---
_id: '1169'
abstract:
- lang: eng
text: Dispersal is a crucial factor in natural evolution, since it determines the
habitat experienced by any population and defines the spatial scale of interactions
between individuals. There is compelling evidence for systematic differences in
dispersal characteristics within the same population, i.e., genotype-dependent
dispersal. The consequences of genotype-dependent dispersal on other evolutionary
phenomena, however, are poorly understood. In this article we investigate the
effect of genotype-dependent dispersal on spatial gene frequency patterns, using
a generalization of the classical diffusion model of selection and dispersal.
Dispersal is characterized by the variance of dispersal (diffusion coefficient)
and the mean displacement (directional advection term). We demonstrate that genotype-dependent
dispersal may change the qualitative behavior of Fisher waves, which change from
being “pulled” to being “pushed” wave fronts as the discrepancy in dispersal between
genotypes increases. The speed of any wave is partitioned into components due
to selection, genotype-dependent variance of dispersal, and genotype-dependent
mean displacement. We apply our findings to wave fronts maintained by selection
against heterozygotes. Furthermore, we identify a benefit of increased variance
of dispersal, quantify its effect on the speed of the wave, and discuss the implications
for the evolution of dispersal strategies.
article_processing_charge: No
author:
- first_name: Sebastian
full_name: Novak, Sebastian
id: 461468AE-F248-11E8-B48F-1D18A9856A87
last_name: Novak
orcid: 0000-0002-2519-824X
- first_name: Richard
full_name: Kollár, Richard
last_name: Kollár
citation:
ama: Novak S, Kollár R. Spatial gene frequency waves under genotype dependent dispersal.
Genetics. 2017;205(1):367-374. doi:10.1534/genetics.116.193946
apa: Novak, S., & Kollár, R. (2017). Spatial gene frequency waves under genotype
dependent dispersal. Genetics. Genetics Society of America. https://doi.org/10.1534/genetics.116.193946
chicago: Novak, Sebastian, and Richard Kollár. “Spatial Gene Frequency Waves under
Genotype Dependent Dispersal.” Genetics. Genetics Society of America, 2017.
https://doi.org/10.1534/genetics.116.193946.
ieee: S. Novak and R. Kollár, “Spatial gene frequency waves under genotype dependent
dispersal,” Genetics, vol. 205, no. 1. Genetics Society of America, pp.
367–374, 2017.
ista: Novak S, Kollár R. 2017. Spatial gene frequency waves under genotype dependent
dispersal. Genetics. 205(1), 367–374.
mla: Novak, Sebastian, and Richard Kollár. “Spatial Gene Frequency Waves under Genotype
Dependent Dispersal.” Genetics, vol. 205, no. 1, Genetics Society of America,
2017, pp. 367–74, doi:10.1534/genetics.116.193946.
short: S. Novak, R. Kollár, Genetics 205 (2017) 367–374.
date_created: 2018-12-11T11:50:31Z
date_published: 2017-01-01T00:00:00Z
date_updated: 2025-07-10T11:50:13Z
day: '01'
ddc:
- '576'
department:
- _id: NiBa
doi: 10.1534/genetics.116.193946
ec_funded: 1
external_id:
isi:
- '000393677300025'
file:
- access_level: open_access
checksum: 7c8ab79cda1f92760bbbbe0f53175bfc
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:10:43Z
date_updated: 2020-07-14T12:44:37Z
file_id: '4833'
file_name: IST-2016-727-v1+1_SFC_Genetics_final.pdf
file_size: 361500
relation: main_file
file_date_updated: 2020-07-14T12:44:37Z
has_accepted_license: '1'
intvolume: ' 205'
isi: 1
issue: '1'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Submitted Version
page: 367 - 374
project:
- _id: 25B1EC9E-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618091'
name: Speed of Adaptation in Population Genetics and Evolutionary Computation
- _id: 25B07788-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '250152'
name: Limits to selection in biology and in evolutionary computation
publication: Genetics
publication_identifier:
issn:
- 0016-6731
publication_status: published
publisher: Genetics Society of America
publist_id: '6188'
pubrep_id: '727'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Spatial gene frequency waves under genotype dependent dispersal
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 205
year: '2017'
...
---
_id: '1191'
abstract:
- lang: eng
text: Variation in genotypes may be responsible for differences in dispersal rates,
directional biases, and growth rates of individuals. These traits may favor certain
genotypes and enhance their spatiotemporal spreading into areas occupied by the
less advantageous genotypes. We study how these factors influence the speed of
spreading in the case of two competing genotypes under the assumption that spatial
variation of the total population is small compared to the spatial variation of
the frequencies of the genotypes in the population. In that case, the dynamics
of the frequency of one of the genotypes is approximately described by a generalized
Fisher–Kolmogorov–Petrovskii–Piskunov (F–KPP) equation. This generalized F–KPP
equation with (nonlinear) frequency-dependent diffusion and advection terms admits
traveling wave solutions that characterize the invasion of the dominant genotype.
Our existence results generalize the classical theory for traveling waves for
the F–KPP with constant coefficients. Moreover, in the particular case of the
quadratic (monostable) nonlinear growth–decay rate in the generalized F–KPP we
study in detail the influence of the variance in diffusion and mean displacement
rates of the two genotypes on the minimal wave propagation speed.
acknowledgement: "We thank Nick Barton, Katarína Bod’ová, and Sr\r\n-\r\ndan Sarikas
for constructive feed-\r\nback and support. Furthermore, we would like to express
our deep gratitude to the anonymous referees (one\r\nof whom, Jimmy Garnier, agreed
to reveal his identity) and the editor Max Souza, for very helpful and\r\ndetailed
comments and suggestions that significantly helped us to improve the manuscript.
This project has\r\nreceived funding from the European Union’s Seventh Framework
Programme for research, technological\r\ndevelopment and demonstration under Grant
Agreement 618091 Speed of Adaptation in Population Genet-\r\nics and Evolutionary
Computation (SAGE) and the European Research Council (ERC) Grant No. 250152\r\n(SN),
from the Scientific Grant Agency of the Slovak Republic under the Grant 1/0459/13
and by the Slovak\r\nResearch and Development Agency under the Contract No. APVV-14-0378
(RK). RK would also like to\r\nthank IST Austria for its hospitality during the
work on this project."
article_processing_charge: No
arxiv: 1
author:
- first_name: Richard
full_name: Kollár, Richard
last_name: Kollár
- first_name: Sebastian
full_name: Novak, Sebastian
id: 461468AE-F248-11E8-B48F-1D18A9856A87
last_name: Novak
orcid: 0000-0002-2519-824X
citation:
ama: Kollár R, Novak S. Existence of traveling waves for the generalized F–KPP equation.
Bulletin of Mathematical Biology. 2017;79(3):525-559. doi:10.1007/s11538-016-0244-3
apa: Kollár, R., & Novak, S. (2017). Existence of traveling waves for the generalized
F–KPP equation. Bulletin of Mathematical Biology. Springer. https://doi.org/10.1007/s11538-016-0244-3
chicago: Kollár, Richard, and Sebastian Novak. “Existence of Traveling Waves for
the Generalized F–KPP Equation.” Bulletin of Mathematical Biology. Springer,
2017. https://doi.org/10.1007/s11538-016-0244-3.
ieee: R. Kollár and S. Novak, “Existence of traveling waves for the generalized
F–KPP equation,” Bulletin of Mathematical Biology, vol. 79, no. 3. Springer,
pp. 525–559, 2017.
ista: Kollár R, Novak S. 2017. Existence of traveling waves for the generalized
F–KPP equation. Bulletin of Mathematical Biology. 79(3), 525–559.
mla: Kollár, Richard, and Sebastian Novak. “Existence of Traveling Waves for the
Generalized F–KPP Equation.” Bulletin of Mathematical Biology, vol. 79,
no. 3, Springer, 2017, pp. 525–59, doi:10.1007/s11538-016-0244-3.
short: R. Kollár, S. Novak, Bulletin of Mathematical Biology 79 (2017) 525–559.
date_created: 2018-12-11T11:50:38Z
date_published: 2017-03-01T00:00:00Z
date_updated: 2025-09-22T09:44:54Z
day: '01'
department:
- _id: NiBa
doi: 10.1007/s11538-016-0244-3
ec_funded: 1
external_id:
arxiv:
- '1607.00944'
isi:
- '000395156200005'
intvolume: ' 79'
isi: 1
issue: '3'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://arxiv.org/abs/1607.00944
month: '03'
oa: 1
oa_version: Preprint
page: 525-559
project:
- _id: 25B1EC9E-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618091'
name: Speed of Adaptation in Population Genetics and Evolutionary Computation
- _id: 25B07788-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '250152'
name: Limits to selection in biology and in evolutionary computation
publication: Bulletin of Mathematical Biology
publication_status: published
publisher: Springer
publist_id: '6160'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Existence of traveling waves for the generalized F–KPP equation
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 79
year: '2017'
...
---
_id: '1199'
abstract:
- lang: eng
text: Much of quantitative genetics is based on the ‘infinitesimal model’, under
which selection has a negligible effect on the genetic variance. This is typically
justified by assuming a very large number of loci with additive effects. However,
it applies even when genes interact, provided that the number of loci is large
enough that selection on each of them is weak relative to random drift. In the
long term, directional selection will change allele frequencies, but even then,
the effects of epistasis on the ultimate change in trait mean due to selection
may be modest. Stabilising selection can maintain many traits close to their optima,
even when the underlying alleles are weakly selected. However, the number of traits
that can be optimised is apparently limited to ~4Ne by the ‘drift load’, and this
is hard to reconcile with the apparent complexity of many organisms. Just as for
the mutation load, this limit can be evaded by a particular form of negative epistasis.
A more robust limit is set by the variance in reproductive success. This suggests
that selection accumulates information most efficiently in the infinitesimal regime,
when selection on individual alleles is weak, and comparable with random drift.
