_access
checksum: 4076ceab32ef588cc233802bab24c1ab
content_type: text/plain
creator: rgrah
date_created: 2020-01-28T10:39:30Z
date_updated: 2020-07-14T12:47:57Z
file_id: '7385'
file_name: READ_ME_MAIN.txt
file_size: 962
relation: main_file
file_date_updated: 2020-07-14T12:47:57Z
has_accepted_license: '1'
keyword:
- Matlab scripts
- analysis of microfluidics
- mathematical model
month: '01'
oa: 1
oa_version: Published Version
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '7652'
relation: used_in_publication
status: public
status: public
title: 'Matlab scripts for the Paper: Gene Amplification as a Form of Population-Level
Gene Expression regulation'
type: research_data
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2020'
...
---
_id: '7680'
abstract:
- lang: eng
text: "Proteins and their complex dynamic interactions regulate cellular mechanisms
from sensing and transducing extracellular signals, to mediating genetic responses,
and sustaining or changing cell morphology. To manipulate these protein-protein
interactions (PPIs) that govern the behavior and fate of cells, synthetically
constructed, genetically encoded tools provide the means to precisely target proteins
of interest (POIs), and control their subcellular localization and activity in
vitro and in vivo. Ideal synthetic tools react to an orthogonal cue, i.e. a trigger
that does not activate any other endogenous process, thereby allowing manipulation
of the POI alone.\r\nIn optogenetics, naturally occurring photosensory domain
from plants, algae and bacteria are re-purposed and genetically fused to POIs.
Illumination with light of a specific wavelength triggers a conformational change
that can mediate PPIs, such as dimerization or oligomerization. By using light
as a trigger, these tools can be activated with high spatial and temporal precision,
on subcellular and millisecond scales. Chemogenetic tools consist of protein domains
that recognize and bind small molecules. By genetic fusion to POIs, these domains
can mediate PPIs upon addition of their specific ligands, which are often synthetically
designed to provide highly specific interactions and exhibit good bioavailability.\r\nMost
optogenetic tools to mediate PPIs are based on well-studied photoreceptors responding
to red, blue or near-UV light, leaving a striking gap in the green band of the
visible light spectrum. Among both optogenetic and chemogenetic tools, there is
an abundance of methods to induce PPIs, but tools to disrupt them require UV illumination,
rely on covalent linkage and subsequent enzymatic cleavage or initially result
in protein clustering of unknown stoichiometry.\r\nThis work describes how the
recently structurally and photochemically characterized green-light responsive
cobalamin-binding domains (CBDs) from bacterial transcription factors were re-purposed
to function as a green-light responsive optogenetic tool. In contrast to previously
engineered optogenetic tools, CBDs do not induce PPI, but rather confer a PPI
already upon expression, which can be rapidly disrupted by illumination. This
was employed to mimic inhibition of constitutive activity of a growth factor receptor,
and successfully implement for cell signalling in mammalian cells and in vivo
to rescue development in zebrafish. This work further describes the development
and application of a chemically induced de-dimerizer (CDD) based on a recently
identified and structurally described bacterial oxyreductase. CDD forms a dimer
upon expression in absence of its cofactor, the flavin derivative F420. Safety
and of domain expression and ligand exposure are demonstrated in vitro and in
vivo in zebrafish. The system is further applied to inhibit cell signalling output
from a chimeric receptor upon F420 treatment.\r\nCBDs and CDD expand the repertoire
of synthetic tools by providing novel mechanisms of mediating PPIs, and by recognizing
previously not utilized cues. In the future, they can readily be combined with
existing synthetic tools to functionally manipulate PPIs in vitro and in vivo."