A review of evidence on selection strength suggests that although most variance
in fitness may be because of alleles with large Nes, substantial amounts of adaptation
may be because of alleles in the infinitesimal regime, in which epistasis has
modest effects.
article_processing_charge: No
author:
- first_name: Nicholas H
full_name: Barton, Nicholas H
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
orcid: 0000-0002-8548-5240
citation:
ama: Barton NH. How does epistasis influence the response to selection? Heredity.
2017;118:96-109. doi:10.1038/hdy.2016.109
apa: Barton, N. H. (2017). How does epistasis influence the response to selection?
Heredity. Nature Publishing Group. https://doi.org/10.1038/hdy.2016.109
chicago: Barton, Nicholas H. “How Does Epistasis Influence the Response to Selection?”
Heredity. Nature Publishing Group, 2017. https://doi.org/10.1038/hdy.2016.109.
ieee: N. H. Barton, “How does epistasis influence the response to selection?,” Heredity,
vol. 118. Nature Publishing Group, pp. 96–109, 2017.
ista: Barton NH. 2017. How does epistasis influence the response to selection? Heredity.
118, 96–109.
mla: Barton, Nicholas H. “How Does Epistasis Influence the Response to Selection?”
Heredity, vol. 118, Nature Publishing Group, 2017, pp. 96–109, doi:10.1038/hdy.2016.109.
short: N.H. Barton, Heredity 118 (2017) 96–109.
date_created: 2018-12-11T11:50:40Z
date_published: 2017-01-01T00:00:00Z
date_updated: 2025-04-15T07:11:02Z
day: '01'
department:
- _id: NiBa
doi: 10.1038/hdy.2016.109
ec_funded: 1
external_id:
isi:
- '000392229100011'
intvolume: ' 118'
isi: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5176114/
month: '01'
oa: 1
oa_version: Submitted Version
page: 96 - 109
project:
- _id: 25B07788-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '250152'
name: Limits to selection in biology and in evolutionary computation
publication: Heredity
publication_status: published
publisher: Nature Publishing Group
publist_id: '6151'
quality_controlled: '1'
related_material:
record:
- id: '9710'
relation: research_data
status: public
scopus_import: '1'
status: public
title: How does epistasis influence the response to selection?
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 118
year: '2017'
...
---
_id: '1336'
abstract:
- lang: eng
text: Evolutionary algorithms (EAs) form a popular optimisation paradigm inspired
by natural evolution. In recent years the field of evolutionary computation has
developed a rigorous analytical theory to analyse the runtimes of EAs on many
illustrative problems. Here we apply this theory to a simple model of natural
evolution. In the Strong Selection Weak Mutation (SSWM) evolutionary regime the
time between occurrences of new mutations is much longer than the time it takes
for a mutated genotype to take over the population. In this situation, the population
only contains copies of one genotype and evolution can be modelled as a stochastic
process evolving one genotype by means of mutation and selection between the resident
and the mutated genotype. The probability of accepting the mutated genotype then
depends on the change in fitness. We study this process, SSWM, from an algorithmic
perspective, quantifying its expected optimisation time for various parameters
and investigating differences to a similar evolutionary algorithm, the well-known
(1+1) EA. We show that SSWM can have a moderate advantage over the (1+1) EA at
crossing fitness valleys and study an example where SSWM outperforms the (1+1)
EA by taking advantage of information on the fitness gradient.
article_processing_charge: No
author:
- first_name: Tiago
full_name: Paixao, Tiago
id: 2C5658E6-F248-11E8-B48F-1D18A9856A87
last_name: Paixao
orcid: 0000-0003-2361-3953
- first_name: Jorge
full_name: Pérez Heredia, Jorge
last_name: Pérez Heredia
- first_name: Dirk
full_name: Sudholt, Dirk
last_name: Sudholt
- first_name: Barbora
full_name: Trubenova, Barbora
id: 42302D54-F248-11E8-B48F-1D18A9856A87
last_name: Trubenova
orcid: 0000-0002-6873-2967
citation:
ama: Paixao T, Pérez Heredia J, Sudholt D, Trubenova B. Towards a runtime comparison
of natural and artificial evolution. Algorithmica. 2017;78(2):681-713.
doi:10.1007/s00453-016-0212-1
apa: Paixao, T., Pérez Heredia, J., Sudholt, D., & Trubenova, B. (2017). Towards
a runtime comparison of natural and artificial evolution. Algorithmica.
Springer. https://doi.org/10.1007/s00453-016-0212-1
chicago: Paixao, Tiago, Jorge Pérez Heredia, Dirk Sudholt, and Barbora Trubenova.
“Towards a Runtime Comparison of Natural and Artificial Evolution.” Algorithmica.
Springer, 2017. https://doi.org/10.1007/s00453-016-0212-1.
ieee: T. Paixao, J. Pérez Heredia, D. Sudholt, and B. Trubenova, “Towards a runtime
comparison of natural and artificial evolution,” Algorithmica, vol. 78,
no. 2. Springer, pp. 681–713, 2017.
ista: Paixao T, Pérez Heredia J, Sudholt D, Trubenova B. 2017. Towards a runtime
comparison of natural and artificial evolution. Algorithmica. 78(2), 681–713.
mla: Paixao, Tiago, et al. “Towards a Runtime Comparison of Natural and Artificial
Evolution.” Algorithmica, vol. 78, no. 2, Springer, 2017, pp. 681–713,
doi:10.1007/s00453-016-0212-1.
short: T. Paixao, J. Pérez Heredia, D. Sudholt, B. Trubenova, Algorithmica 78 (2017)
681–713.
date_created: 2018-12-11T11:51:27Z
date_published: 2017-06-01T00:00:00Z
date_updated: 2026-04-16T09:55:33Z
day: '01'
ddc:
- '576'
department:
- _id: NiBa
- _id: CaGu
doi: 10.1007/s00453-016-0212-1
ec_funded: 1
external_id:
isi:
- '000400379500013'
file:
- access_level: open_access
checksum: 7873f665a0c598ac747c908f34cb14b9
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:10:19Z
date_updated: 2020-07-14T12:44:44Z
file_id: '4805'
file_name: IST-2016-658-v1+1_s00453-016-0212-1.pdf
file_size: 710206
relation: main_file
file_date_updated: 2020-07-14T12:44:44Z
has_accepted_license: '1'
intvolume: ' 78'
isi: 1
issue: '2'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: 681 - 713
project:
- _id: 25B1EC9E-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618091'
name: Speed of Adaptation in Population Genetics and Evolutionary Computation
publication: Algorithmica
publication_identifier:
issn:
- 0178-4617
publication_status: published
publisher: Springer
publist_id: '5931'
pubrep_id: '658'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Towards a runtime comparison of natural and artificial 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: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 78
year: '2017'
...
---
_id: '1351'
abstract:
- lang: eng
text: The behaviour of gene regulatory networks (GRNs) is typically analysed using
simulation-based statistical testing-like methods. In this paper, we demonstrate
that we can replace this approach by a formal verification-like method that gives
higher assurance and scalability. We focus on Wagner’s weighted GRN model with
varying weights, which is used in evolutionary biology. In the model, weight parameters
represent the gene interaction strength that may change due to genetic mutations.
For a property of interest, we synthesise the constraints over the parameter space
that represent the set of GRNs satisfying the property. We experimentally show
that our parameter synthesis procedure computes the mutational robustness of GRNs—an
important problem of interest in evolutionary biology—more efficiently than the
classical simulation method. We specify the property in linear temporal logic.
We employ symbolic bounded model checking and SMT solving to compute the space
of GRNs that satisfy the property, which amounts to synthesizing a set of linear
constraints on the weights.
article_processing_charge: No
author:
- first_name: Mirco
full_name: Giacobbe, Mirco
id: 3444EA5E-F248-11E8-B48F-1D18A9856A87
last_name: Giacobbe
orcid: 0000-0001-8180-0904
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
- first_name: Ashutosh
full_name: Gupta, Ashutosh
id: 335E5684-F248-11E8-B48F-1D18A9856A87
last_name: Gupta
- first_name: Thomas A
full_name: Henzinger, Thomas A
id: 40876CD8-F248-11E8-B48F-1D18A9856A87
last_name: Henzinger
orcid: 0000−0002−2985−7724
- first_name: Tiago
full_name: Paixao, Tiago
id: 2C5658E6-F248-11E8-B48F-1D18A9856A87
last_name: Paixao
orcid: 0000-0003-2361-3953
- first_name: Tatjana
full_name: Petrov, Tatjana
id: 3D5811FC-F248-11E8-B48F-1D18A9856A87
last_name: Petrov
orcid: 0000-0002-9041-0905
citation:
ama: Giacobbe M, Guet CC, Gupta A, Henzinger TA, Paixao T, Petrov T. Model checking
the evolution of gene regulatory networks. Acta Informatica. 2017;54(8):765-787.
doi:10.1007/s00236-016-0278-x
apa: Giacobbe, M., Guet, C. C., Gupta, A., Henzinger, T. A., Paixao, T., & Petrov,
T. (2017). Model checking the evolution of gene regulatory networks. Acta Informatica.
Springer. https://doi.org/10.1007/s00236-016-0278-x
chicago: Giacobbe, Mirco, Calin C Guet, Ashutosh Gupta, Thomas A Henzinger, Tiago
Paixao, and Tatjana Petrov. “Model Checking the Evolution of Gene Regulatory Networks.”
Acta Informatica. Springer, 2017. https://doi.org/10.1007/s00236-016-0278-x.
ieee: M. Giacobbe, C. C. Guet, A. Gupta, T. A. Henzinger, T. Paixao, and T. Petrov,
“Model checking the evolution of gene regulatory networks,” Acta Informatica,
vol. 54, no. 8. Springer, pp. 765–787, 2017.
ista: Giacobbe M, Guet CC, Gupta A, Henzinger TA, Paixao T, Petrov T. 2017. Model
checking the evolution of gene regulatory networks. Acta Informatica. 54(8), 765–787.
mla: Giacobbe, Mirco, et al. “Model Checking the Evolution of Gene Regulatory Networks.”