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Stephanie
full_name: Kainrath, Stephanie
id: 32CFBA64-F248-11E8-B48F-1D18A9856A87
last_name: Kainrath
citation:
ama: Kainrath S. Synthetic tools for optogenetic and chemogenetic inhibition of
cellular signals. 2020. doi:10.15479/AT:ISTA:7680
apa: Kainrath, S. (2020). Synthetic tools for optogenetic and chemogenetic inhibition
of cellular signals. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:7680
chicago: Kainrath, Stephanie. “Synthetic Tools for Optogenetic and Chemogenetic
Inhibition of Cellular Signals.” Institute of Science and Technology Austria,
2020. https://doi.org/10.15479/AT:ISTA:7680.
ieee: S. Kainrath, “Synthetic tools for optogenetic and chemogenetic inhibition
of cellular signals,” Institute of Science and Technology Austria, 2020.
ista: Kainrath S. 2020. Synthetic tools for optogenetic and chemogenetic inhibition
of cellular signals. Institute of Science and Technology Austria.
mla: Kainrath, Stephanie. Synthetic Tools for Optogenetic and Chemogenetic Inhibition
of Cellular Signals. Institute of Science and Technology Austria, 2020, doi:10.15479/AT:ISTA:7680.
short: S. Kainrath, Synthetic Tools for Optogenetic and Chemogenetic Inhibition
of Cellular Signals, Institute of Science and Technology Austria, 2020.
date_created: 2020-04-24T16:00:51Z
date_published: 2020-04-24T00:00:00Z
date_updated: 2023-09-22T09:20:10Z
day: '24'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: CaGu
doi: 10.15479/AT:ISTA:7680
file:
- access_level: open_access
checksum: fb9a4468eb27be92690728e35c823796
content_type: application/pdf
creator: stgingl
date_created: 2020-04-28T11:19:21Z
date_updated: 2021-10-31T23:30:05Z
embargo: 2021-10-30
file_id: '7692'
file_name: Thesis_without-signatures_PDFA.pdf
file_size: 3268017
relation: main_file
- access_level: closed
checksum: f6c80ca97104a631a328cb79a2c53493
content_type: application/octet-stream
creator: stgingl
date_created: 2020-04-28T11:19:24Z
date_updated: 2021-10-31T23:30:05Z
embargo_to: open_access
file_id: '7693'
file_name: Thesis_without signatures.docx
file_size: 5167703
relation: source_file
file_date_updated: 2021-10-31T23:30:05Z
has_accepted_license: '1'
language:
- iso: eng
month: '04'
oa: 1
oa_version: None
page: '98'
publication_identifier:
eissn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '1028'
relation: dissertation_contains
status: public
status: public
supervisor:
- first_name: Harald L
full_name: Janovjak, Harald L
id: 33BA6C30-F248-11E8-B48F-1D18A9856A87
last_name: Janovjak
orcid: 0000-0002-8023-9315
title: Synthetic tools for optogenetic and chemogenetic inhibition of cellular signals
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2020'
...
---
_id: '7652'
abstract:
- lang: eng
text: Organisms cope with change by taking advantage of transcriptional regulators.
However, when faced with rare environments, the evolution of transcriptional regulators
and their promoters may be too slow. Here, we investigate whether the intrinsic
instability of gene duplication and amplification provides a generic alternative
to canonical gene regulation. Using real-time monitoring of gene-copy-number mutations
in Escherichia coli, we show that gene duplications and amplifications enable
adaptation to fluctuating environments by rapidly generating copy-number and,
therefore, expression-level polymorphisms. This amplification-mediated gene expression
tuning (AMGET) occurs on timescales that are similar to canonical gene regulation
and can respond to rapid environmental changes. Mathematical modelling shows that
amplifications also tune gene expression in stochastic environments in which transcription-factor-based
schemes are hard to evolve or maintain. The fleeting nature of gene amplifications
gives rise to a generic population-level mechanism that relies on genetic heterogeneity
to rapidly tune the expression of any gene, without leaving any genomic signature.
acknowledgement: We thank L. Hurst, N. Barton, M. Pleska, M. Steinrück, B. Kavcic
and A. Staron for input on the manuscript, and To. Bergmiller and R. Chait for help
with microfluidics experiments. I.T. is a recipient the OMV fellowship. R.G. is
a recipient of a DOC (Doctoral Fellowship Programme of the Austrian Academy of Sciences)
Fellowship of the Austrian Academy of Sciences.