Acta Informatica, vol. 54, no. 8, Springer, 2017, pp. 765–87, doi:10.1007/s00236-016-0278-x.
short: M. Giacobbe, C.C. Guet, A. Gupta, T.A. Henzinger, T. Paixao, T. Petrov, Acta
Informatica 54 (2017) 765–787.
corr_author: '1'
date_created: 2018-12-11T11:51:32Z
date_published: 2017-12-01T00:00:00Z
date_updated: 2025-07-10T11:50:42Z
day: '01'
ddc:
- '006'
- '576'
department:
- _id: ToHe
- _id: CaGu
- _id: NiBa
doi: 10.1007/s00236-016-0278-x
ec_funded: 1
external_id:
isi:
- '000414343200003'
file:
- access_level: open_access
checksum: 4e661d9135d7f8c342e8e258dee76f3e
content_type: application/pdf
creator: dernst
date_created: 2019-01-17T15:57:29Z
date_updated: 2020-07-14T12:44:46Z
file_id: '5841'
file_name: 2017_ActaInformatica_Giacobbe.pdf
file_size: 755241
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file_date_updated: 2020-07-14T12:44:46Z
has_accepted_license: '1'
intvolume: ' 54'
isi: 1
issue: '8'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
page: 765 - 787
project:
- _id: 25EE3708-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '267989'
name: Quantitative Reactive Modeling
- _id: 25832EC2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: S 11407_N23
name: Rigorous Systems Engineering
- _id: 25F42A32-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Z211
name: Formal methods for the design and analysis of complex systems
- _id: 25B1EC9E-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618091'
name: Speed of Adaptation in Population Genetics and Evolutionary Computation
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 25B07788-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '250152'
name: Limits to selection in biology and in evolutionary computation
publication: Acta Informatica
publication_identifier:
issn:
- 0001-5903
publication_status: published
publisher: Springer
publist_id: '5898'
pubrep_id: '649'
quality_controlled: '1'
related_material:
record:
- id: '1835'
relation: earlier_version
status: public
scopus_import: '1'
status: public
title: Model checking the evolution of gene regulatory networks
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: 54
year: '2017'
...
---
_id: '570'
abstract:
- lang: eng
text: 'Most phenotypes are determined by molecular systems composed of specifically
interacting molecules. However, unlike for individual components, little is known
about the distributions of mutational effects of molecular systems as a whole.
We ask how the distribution of mutational effects of a transcriptional regulatory
system differs from the distributions of its components, by first independently,
and then simultaneously, mutating a transcription factor and the associated promoter
it represses. We find that the system distribution exhibits increased phenotypic
variation compared to individual component distributions - an effect arising from
intermolecular epistasis between the transcription factor and its DNA-binding
site. In large part, this epistasis can be qualitatively attributed to the structure
of the transcriptional regulatory system and could therefore be a common feature
in prokaryotes. Counter-intuitively, intermolecular epistasis can alleviate the
constraints of individual components, thereby increasing phenotypic variation
that selection could act on and facilitating adaptive evolution. '
article_number: e28921
article_processing_charge: No
author:
- first_name: Mato
full_name: Lagator, Mato
id: 345D25EC-F248-11E8-B48F-1D18A9856A87
last_name: Lagator
- first_name: Srdjan
full_name: Sarikas, Srdjan
id: 35F0286E-F248-11E8-B48F-1D18A9856A87
last_name: Sarikas
- first_name: Hande
full_name: Acar, Hande
id: 2DDF136A-F248-11E8-B48F-1D18A9856A87
last_name: Acar
orcid: 0000-0003-1986-9753
- first_name: Jonathan P
full_name: Bollback, Jonathan P
id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
last_name: Bollback
orcid: 0000-0002-4624-4612
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Lagator M, Sarikas S, Acar H, Bollback JP, Guet CC. Regulatory network structure
determines patterns of intermolecular epistasis. eLife. 2017;6. doi:10.7554/eLife.28921
apa: Lagator, M., Sarikas, S., Acar, H., Bollback, J. P., & Guet, C. C. (2017).
Regulatory network structure determines patterns of intermolecular epistasis.
ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.28921
chicago: Lagator, Mato, Srdjan Sarikas, Hande Acar, Jonathan P Bollback, and Calin
C Guet. “Regulatory Network Structure Determines Patterns of Intermolecular Epistasis.”
ELife. eLife Sciences Publications, 2017. https://doi.org/10.7554/eLife.28921.
ieee: M. Lagator, S. Sarikas, H. Acar, J. P. Bollback, and C. C. Guet, “Regulatory
network structure determines patterns of intermolecular epistasis,” eLife,
vol. 6. eLife Sciences Publications, 2017.
ista: Lagator M, Sarikas S, Acar H, Bollback JP, Guet CC. 2017. Regulatory network
structure determines patterns of intermolecular epistasis. eLife. 6, e28921.
mla: Lagator, Mato, et al. “Regulatory Network Structure Determines Patterns of
Intermolecular Epistasis.” ELife, vol. 6, e28921, eLife Sciences Publications,
2017, doi:10.7554/eLife.28921.
short: M. Lagator, S. Sarikas, H. Acar, J.P. Bollback, C.C. Guet, ELife 6 (2017).
corr_author: '1'
date_created: 2018-12-11T11:47:14Z
date_published: 2017-11-13T00:00:00Z
date_updated: 2025-09-11T07:40:30Z
day: '13'
ddc:
- '576'
department:
- _id: CaGu
- _id: JoBo
- _id: NiBa
doi: 10.7554/eLife.28921
ec_funded: 1
external_id:
isi:
- '000425868200001'
file:
- access_level: open_access
checksum: 273ab17f33305e4eaafd911ff88e7c5b
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:42Z
date_updated: 2020-07-14T12:47:10Z
file_id: '5096'
file_name: IST-2017-918-v1+1_elife-28921-figures-v3.pdf
file_size: 8453470
relation: main_file
- access_level: open_access
checksum: b433f90576c7be597cd43367946f8e7f
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:43Z
date_updated: 2020-07-14T12:47:10Z
file_id: '5097'
file_name: IST-2017-918-v1+2_elife-28921-v3.pdf
file_size: 1953221
relation: main_file
file_date_updated: 2020-07-14T12:47:10Z
has_accepted_license: '1'
intvolume: ' 6'
isi: 1
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 2578D616-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '648440'
name: Selective Barriers to Horizontal Gene Transfer
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
publist_id: '7244'
pubrep_id: '918'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Regulatory network structure determines patterns of intermolecular epistasis
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 6
year: '2017'
...
---
_id: '611'
abstract:
- lang: eng
text: Small RNAs (sRNAs) regulate genes in plants and animals. Here, we show that
population-wide differences in color patterns in snapdragon flowers are caused
by an inverted duplication that generates sRNAs. The complexity and size of the
transcripts indicate that the duplication represents an intermediate on the pathway
to microRNA evolution. The sRNAs repress a pigment biosynthesis gene, creating
a yellow highlight at the site of pollinator entry. The inverted duplication exhibits
steep clines in allele frequency in a natural hybrid zone, showing that the allele
is under selection. Thus, regulatory interactions of evolutionarily recent sRNAs
can be acted upon by selection and contribute to the evolution of phenotypic diversity.
article_processing_charge: No
author:
- first_name: Desmond
full_name: Bradley, Desmond
last_name: Bradley
- first_name: Ping
full_name: Xu, Ping
last_name: Xu
- first_name: Irina
full_name: Mohorianu, Irina
last_name: Mohorianu
- first_name: Annabel
full_name: Whibley, Annabel
last_name: Whibley
- first_name: David
full_name: Field, David
id: 419049E2-F248-11E8-B48F-1D18A9856A87
last_name: Field
orcid: 0000-0002-4014-8478
- first_name: Hugo
full_name: Tavares, Hugo
last_name: Tavares
- first_name: Matthew
full_name: Couchman, Matthew
last_name: Couchman
- first_name: Lucy
full_name: Copsey, Lucy
last_name: Copsey
- first_name: Rosemary
full_name: Carpenter, Rosemary
last_name: Carpenter
- first_name: Miaomiao
full_name: Li, Miaomiao
last_name: Li
- first_name: Qun
full_name: Li, Qun
last_name: Li
- first_name: Yongbiao
full_name: Xue, Yongbiao
last_name: Xue
- first_name: Tamas
full_name: Dalmay, Tamas
last_name: Dalmay
- first_name: Enrico
full_name: Coen, Enrico
last_name: Coen
citation:
ama: Bradley D, Xu P, Mohorianu I, et al. Evolution of flower color pattern through
selection on regulatory small RNAs. Science. 2017;358(6365):925-928. doi:10.1126/science.aao3526
apa: Bradley, D., Xu, P., Mohorianu, I., Whibley, A., Field, D., Tavares, H., …
Coen, E. (2017). Evolution of flower color pattern through selection on regulatory
small RNAs. Science. American Association for the Advancement of Science.
https://doi.org/10.1126/science.aao3526
chicago: Bradley, Desmond, Ping Xu, Irina Mohorianu, Annabel Whibley, David Field,
Hugo Tavares, Matthew Couchman, et al. “Evolution of Flower Color Pattern through
Selection on Regulatory Small RNAs.” Science. American Association for
the Advancement of Science, 2017. https://doi.org/10.1126/science.aao3526.
ieee: D. Bradley et al., “Evolution of flower color pattern through selection
on regulatory small RNAs,” Science, vol. 358, no. 6365. American Association
for the Advancement of Science, pp. 925–928, 2017.
ista: Bradley D, Xu P, Mohorianu I, Whibley A, Field D, Tavares H, Couchman M, Copsey
L, Carpenter R, Li M, Li Q, Xue Y, Dalmay T, Coen E. 2017. Evolution of flower
color pattern through selection on regulatory small RNAs. Science. 358(6365),
925–928.
mla: Bradley, Desmond, et al. “Evolution of Flower Color Pattern through Selection
on Regulatory Small RNAs.” Science, vol. 358, no. 6365, American Association
for the Advancement of Science, 2017, pp. 925–28, doi:10.1126/science.aao3526.
short: D. Bradley, P. Xu, I. Mohorianu, A. Whibley, D. Field, H. Tavares, M. Couchman,
L. Copsey, R. Carpenter, M. Li, Q. Li, Y. Xue, T. Dalmay, E. Coen, Science 358
(2017) 925–928.
date_created: 2018-12-11T11:47:29Z
date_published: 2017-11-17T00:00:00Z
date_updated: 2025-09-11T07:34:49Z
day: '17'
department:
- _id: NiBa
doi: 10.1126/science.aao3526
external_id:
isi:
- '000415293000047'
intvolume: ' 358'
isi: 1
issue: '6365'
language:
- iso: eng
month: '11'
oa_version: None
page: 925 - 928
publication: Science
publication_identifier:
issn:
- 0036-8075
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '7193'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Evolution of flower color pattern through selection on regulatory small RNAs
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 358
year: '2017'
...
---
_id: '614'
abstract:
- lang: eng
text: 'Moths and butterflies (Lepidoptera) usually have a pair of differentiated
WZ sex chromosomes. However, in most lineages outside of the division Ditrysia,
as well as in the sister order Trichoptera, females lack a W chromosome. The W
is therefore thought to have been acquired secondarily. Here we compare the genomes
of three Lepidoptera species (one Dytrisia and two non-Dytrisia) to test three
models accounting for the origin of the W: (1) a Z-autosome fusion; (2) a sex
chromosome turnover; and (3) a non-canonical mechanism (e.g., through the recruitment
of a B chromosome). We show that the gene content of the Z is highly conserved
across Lepidoptera (rejecting a sex chromosome turnover) and that very few genes
moved onto the Z in the common ancestor of the Ditrysia (arguing against a Z-autosome
fusion). Our comparative genomics analysis therefore supports the secondary acquisition
of the Lepidoptera W by a non-canonical mechanism, and it confirms the extreme
stability of well-differentiated sex chromosomes.'
article_number: '1486'
article_processing_charge: No
article_type: original
author:
- first_name: Christelle
full_name: Fraisse, Christelle
id: 32DF5794-F248-11E8-B48F-1D18A9856A87
last_name: Fraisse
orcid: 0000-0001-8441-5075
- first_name: Marion A
full_name: Picard, Marion A
id: 2C921A7A-F248-11E8-B48F-1D18A9856A87
last_name: Picard
orcid: 0000-0002-8101-2518
- first_name: Beatriz
full_name: Vicoso, Beatriz
id: 49E1C5C6-F248-11E8-B48F-1D18A9856A87
last_name: Vicoso
orcid: 0000-0002-4579-8306
citation:
ama: Fraisse C, Picard MAL, Vicoso B. The deep conservation of the Lepidoptera Z
chromosome suggests a non canonical origin of the W. Nature Communications.
2017;8(1). doi:10.1038/s41467-017-01663-5
apa: Fraisse, C., Picard, M. A. L., & Vicoso, B. (2017). The deep conservation
of the Lepidoptera Z chromosome suggests a non canonical origin of the W. Nature
Communications. Nature Publishing Group. https://doi.org/10.1038/s41467-017-01663-5
chicago: Fraisse, Christelle, Marion A L Picard, and Beatriz Vicoso. “The Deep Conservation
of the Lepidoptera Z Chromosome Suggests a Non Canonical Origin of the W.” Nature
Communications. Nature Publishing Group, 2017. https://doi.org/10.1038/s41467-017-01663-5.
ieee: C. Fraisse, M. A. L. Picard, and B. Vicoso, “The deep conservation of the
Lepidoptera Z chromosome suggests a non canonical origin of the W,” Nature
Communications, vol. 8, no. 1. Nature Publishing Group, 2017.
ista: Fraisse C, Picard MAL, Vicoso B. 2017. The deep conservation of the Lepidoptera
Z chromosome suggests a non canonical origin of the W. Nature Communications.
8(1), 1486.
mla: Fraisse, Christelle, et al. “The Deep Conservation of the Lepidoptera Z Chromosome
Suggests a Non Canonical Origin of the W.” Nature Communications, vol.
8, no. 1, 1486, Nature Publishing Group, 2017, doi:10.1038/s41467-017-01663-5.
short: C. Fraisse, M.A.L. Picard, B. Vicoso, Nature Communications 8 (2017).
corr_author: '1'
date_created: 2018-12-11T11:47:30Z
date_published: 2017-12-01T00:00:00Z
date_updated: 2025-09-11T07:33:34Z
day: '01'
ddc:
- '570'
- '576'
department:
- _id: BeVi
- _id: NiBa
doi: 10.1038/s41467-017-01663-5
external_id:
isi:
- '000415124000013'
pmid:
- '29133797'
file:
- access_level: open_access
checksum: 4da2651303c8afc2f7fc419be42a2433
content_type: application/pdf
creator: dernst
date_created: 2020-03-03T15:55:50Z
date_updated: 2020-07-14T12:47:20Z
file_id: '7562'
file_name: 2017_NatureComm_Fraisse.pdf
file_size: 1201520
relation: main_file
file_date_updated: 2020-07-14T12:47:20Z
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
issue: '1'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 250ED89C-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P28842-B22
name: Sex chromosome evolution under male- and female- heterogamety
publication: Nature Communications
publication_identifier:
issn:
- 2041-1723
publication_status: published
publisher: Nature Publishing Group
publist_id: '7190'
pubrep_id: '910'
quality_controlled: '1'
related_material:
record:
- id: '7163'
relation: popular_science
status: public
scopus_import: '1'
status: public
title: The deep conservation of the Lepidoptera Z chromosome suggests a non canonical
origin of the W
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 8
year: '2017'
...
---
_id: '626'
abstract:
- lang: eng
text: 'Our focus here is on the infinitesimal model. In this model, one or several
quantitative traits are described as the sum of a genetic and a non-genetic component,
the first being distributed within families as a normal random variable centred
at the average of the parental genetic components, and with a variance independent
of the parental traits. Thus, the variance that segregates within families is
not perturbed by selection, and can be predicted from the variance components.
This does not necessarily imply that the trait distribution across the whole population
should be Gaussian, and indeed selection or population structure may have a substantial
effect on the overall trait distribution. One of our main aims is to identify
some general conditions on the allelic effects for the infinitesimal model to
be accurate. We first review the long history of the infinitesimal model in quantitative
genetics. Then we formulate the model at the phenotypic level in terms of individual
trait values and relationships between individuals, but including different evolutionary
processes: genetic drift, recombination, selection, mutation, population structure,
…. We give a range of examples of its application to evolutionary questions related
to stabilising selection, assortative mating, effective population size and response
to selection, habitat preference and speciation. We provide a mathematical justification
of the model as the limit as the number M of underlying loci tends to infinity
of a model with Mendelian inheritance, mutation and environmental noise, when
the genetic component of the trait is purely additive. We also show how the model
generalises to include epistatic effects. We prove in particular that, within
each family, the genetic components of the individual trait values in the current
generation are indeed normally distributed with a variance independent of ancestral
traits, up to an error of order 1∕M. Simulations suggest that in some cases the
convergence may be as fast as 1∕M.'
article_processing_charge: No
author:
- first_name: Nicholas H
full_name: Barton, Nicholas H
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
orcid: 0000-0002-8548-5240
- first_name: Alison
full_name: Etheridge, Alison
last_name: Etheridge
- first_name: Amandine
full_name: Véber, Amandine
last_name: Véber
citation:
ama: 'Barton NH, Etheridge A, Véber A. The infinitesimal model: Definition derivation
and implications. Theoretical Population Biology. 2017;118:50-73. doi:10.1016/j.tpb.2017.06.001'
apa: 'Barton, N. H., Etheridge, A., & Véber, A. (2017). The infinitesimal model:
Definition derivation and implications. Theoretical Population Biology.
Academic Press. https://doi.org/10.1016/j.tpb.2017.06.001'
chicago: 'Barton, Nicholas H, Alison Etheridge, and Amandine Véber. “The Infinitesimal
Model: Definition Derivation and Implications.” Theoretical Population Biology.
Academic Press, 2017. https://doi.org/10.1016/j.tpb.2017.06.001.'
ieee: 'N. H. Barton, A. Etheridge, and A. Véber, “The infinitesimal model: Definition
derivation and implications,” Theoretical Population Biology, vol. 118.
Academic Press, pp. 50–73, 2017.'
ista: 'Barton NH, Etheridge A, Véber A. 2017. The infinitesimal model: Definition
derivation and implications. Theoretical Population Biology. 118, 50–73.'
mla: 'Barton, Nicholas H., et al. “The Infinitesimal Model: Definition Derivation
and Implications.” Theoretical Population Biology, vol. 118, Academic Press,
2017, pp. 50–73, doi:10.1016/j.tpb.2017.06.001.'
short: N.H. Barton, A. Etheridge, A. Véber, Theoretical Population Biology 118 (2017)
50–73.
corr_author: '1'
date_created: 2018-12-11T11:47:34Z
date_published: 2017-12-01T00:00:00Z
date_updated: 2025-09-11T07:29:31Z
day: '01'
ddc:
- '576'
department:
- _id: NiBa
doi: 10.1016/j.tpb.2017.06.001
ec_funded: 1
external_id:
isi:
- '000417668700005'
file:
- access_level: open_access
checksum: 7dd02bfcfe8f244f4a6c19091aedf2c8
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:12:45Z
date_updated: 2020-07-14T12:47:25Z
file_id: '4964'
file_name: IST-2017-908-v1+1_1-s2.0-S0040580917300886-main_1_.pdf
file_size: 1133924
relation: main_file
file_date_updated: 2020-07-14T12:47:25Z
has_accepted_license: '1'
intvolume: ' 118'
isi: 1
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
page: 50 - 73
project:
- _id: 25B07788-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '250152'
name: Limits to selection in biology and in evolutionary computation
publication: Theoretical Population Biology
publication_identifier:
issn:
- 0040-5809
publication_status: published
publisher: Academic Press
publist_id: '7169'
pubrep_id: '908'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'The infinitesimal model: Definition derivation and implications'
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 118
year: '2017'
...