article_processing_charge: No
article_type: original
author:
- first_name: Isabella
full_name: Tomanek, Isabella
id: 3981F020-F248-11E8-B48F-1D18A9856A87
last_name: Tomanek
orcid: 0000-0001-6197-363X
- first_name: Rok
full_name: Grah, Rok
id: 483E70DE-F248-11E8-B48F-1D18A9856A87
last_name: Grah
orcid: 0000-0003-2539-3560
- first_name: M.
full_name: Lagator, M.
last_name: Lagator
- first_name: A. M. C.
full_name: Andersson, A. M. C.
last_name: Andersson
- first_name: Jonathan P
full_name: Bollback, Jonathan P
id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
last_name: Bollback
orcid: 0000-0002-4624-4612
- first_name: Gašper
full_name: Tkačik, Gašper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkačik
orcid: 0000-0002-6699-1455
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Tomanek I, Grah R, Lagator M, et al. Gene amplification as a form of population-level
gene expression regulation. Nature Ecology & Evolution. 2020;4(4):612-625.
doi:10.1038/s41559-020-1132-7
apa: Tomanek, I., Grah, R., Lagator, M., Andersson, A. M. C., Bollback, J. P., Tkačik,
G., & Guet, C. C. (2020). Gene amplification as a form of population-level
gene expression regulation. Nature Ecology & Evolution. Springer Nature.
https://doi.org/10.1038/s41559-020-1132-7
chicago: Tomanek, Isabella, Rok Grah, M. Lagator, A. M. C. Andersson, Jonathan P
Bollback, Gašper Tkačik, and Calin C Guet. “Gene Amplification as a Form of Population-Level
Gene Expression Regulation.” Nature Ecology & Evolution. Springer Nature,
2020. https://doi.org/10.1038/s41559-020-1132-7.
ieee: I. Tomanek et al., “Gene amplification as a form of population-level
gene expression regulation,” Nature Ecology & Evolution, vol. 4, no.
4. Springer Nature, pp. 612–625, 2020.
ista: Tomanek I, Grah R, Lagator M, Andersson AMC, Bollback JP, Tkačik G, Guet CC.
2020. Gene amplification as a form of population-level gene expression regulation.
Nature Ecology & Evolution. 4(4), 612–625.
mla: Tomanek, Isabella, et al. “Gene Amplification as a Form of Population-Level
Gene Expression Regulation.” Nature Ecology & Evolution, vol. 4, no.
4, Springer Nature, 2020, pp. 612–25, doi:10.1038/s41559-020-1132-7.
short: I. Tomanek, R. Grah, M. Lagator, A.M.C. Andersson, J.P. Bollback, G. Tkačik,
C.C. Guet, Nature Ecology & Evolution 4 (2020) 612–625.
date_created: 2020-04-08T15:20:53Z
date_published: 2020-04-01T00:00:00Z
date_updated: 2024-03-28T23:30:37Z
day: '01'
ddc:
- '570'
department:
- _id: GaTk
- _id: CaGu
doi: 10.1038/s41559-020-1132-7
external_id:
isi:
- '000519008300005'
file:
- access_level: open_access
checksum: ef3bbf42023e30b2c24a6278025d2040
content_type: application/pdf
creator: dernst
date_created: 2020-10-09T09:56:01Z
date_updated: 2020-10-09T09:56:01Z
file_id: '8640'
file_name: 2020_NatureEcolEvo_Tomanek.pdf
file_size: 745242
relation: main_file
success: 1
file_date_updated: 2020-10-09T09:56:01Z
has_accepted_license: '1'
intvolume: ' 4'
isi: 1
issue: '4'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Submitted Version
page: 612-625
project:
- _id: 267C84F4-B435-11E9-9278-68D0E5697425
name: Biophysically realistic genotype-phenotype maps for regulatory networks
publication: Nature Ecology & Evolution
publication_identifier:
issn:
- 2397-334X
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/how-to-thrive-without-gene-regulation/
record:
- id: '8155'
relation: dissertation_contains
status: public
- id: '7383'
relation: research_data
status: public
- id: '7016'
relation: research_data
status: public
- id: '8653'
relation: used_in_publication
status: public
scopus_import: '1'
status: public
title: Gene amplification as a form of population-level gene expression regulation
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 4
year: '2020'
...