---
OA_place: publisher
_id: '6291'
abstract:
- lang: eng
text: Bacteria and their pathogens – phages – are the most abundant living entities
on Earth. Throughout their coevolution, bacteria have evolved multiple immune
systems to overcome the ubiquitous threat from the phages. Although the molecu-
lar details of these immune systems’ functions are relatively well understood,
their epidemiological consequences for the phage-bacterial communities have been
largely neglected. In this thesis we employed both experimental and theoretical
methods to explore whether herd and social immunity may arise in bacterial popu-
lations. Using our experimental system consisting of Escherichia coli strains
with a CRISPR based immunity to the T7 phage we show that herd immunity arises
in phage-bacterial communities and that it is accentuated when the populations
are spatially structured. By fitting a mathematical model, we inferred expressions
for the herd immunity threshold and the velocity of spread of a phage epidemic
in partially resistant bacterial populations, which both depend on the bacterial
growth rate, phage burst size and phage latent period. We also investigated the
poten- tial for social immunity in Streptococcus thermophilus and its phage 2972
using a bioinformatic analysis of potentially coding short open reading frames
with a signalling signature, encoded within the CRISPR associated genes. Subsequently,
we tested one identified potentially signalling peptide and found that its addition
to a phage-challenged culture increases probability of survival of bacteria two
fold, although the results were only marginally significant. Together, these results
demonstrate that the ubiquitous arms races between bacteria and phages have further
consequences at the level of the population.
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Pavel
full_name: Payne, Pavel
id: 35F78294-F248-11E8-B48F-1D18A9856A87
last_name: Payne
orcid: 0000-0002-2711-9453
citation:
ama: Payne P. Bacterial herd and social immunity to phages. 2017.
apa: Payne, P. (2017). Bacterial herd and social immunity to phages. Institute
of Science and Technology Austria.
chicago: Payne, Pavel. “Bacterial Herd and Social Immunity to Phages.” Institute
of Science and Technology Austria, 2017.
ieee: P. Payne, “Bacterial herd and social immunity to phages,” Institute of Science
and Technology Austria, 2017.
ista: Payne P. 2017. Bacterial herd and social immunity to phages. Institute of
Science and Technology Austria.
mla: Payne, Pavel. Bacterial Herd and Social Immunity to Phages. Institute
of Science and Technology Austria, 2017.
short: P. Payne, Bacterial Herd and Social Immunity to Phages, Institute of Science
and Technology Austria, 2017.
corr_author: '1'
date_created: 2019-04-09T15:16:45Z
date_published: 2017-02-01T00:00:00Z
date_updated: 2026-04-08T14:16:28Z
day: '01'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: NiBa
- _id: JoBo
file:
- access_level: closed
checksum: a0fc5c26a89c0ea759947ffba87d0d8f
content_type: application/pdf
creator: dernst
date_created: 2019-04-09T15:15:32Z
date_updated: 2020-07-14T12:47:27Z
file_id: '6292'
file_name: thesis_pavel_payne_final_w_signature_page.pdf
file_size: 3025175
relation: main_file
- access_level: open_access
checksum: af531e921a7f64a9e0af4cd8783b2226
content_type: application/pdf
creator: dernst
date_created: 2021-02-22T13:45:59Z
date_updated: 2021-02-22T13:45:59Z
file_id: '9187'
file_name: 2017_Payne_Thesis.pdf
file_size: 3111536
relation: main_file
success: 1
file_date_updated: 2021-02-22T13:45:59Z
has_accepted_license: '1'
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
page: '83'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
status: public
supervisor:
- 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: Nicholas H
full_name: Barton, Nicholas H
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
orcid: 0000-0002-8548-5240
title: Bacterial herd and social immunity to phages
type: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2017'
...
---
_id: '1063'
abstract:
- lang: eng
text: Severe environmental change can drive a population extinct unless the population
adapts in time to the new conditions (“evolutionary rescue”). How does biparental
sexual reproduction influence the chances of population persistence compared to
clonal reproduction or selfing? In this article, we set up a one‐locus two‐allele
model for adaptation in diploid species, where rescue is contingent on the establishment
of the mutant homozygote. Reproduction can occur by random mating, selfing, or
clonally. Random mating generates and destroys the rescue mutant; selfing is efficient
at generating it but at the same time depletes the heterozygote, which can lead
to a low mutant frequency in the standing genetic variation. Due to these (and
other) antagonistic effects, we find a nontrivial dependence of population survival
on the rate of sex/selfing, which is strongly influenced by the dominance coefficient
of the mutation before and after the environmental change. Importantly, since
mating with the wild‐type breaks the mutant homozygote up, a slow decay of the
wild‐type population size can impede rescue in randomly mating populations.
article_processing_charge: No
author:
- first_name: Hildegard
full_name: Uecker, Hildegard
id: 2DB8F68A-F248-11E8-B48F-1D18A9856A87
last_name: Uecker
orcid: 0000-0001-9435-2813
biorxivid: 1
citation:
ama: Uecker H. Evolutionary rescue in randomly mating, selfing, and clonal populations.
Evolution. 2017;71(4):845-858. doi:10.1111/evo.13191
apa: Uecker, H. (2017). Evolutionary rescue in randomly mating, selfing, and clonal
populations. Evolution. Wiley. https://doi.org/10.1111/evo.13191
chicago: Uecker, Hildegard. “Evolutionary Rescue in Randomly Mating, Selfing, and
Clonal Populations.” Evolution. Wiley, 2017. https://doi.org/10.1111/evo.13191.
ieee: H. Uecker, “Evolutionary rescue in randomly mating, selfing, and clonal populations,”
Evolution, vol. 71, no. 4. Wiley, pp. 845–858, 2017.
ista: Uecker H. 2017. Evolutionary rescue in randomly mating, selfing, and clonal
populations. Evolution. 71(4), 845–858.
mla: Uecker, Hildegard. “Evolutionary Rescue in Randomly Mating, Selfing, and Clonal
Populations.” Evolution, vol. 71, no. 4, Wiley, 2017, pp. 845–58, doi:10.1111/evo.13191.
short: H. Uecker, Evolution 71 (2017) 845–858.
das_tickbox: '1'
date_created: 2018-12-11T11:49:57Z
date_published: 2017-04-01T00:00:00Z
date_updated: 2026-06-22T14:05:53Z
day: '01'
department:
- _id: NiBa
doi: 10.1111/evo.13191
ec_funded: 1
external_id:
biorxivid:
- 10.1101/081042
isi:
- '000398545200003'
intvolume: ' 71'
isi: 1
issue: '4'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/081042
month: '04'
oa: 1
oa_version: Submitted Version
page: 845 - 858
project:
- _id: 25B07788-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '250152'
name: Limits to selection in biology and in evolutionary computation
publication: Evolution
publication_identifier:
issn:
- 0014-3820
publication_status: published
publisher: Wiley
publist_id: '6327'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Evolutionary rescue in randomly mating, selfing, and clonal populations
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 71
year: '2017'
...
---
_id: '1074'
abstract:
- lang: eng
text: Recently it has become feasible to detect long blocks of nearly identical
sequence shared between pairs of genomes. These IBD blocks are direct traces of
recent coalescence events and, as such, contain ample signal to infer recent demography.
Here, we examine sharing of such blocks in two-dimensional populations with local
migration. Using a diffusion approximation to trace genetic ancestry, we derive
analytical formulae for patterns of isolation by distance of IBD blocks, which
can also incorporate recent population density changes. We introduce an inference
scheme that uses a composite likelihood approach to fit these formulae. We then
extensively evaluate our theory and inference method on a range of scenarios using
simulated data. We first validate the diffusion approximation by showing that
the theoretical results closely match the simulated block sharing patterns. We
then demonstrate that our inference scheme can accurately and robustly infer dispersal
rate and effective density, as well as bounds on recent dynamics of population
density. To demonstrate an application, we use our estimation scheme to explore
the fit of a diffusion model to Eastern European samples in the POPRES data set.
We show that ancestry diffusing with a rate of σ ≈ 50–100 km/√gen during the last
centuries, combined with accelerating population growth, can explain the observed
exponential decay of block sharing with increasing pairwise sample distance.
article_processing_charge: No
author:
- first_name: Harald
full_name: Ringbauer, Harald
id: 417FCFF4-F248-11E8-B48F-1D18A9856A87
last_name: Ringbauer
orcid: 0000-0002-4884-9682
- first_name: Graham
full_name: Coop, Graham
last_name: Coop
- first_name: Nicholas H
full_name: Barton, Nicholas H
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
orcid: 0000-0002-8548-5240
citation:
ama: Ringbauer H, Coop G, Barton NH. Inferring recent demography from isolation
by distance of long shared sequence blocks. Genetics. 2017;205(3):1335-1351.
doi:10.1534/genetics.116.196220
apa: Ringbauer, H., Coop, G., & Barton, N. H. (2017). Inferring recent demography
from isolation by distance of long shared sequence blocks. Genetics. Genetics
Society of America. https://doi.org/10.1534/genetics.116.196220
chicago: Ringbauer, Harald, Graham Coop, and Nicholas H Barton. “Inferring Recent
Demography from Isolation by Distance of Long Shared Sequence Blocks.” Genetics.
Genetics Society of America, 2017. https://doi.org/10.1534/genetics.116.196220.
ieee: H. Ringbauer, G. Coop, and N. H. Barton, “Inferring recent demography from
isolation by distance of long shared sequence blocks,” Genetics, vol. 205,
no. 3. Genetics Society of America, pp. 1335–1351, 2017.
ista: Ringbauer H, Coop G, Barton NH. 2017. Inferring recent demography from isolation
by distance of long shared sequence blocks. Genetics. 205(3), 1335–1351.
mla: Ringbauer, Harald, et al. “Inferring Recent Demography from Isolation by Distance
of Long Shared Sequence Blocks.” Genetics, vol. 205, no. 3, Genetics Society
of America, 2017, pp. 1335–51, doi:10.1534/genetics.116.196220.
short: H. Ringbauer, G. Coop, N.H. Barton, Genetics 205 (2017) 1335–1351.
date_created: 2018-12-11T11:50:00Z
date_published: 2017-03-01T00:00:00Z
date_updated: 2026-04-08T14:06:35Z
day: '01'
department:
- _id: NiBa
doi: 10.1534/genetics.116.196220
ec_funded: 1
external_id:
isi:
- '000395807200023'
intvolume: ' 205'
isi: 1
issue: '3'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.biorxiv.org/content/early/2016/09/23/076810
month: '03'
oa: 1
oa_version: Preprint
page: 1335 - 1351
project:
- _id: 25B07788-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '250152'
name: Limits to selection in biology and in evolutionary computation
publication: Genetics
publication_identifier:
issn:
- 0016-6731
publication_status: published
publisher: Genetics Society of America
publist_id: '6307'
quality_controlled: '1'
related_material:
record:
- id: '200'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Inferring recent demography from isolation by distance of long shared sequence
blocks
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 205
year: '2017'
...
---
_id: '1077'
abstract:
- lang: eng
text: Viral capsids are structurally constrained by interactions among the amino
acids (AAs) of their constituent proteins. Therefore, epistasis is expected to
evolve among physically interacting sites and to influence the rates of substitution.
To study the evolution of epistasis, we focused on the major structural protein
of the fX174 phage family by first reconstructing the ancestral protein sequences
of 18 species using a Bayesian statistical framework. The inferred ancestral reconstruction
differed at eight AAs, for a total of 256 possible ancestral haplotypes. For each
ancestral haplotype and the extant species, we estimated, in silico, the distribution
of free energies and epistasis of the capsid structure. We found that free energy
has not significantly increased but epistasis has. We decomposed epistasis up
to fifth order and found that higher-order epistasis sometimes compensates pairwise
interactions making the free energy seem additive. The dN/dS ratio is low, suggesting
strong purifying selection, and that structure is under stabilizing selection.
We synthesized phages carrying ancestral haplotypes of the coat protein gene and
measured their fitness experimentally. Our findings indicate that stabilizing
mutations can have higher fitness, and that fitness optima do not necessarily
coincide with energy minima.
article_number: '20160139'
article_processing_charge: Yes (in subscription journal)
author:
- first_name: Rodrigo A
full_name: Fernandes Redondo, Rodrigo A
id: 409D5C96-F248-11E8-B48F-1D18A9856A87
last_name: Fernandes Redondo
orcid: 0000-0002-5837-2793
- first_name: Harold
full_name: Vladar, Harold
id: 2A181218-F248-11E8-B48F-1D18A9856A87
last_name: Vladar
orcid: 0000-0002-5985-7653
- first_name: Tomasz
full_name: Włodarski, Tomasz
last_name: Włodarski
- first_name: Jonathan P
full_name: Bollback, Jonathan P
id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
last_name: Bollback
orcid: 0000-0002-4624-4612
citation:
ama: Fernandes Redondo RA, de Vladar H, Włodarski T, Bollback JP. Evolutionary interplay
between structure, energy and epistasis in the coat protein of the ϕX174 phage
family. Journal of the Royal Society Interface. 2017;14(126). doi:10.1098/rsif.2016.0139
apa: Fernandes Redondo, R. A., de Vladar, H., Włodarski, T., & Bollback, J.
P. (2017). Evolutionary interplay between structure, energy and epistasis in the
coat protein of the ϕX174 phage family. Journal of the Royal Society Interface.
Royal Society of London. https://doi.org/10.1098/rsif.2016.0139
chicago: Fernandes Redondo, Rodrigo A, Harold de Vladar, Tomasz Włodarski, and Jonathan
P Bollback. “Evolutionary Interplay between Structure, Energy and Epistasis in
the Coat Protein of the ΦX174 Phage Family.” Journal of the Royal Society Interface.
Royal Society of London, 2017. https://doi.org/10.1098/rsif.2016.0139.
ieee: R. A. Fernandes Redondo, H. de Vladar, T. Włodarski, and J. P. Bollback, “Evolutionary
interplay between structure, energy and epistasis in the coat protein of the ϕX174
phage family,” Journal of the Royal Society Interface, vol. 14, no. 126.
Royal Society of London, 2017.
ista: Fernandes Redondo RA, de Vladar H, Włodarski T, Bollback JP. 2017. Evolutionary
interplay between structure, energy and epistasis in the coat protein of the ϕX174
phage family. Journal of the Royal Society Interface. 14(126), 20160139.
mla: Fernandes Redondo, Rodrigo A., et al. “Evolutionary Interplay between Structure,
Energy and Epistasis in the Coat Protein of the ΦX174 Phage Family.” Journal
of the Royal Society Interface, vol. 14, no. 126, 20160139, Royal Society
of London, 2017, doi:10.1098/rsif.2016.0139.
short: R.A. Fernandes Redondo, H. de Vladar, T. Włodarski, J.P. Bollback, Journal
of the Royal Society Interface 14 (2017).
date_created: 2018-12-11T11:50:01Z
date_published: 2017-01-04T00:00:00Z
date_updated: 2025-07-10T11:49:59Z
day: '04'
ddc:
- '570'
department:
- _id: NiBa
- _id: JoBo
doi: 10.1098/rsif.2016.0139
ec_funded: 1
external_id:
isi:
- '000393380400001'
file:
- access_level: open_access
content_type: application/pdf
creator: dernst
date_created: 2019-01-18T09:14:02Z
date_updated: 2019-01-18T09:14:02Z
file_id: '5843'
file_name: 2017_JRSI_Redondo.pdf
file_size: 1092015
relation: main_file
success: 1
file_date_updated: 2019-01-18T09:14:02Z
has_accepted_license: '1'
intvolume: ' 14'
isi: 1
issue: '126'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
project:
- _id: 25B07788-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '250152'
name: Limits to selection in biology and in evolutionary computation
- _id: 2578D616-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '648440'
name: Selective Barriers to Horizontal Gene Transfer
publication: Journal of the Royal Society Interface
publication_identifier:
issn:
- 1742-5689
publication_status: published
publisher: Royal Society of London
publist_id: '6303'
quality_controlled: '1'
related_material:
record:
- id: '9864'
relation: research_data
status: public
scopus_import: '1'
status: public
title: Evolutionary interplay between structure, energy and epistasis in the coat
protein of the ϕX174 phage family
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 14
year: '2017'
...
---
_id: '910'
abstract:
- lang: eng
text: "Frequency-independent selection is generally considered as a force that acts
to reduce the genetic variation in evolving populations, yet rigorous arguments
for this idea are scarce. When selection fluctuates in time, it is unclear whether
frequency-independent selection may maintain genetic polymorphism without invoking
additional mechanisms. We show that constant frequency-independent selection with
arbitrary epistasis on a well-mixed haploid population eliminates genetic variation
if we assume linkage equilibrium between alleles. To this end, we introduce the
notion of frequency-independent selection at the level of alleles, which is sufficient
to prove our claim and contains the notion of frequency-independent selection
on haploids. When selection and recombination are weak but of the same order,
there may be strong linkage disequilibrium; numerical calculations show that stable
equilibria are highly unlikely. Using the example of a diallelic two-locus model,
we then demonstrate that frequency-independent selection that fluctuates in time
can maintain stable polymorphism if linkage disequilibrium changes its sign periodically.
We put our findings in the context of results from the existing literature and
point out those scenarios in which the possible role of frequency-independent
selection in maintaining genetic variation remains unclear.\r\n"
article_processing_charge: No
author:
- first_name: Sebastian
full_name: Novak, Sebastian
id: 461468AE-F248-11E8-B48F-1D18A9856A87
last_name: Novak
orcid: 0000-0002-2519-824X
- first_name: Nicholas H
full_name: Barton, Nicholas H
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
orcid: 0000-0002-8548-5240
citation:
ama: Novak S, Barton NH. When does frequency-independent selection maintain genetic
variation? Genetics. 2017;207(2):653-668. doi:10.1534/genetics.117.300129
apa: Novak, S., & Barton, N. H. (2017). When does frequency-independent selection
maintain genetic variation? Genetics. Genetics Society of America. https://doi.org/10.1534/genetics.117.300129
chicago: Novak, Sebastian, and Nicholas H Barton. “When Does Frequency-Independent
Selection Maintain Genetic Variation?” Genetics. Genetics Society of America,
2017. https://doi.org/10.1534/genetics.117.300129.
ieee: S. Novak and N. H. Barton, “When does frequency-independent selection maintain
genetic variation?,” Genetics, vol. 207, no. 2. Genetics Society of America,
pp. 653–668, 2017.
ista: Novak S, Barton NH. 2017. When does frequency-independent selection maintain
genetic variation? Genetics. 207(2), 653–668.
mla: Novak, Sebastian, and Nicholas H. Barton. “When Does Frequency-Independent
Selection Maintain Genetic Variation?” Genetics, vol. 207, no. 2, Genetics
Society of America, 2017, pp. 653–68, doi:10.1534/genetics.117.300129.
short: S. Novak, N.H. Barton, Genetics 207 (2017) 653–668.
corr_author: '1'
date_created: 2018-12-11T11:49:09Z
date_published: 2017-10-01T00:00:00Z
date_updated: 2025-04-15T08:22:21Z
day: '01'
ddc:
- '576'
department:
- _id: NiBa
doi: 10.1534/genetics.117.300129
ec_funded: 1
external_id:
isi:
- '000412232600019'
file:
- access_level: open_access
checksum: f7c32dabf52e6d9e709d9203761e39fd
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:17:12Z
date_updated: 2020-07-14T12:48:15Z
file_id: '5264'
file_name: IST-2018-974-v1+1_manuscript.pdf
file_size: 494268
relation: main_file
file_date_updated: 2020-07-14T12:48:15Z
has_accepted_license: '1'
intvolume: ' 207'
isi: 1
issue: '2'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Submitted Version
page: 653 - 668
project:
- _id: 25B1EC9E-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618091'
name: Speed of Adaptation in Population Genetics and Evolutionary Computation
publication: Genetics
publication_status: published
publisher: Genetics Society of America
publist_id: '6533'
pubrep_id: '974'
quality_controlled: '1'
scopus_import: '1'
status: public
title: When does frequency-independent selection maintain genetic variation?
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 207
year: '2017'
...
---
_id: '952'
abstract:
- lang: eng
text: A novel strategy for controlling the spread of arboviral diseases such as
dengue, Zika and chikungunya is to transform mosquito populations with virus-suppressing
Wolbachia. In general, Wolbachia transinfected into mosquitoes induce fitness
costs through lower viability or fecundity. These maternally inherited bacteria
also produce a frequency-dependent advantage for infected females by inducing
cytoplasmic incompatibility (CI), which kills the embryos produced by uninfected
females mated to infected males. These competing effects, a frequency-dependent
advantage and frequency-independent costs, produce bistable Wolbachia frequency
dynamics. Above a threshold frequency, denoted pˆ, CI drives fitness-decreasing
Wolbachia transinfections through local populations; but below pˆ, infection frequencies
tend to decline to zero. If pˆ is not too high, CI also drives spatial spread
once infections become established over sufficiently large areas. We illustrate
how simple models provide testable predictions concerning the spatial and temporal
dynamics of Wolbachia introductions, focusing on rate of spatial spread, the shape
of spreading waves, and the conditions for initiating spread from local introductions.
First, we consider the robustness of diffusion-based predictions to incorporating
two important features of wMel-Aedes aegypti biology that may be inconsistent
with the diffusion approximations, namely fast local dynamics induced by complete
CI (i.e., all embryos produced from incompatible crosses die) and long-tailed,
non-Gaussian dispersal. With complete CI, our numerical analyses show that long-tailed
dispersal changes wave-width predictions only slightly; but it can significantly
reduce wave speed relative to the diffusion prediction; it also allows smaller
local introductions to initiate spatial spread. Second, we use approximations
for pˆ and dispersal distances to predict the outcome of 2013 releases of wMel-infected
Aedes aegypti in Cairns, Australia, Third, we describe new data from Ae. aegypti
populations near Cairns, Australia that demonstrate long-distance dispersal and
provide an approximate lower bound on pˆ for wMel in northeastern Australia. Finally,
we apply our analyses to produce operational guidelines for efficient transformation
of vector populations over large areas. We demonstrate that even very slow spatial
spread, on the order of 10-20 m/month (as predicted), can produce area-wide population
transformation within a few years following initial releases covering about 20-30%
of the target area.
article_processing_charge: No
author:
- first_name: Michael
full_name: Turelli, Michael
last_name: Turelli
- first_name: Nicholas H
full_name: Barton, Nicholas H
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
orcid: 0000-0002-8548-5240
citation:
ama: 'Turelli M, Barton NH. Deploying dengue-suppressing Wolbachia: Robust models
predict slow but effective spatial spread in Aedes aegypti. Theoretical Population
Biology. 2017;115:45-60. doi:10.1016/j.tpb.2017.03.003'
apa: 'Turelli, M., & Barton, N. H. (2017). Deploying dengue-suppressing Wolbachia:
Robust models predict slow but effective spatial spread in Aedes aegypti. Theoretical
Population Biology. Elsevier. https://doi.org/10.1016/j.tpb.2017.03.003'
chicago: 'Turelli, Michael, and Nicholas H Barton. “Deploying Dengue-Suppressing
Wolbachia: Robust Models Predict Slow but Effective Spatial Spread in Aedes Aegypti.”
Theoretical Population Biology. Elsevier, 2017. https://doi.org/10.1016/j.tpb.2017.03.003.'
ieee: 'M. Turelli and N. H. Barton, “Deploying dengue-suppressing Wolbachia: Robust
models predict slow but effective spatial spread in Aedes aegypti,” Theoretical
Population Biology, vol. 115. Elsevier, pp. 45–60, 2017.'
ista: 'Turelli M, Barton NH. 2017. Deploying dengue-suppressing Wolbachia: Robust
models predict slow but effective spatial spread in Aedes aegypti. Theoretical
Population Biology. 115, 45–60.'
mla: 'Turelli, Michael, and Nicholas H. Barton. “Deploying Dengue-Suppressing Wolbachia:
Robust Models Predict Slow but Effective Spatial Spread in Aedes Aegypti.” Theoretical
Population Biology, vol. 115, Elsevier, 2017, pp. 45–60, doi:10.1016/j.tpb.2017.03.003.'
short: M. Turelli, N.H. Barton, Theoretical Population Biology 115 (2017) 45–60.
date_created: 2018-12-11T11:49:22Z
date_published: 2017-06-01T00:00:00Z
date_updated: 2025-07-10T12:01:49Z
day: '01'
ddc:
- '576'
department:
- _id: NiBa
doi: 10.1016/j.tpb.2017.03.003
external_id:
pmid:
- '28411063'
file:
- access_level: open_access
checksum: 9aeff86fa7de69f7a15cf4fc60d57d01
content_type: application/pdf
creator: dernst
date_created: 2019-04-17T06:39:45Z
date_updated: 2020-07-14T12:48:16Z
file_id: '6327'
file_name: 2017_TheoreticalPopulationBio_Turelli.pdf
file_size: 2073856
relation: main_file
file_date_updated: 2020-07-14T12:48:16Z
has_accepted_license: '1'
intvolume: ' 115'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Submitted Version
page: 45 - 60
pmid: 1
publication: Theoretical Population Biology
publication_identifier:
issn:
- 0040-5809
publication_status: published
publisher: Elsevier
publist_id: '6463'
pubrep_id: '972'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Deploying dengue-suppressing Wolbachia: Robust models predict slow but effective
spatial spread in Aedes aegypti'
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 115
year: '2017'
...
---
_id: '953'
abstract:
- lang: eng
text: 'The role of natural selection in the evolution of adaptive phenotypes has
undergone constant probing by evolutionary biologists, employing both theoretical
and empirical approaches. As Darwin noted, natural selection can act together
with other processes, including random changes in the frequencies of phenotypic
differences that are not under strong selection, and changes in the environment,
which may reflect evolutionary changes in the organisms themselves. As understanding
of genetics developed after 1900, the new genetic discoveries were incorporated
into evolutionary biology. The resulting general principles were summarized by
Julian Huxley in his 1942 book Evolution: the modern synthesis. Here, we examine
how recent advances in genetics, developmental biology and molecular biology,
including epigenetics, relate to today''s understanding of the evolution of adaptations.
We illustrate how careful genetic studies have repeatedly shown that apparently
puzzling results in a wide diversity of organisms involve processes that are consistent
with neo-Darwinism. They do not support important roles in adaptation for processes
such as directed mutation or the inheritance of acquired characters, and therefore
no radical revision of our understanding of the mechanism of adaptive evolution
is needed.'
article_number: '20162864'
article_processing_charge: No
author:
- first_name: Deborah
full_name: Charlesworth, Deborah
last_name: Charlesworth
- first_name: Nicholas H
full_name: Barton, Nicholas H
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
orcid: 0000-0002-8548-5240
- first_name: Brian
full_name: Charlesworth, Brian
last_name: Charlesworth
citation:
ama: Charlesworth D, Barton NH, Charlesworth B. The sources of adaptive evolution.
Proceedings of the Royal Society of London Series B Biological Sciences.
2017;284(1855). doi:10.1098/rspb.2016.2864
apa: Charlesworth, D., Barton, N. H., & Charlesworth, B. (2017). The sources
of adaptive evolution. Proceedings of the Royal Society of London Series B
Biological Sciences. Royal Society, The. https://doi.org/10.1098/rspb.2016.2864
chicago: Charlesworth, Deborah, Nicholas H Barton, and Brian Charlesworth. “The
Sources of Adaptive Evolution.” Proceedings of the Royal Society of London
Series B Biological Sciences. Royal Society, The, 2017. https://doi.org/10.1098/rspb.2016.2864.
ieee: D. Charlesworth, N. H. Barton, and B. Charlesworth, “The sources of adaptive
evolution,” Proceedings of the Royal Society of London Series B Biological
Sciences, vol. 284, no. 1855. Royal Society, The, 2017.
ista: Charlesworth D, Barton NH, Charlesworth B. 2017. The sources of adaptive evolution.
Proceedings of the Royal Society of London Series B Biological Sciences. 284(1855),
20162864.
mla: Charlesworth, Deborah, et al. “The Sources of Adaptive Evolution.” Proceedings
of the Royal Society of London Series B Biological Sciences, vol. 284, no.
1855, 20162864, Royal Society, The, 2017, doi:10.1098/rspb.2016.2864.
short: D. Charlesworth, N.H. Barton, B. Charlesworth, Proceedings of the Royal Society
of London Series B Biological Sciences 284 (2017).
date_created: 2018-12-11T11:49:23Z
date_published: 2017-05-31T00:00:00Z
date_updated: 2023-09-22T10:01:48Z
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doi: 10.1098/rspb.2016.2864
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publication_status: published
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title: The sources of adaptive evolution
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...
---
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abstract:
- lang: eng
text: Understanding the relation between genotype and phenotype remains a major
challenge. The difficulty of predicting individual mutation effects, and particularly
the interactions between them, has prevented the development of a comprehensive
theory that links genotypic changes to their phenotypic effects. We show that
a general thermodynamic framework for gene regulation, based on a biophysical
understanding of protein-DNA binding, accurately predicts the sign of epistasis
in a canonical cis-regulatory element consisting of overlapping RNA polymerase
and repressor binding sites. Sign and magnitude of individual mutation effects
are sufficient to predict the sign of epistasis and its environmental dependence.
Thus, the thermodynamic model offers the correct null prediction for epistasis
between mutations across DNA-binding sites. Our results indicate that a predictive
theory for the effects of cis-regulatory mutations is possible from first principles,
as long as the essential molecular mechanisms and the constraints these impose
on a biological system are accounted for.
article_number: e25192
article_processing_charge: Yes
author:
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full_name: Lagator, Mato
id: 345D25EC-F248-11E8-B48F-1D18A9856A87
last_name: Lagator
- first_name: Tiago
full_name: Paixao, Tiago
id: 2C5658E6-F248-11E8-B48F-1D18A9856A87
last_name: Paixao
orcid: 0000-0003-2361-3953
- first_name: Nicholas H
full_name: Barton, Nicholas H
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
orcid: 0000-0002-8548-5240
- first_name: Jonathan P
full_name: Bollback, Jonathan P
id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
last_name: Bollback
orcid: 0000-0002-4624-4612
- first_name: Calin C
full_name: Guet, Calin C
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last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Lagator M, Paixao T, Barton NH, Bollback JP, Guet CC. On the mechanistic nature
of epistasis in a canonical cis-regulatory element. eLife. 2017;6. doi:10.7554/eLife.25192
apa: Lagator, M., Paixao, T., Barton, N. H., Bollback, J. P., & Guet, C. C.
(2017). On the mechanistic nature of epistasis in a canonical cis-regulatory element.
ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.25192
chicago: Lagator, Mato, Tiago Paixao, Nicholas H Barton, Jonathan P Bollback, and
Calin C Guet. “On the Mechanistic Nature of Epistasis in a Canonical Cis-Regulatory
Element.” ELife. eLife Sciences Publications, 2017. https://doi.org/10.7554/eLife.25192.
ieee: M. Lagator, T. Paixao, N. H. Barton, J. P. Bollback, and C. C. Guet, “On the
mechanistic nature of epistasis in a canonical cis-regulatory element,” eLife,
vol. 6. eLife Sciences Publications, 2017.
ista: Lagator M, Paixao T, Barton NH, Bollback JP, Guet CC. 2017. On the mechanistic
nature of epistasis in a canonical cis-regulatory element. eLife. 6, e25192.
mla: Lagator, Mato, et al. “On the Mechanistic Nature of Epistasis in a Canonical
Cis-Regulatory Element.” ELife, vol. 6, e25192, eLife Sciences Publications,
2017, doi:10.7554/eLife.25192.
short: M. Lagator, T. Paixao, N.H. Barton, J.P. Bollback, C.C. Guet, ELife 6 (2017).
date_created: 2018-12-11T11:49:23Z
date_published: 2017-05-18T00:00:00Z
date_updated: 2025-07-10T12:01:50Z
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ddc:
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department:
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doi: 10.7554/eLife.25192
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abstract:
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text: 'Gene expression is controlled by networks of regulatory proteins that interact
specifically with external signals and DNA regulatory sequences. These interactions
force the network components to co-evolve so as to continually maintain function.
Yet, existing models of evolution mostly focus on isolated genetic elements. In
contrast, we study the essential process by which regulatory networks grow: the
duplication and subsequent specialization of network components. We synthesize
a biophysical model of molecular interactions with the evolutionary framework
to find the conditions and pathways by which new regulatory functions emerge.
We show that specialization of new network components is usually slow, but can
be drastically accelerated in the presence of regulatory crosstalk and mutations
that promote promiscuous interactions between network components.'
article_number: '216'
article_processing_charge: Yes (in subscription journal)
author:
- first_name: Tamar
full_name: Friedlander, Tamar
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last_name: Friedlander
- first_name: Roshan
full_name: Prizak, Roshan
id: 4456104E-F248-11E8-B48F-1D18A9856A87
last_name: Prizak
- first_name: Nicholas H
full_name: Barton, Nicholas H
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
orcid: 0000-0002-8548-5240
- first_name: Gasper
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last_name: Tkacik
orcid: 0000-0002-6699-1455
citation:
ama: Friedlander T, Prizak R, Barton NH, Tkačik G. Evolution of new regulatory functions
on biophysically realistic fitness landscapes. Nature Communications. 2017;8(1).
doi:10.1038/s41467-017-00238-8
apa: Friedlander, T., Prizak, R., Barton, N. H., & Tkačik, G. (2017). Evolution
of new regulatory functions on biophysically realistic fitness landscapes. Nature
Communications. Nature Publishing Group. https://doi.org/10.1038/s41467-017-00238-8
chicago: Friedlander, Tamar, Roshan Prizak, Nicholas H Barton, and Gašper Tkačik.
“Evolution of New Regulatory Functions on Biophysically Realistic Fitness Landscapes.”
Nature Communications. Nature Publishing Group, 2017. https://doi.org/10.1038/s41467-017-00238-8.
ieee: T. Friedlander, R. Prizak, N. H. Barton, and G. Tkačik, “Evolution of new
regulatory functions on biophysically realistic fitness landscapes,” Nature
Communications, vol. 8, no. 1. Nature Publishing Group, 2017.
ista: Friedlander T, Prizak R, Barton NH, Tkačik G. 2017. Evolution of new regulatory
functions on biophysically realistic fitness landscapes. Nature Communications.
8(1), 216.
mla: Friedlander, Tamar, et al. “Evolution of New Regulatory Functions on Biophysically
Realistic Fitness Landscapes.” Nature Communications, vol. 8, no. 1, 216,
Nature Publishing Group, 2017, doi:10.1038/s41467-017-00238-8.
short: T. Friedlander, R. Prizak, N.H. Barton, G. Tkačik, Nature Communications
8 (2017).
corr_author: '1'
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department:
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- _id: NiBa
doi: 10.1038/s41467-017-00238-8
ec_funded: 1
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oa: 1
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grant_number: '291734'
name: International IST Postdoc Fellowship Programme
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grant_number: '250152'
name: Limits to selection in biology and in evolutionary computation
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publisher: Nature Publishing Group
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title: Evolution of new regulatory functions on biophysically realistic fitness landscapes
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---
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abstract:
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text: Mathematica notebooks used to generate figures.
article_processing_charge: No
author:
- first_name: Alison
full_name: Etheridge, Alison
last_name: Etheridge
- first_name: Nicholas H
full_name: Barton, Nicholas H
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
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citation:
ama: 'Etheridge A, Barton NH. Data for: Establishment in a new habitat by polygenic
adaptation. 2017. doi:10.17632/nw68fxzjpm.1'
apa: 'Etheridge, A., & Barton, N. H. (2017). Data for: Establishment in a new
habitat by polygenic adaptation. Mendeley Data. https://doi.org/10.17632/nw68fxzjpm.1'
chicago: 'Etheridge, Alison, and Nicholas H Barton. “Data for: Establishment in
a New Habitat by Polygenic Adaptation.” Mendeley Data, 2017. https://doi.org/10.17632/nw68fxzjpm.1.'
ieee: 'A. Etheridge and N. H. Barton, “Data for: Establishment in a new habitat
by polygenic adaptation.” Mendeley Data, 2017.'
ista: 'Etheridge A, Barton NH. 2017. Data for: Establishment in a new habitat by
polygenic adaptation, Mendeley Data, 10.17632/nw68fxzjpm.1.'
mla: 'Etheridge, Alison, and Nicholas H. Barton. Data for: Establishment in a
New Habitat by Polygenic Adaptation. Mendeley Data, 2017, doi:10.17632/nw68fxzjpm.1.'
short: A. Etheridge, N.H. Barton, (2017).
date_created: 2021-08-09T13:18:55Z
date_published: 2017-12-29T00:00:00Z
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...
---
_id: '7163'
abstract:
- lang: eng
text: The de novo genome assemblies generated for this study, and the associated
metadata.
article_processing_charge: No
author:
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full_name: Fraisse, Christelle
id: 32DF5794-F248-11E8-B48F-1D18A9856A87
last_name: Fraisse
orcid: 0000-0001-8441-5075
citation:
ama: Fraisse C. Supplementary Files for “The deep conservation of the Lepidoptera
Z chromosome suggests a non canonical origin of the W.” 2017. doi:10.15479/AT:ISTA:7163
apa: Fraisse, C. (2017). Supplementary Files for “The deep conservation of the Lepidoptera
Z chromosome suggests a non canonical origin of the W.” Institute of Science and
Technology Austria. https://doi.org/10.15479/AT:ISTA:7163
chicago: Fraisse, Christelle. “Supplementary Files for ‘The Deep Conservation of
the Lepidoptera Z Chromosome Suggests a Non Canonical Origin of the W.’” Institute
of Science and Technology Austria, 2017. https://doi.org/10.15479/AT:ISTA:7163.
ieee: C. Fraisse, “Supplementary Files for ‘The deep conservation of the Lepidoptera
Z chromosome suggests a non canonical origin of the W.’” Institute of Science
and Technology Austria, 2017.
ista: Fraisse C. 2017. Supplementary Files for ‘The deep conservation of the Lepidoptera
Z chromosome suggests a non canonical origin of the W’, Institute of Science and
Technology Austria, 10.15479/AT:ISTA:7163.
mla: Fraisse, Christelle. Supplementary Files for “The Deep Conservation of the
Lepidoptera Z Chromosome Suggests a Non Canonical Origin of the W.” Institute
of Science and Technology Austria, 2017, doi:10.15479/AT:ISTA:7163.
short: C. Fraisse, (2017).
contributor:
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last_name: Picard
orcid: 0000-0002-8101-2518
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id: 49E1C5C6-F248-11E8-B48F-1D18A9856A87
last_name: Vicoso
orcid: 0000-0002-4579-8306
date_created: 2019-12-09T23:03:03Z
date_published: 2017-12-01T00:00:00Z
date_updated: 2025-09-11T07:33:33Z
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ddc:
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- _id: NiBa
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grant_number: P28842-B22
name: Sex chromosome evolution under male- and female- heterogamety
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