---
_id: '39'
abstract:
- lang: eng
  text: We study how a block of genome with a large number of weakly selected loci
    introgresses under directional selection into a genetically homogeneous population.
    We derive exact expressions for the expected rate of growth of any fragment of
    the introduced block during the initial phase of introgression, and show that
    the growth rate of a single-locus variant is largely insensitive to its own additive
    effect, but depends instead on the combined effect of all loci within a characteristic
    linkage scale. The expected growth rate of a fragment is highly correlated with
    its long-term introgression probability in populations of moderate size, and can
    hence identify variants that are likely to introgress across replicate populations.
    We clarify how the introgression probability of an individual variant is determined
    by the interplay between hitchhiking with relatively large fragments during the
    early phase of introgression and selection on fine-scale variation within these,
    which at longer times results in differential introgression probabilities for
    beneficial and deleterious loci within successful fragments. By simulating individuals,
    we also investigate how introgression probabilities at individual loci depend
    on the variance of fitness effects, the net fitness of the introduced block, and
    the size of the recipient population, and how this shapes the net advance under
    selection. Our work suggests that even highly replicable substitutions may be
    associated with a range of selective effects, which makes it challenging to fine
    map the causal loci that underlie polygenic adaptation.
article_processing_charge: No
article_type: original
author:
- first_name: Himani
  full_name: Sachdeva, Himani
  id: 42377A0A-F248-11E8-B48F-1D18A9856A87
  last_name: Sachdeva
- 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: Sachdeva H, Barton NH. Replicability of introgression under linked, polygenic
    selection. <i>Genetics</i>. 2018;210(4):1411-1427. doi:<a href="https://doi.org/10.1534/genetics.118.301429">10.1534/genetics.118.301429</a>
  apa: Sachdeva, H., &#38; Barton, N. H. (2018). Replicability of introgression under
    linked, polygenic selection. <i>Genetics</i>. Genetics Society of America. <a
    href="https://doi.org/10.1534/genetics.118.301429">https://doi.org/10.1534/genetics.118.301429</a>
  chicago: Sachdeva, Himani, and Nicholas H Barton. “Replicability of Introgression
    under Linked, Polygenic Selection.” <i>Genetics</i>. Genetics Society of America,
    2018. <a href="https://doi.org/10.1534/genetics.118.301429">https://doi.org/10.1534/genetics.118.301429</a>.
  ieee: H. Sachdeva and N. H. Barton, “Replicability of introgression under linked,
    polygenic selection,” <i>Genetics</i>, vol. 210, no. 4. Genetics Society of America,
    pp. 1411–1427, 2018.
  ista: Sachdeva H, Barton NH. 2018. Replicability of introgression under linked,
    polygenic selection. Genetics. 210(4), 1411–1427.
  mla: Sachdeva, Himani, and Nicholas H. Barton. “Replicability of Introgression under
    Linked, Polygenic Selection.” <i>Genetics</i>, vol. 210, no. 4, Genetics Society
    of America, 2018, pp. 1411–27, doi:<a href="https://doi.org/10.1534/genetics.118.301429">10.1534/genetics.118.301429</a>.
  short: H. Sachdeva, N.H. Barton, Genetics 210 (2018) 1411–1427.
date_created: 2018-12-11T11:44:18Z
date_published: 2018-12-04T00:00:00Z
date_updated: 2025-07-10T11:52:33Z
day: '04'
department:
- _id: NiBa
doi: 10.1534/genetics.118.301429
external_id:
  isi:
  - '000452315900021'
intvolume: '       210'
isi: 1
issue: '4'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://www.biorxiv.org/content/10.1101/379578v1
month: '12'
oa: 1
oa_version: Preprint
page: 1411-1427
publication: Genetics
publication_identifier:
  issn:
  - 0016-6731
publication_status: published
publisher: Genetics Society of America
quality_controlled: '1'
scopus_import: '1'
status: public
title: Replicability of introgression under linked, polygenic selection
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 210
year: '2018'
...
---
_id: '40'
abstract:
- lang: eng
  text: Hanemaaijer et al. (Molecular Ecology, 27, 2018) describe the genetic consequences
    of the introgression of an insecticide resistance allele into a mosquito population.
    Linked alleles initially increased, but many of these later declined. It is hard
    to determine whether this decline was due to counter‐selection, rather than simply
    to chance.
article_processing_charge: Yes (via OA deal)
article_type: letter_note
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. The consequences of an introgression event. <i>Molecular Ecology</i>.
    2018;27(24):4973-4975. doi:<a href="https://doi.org/10.1111/mec.14950">10.1111/mec.14950</a>
  apa: Barton, N. H. (2018). The consequences of an introgression event. <i>Molecular
    Ecology</i>. Wiley. <a href="https://doi.org/10.1111/mec.14950">https://doi.org/10.1111/mec.14950</a>
  chicago: Barton, Nicholas H. “The Consequences of an Introgression Event.” <i>Molecular
    Ecology</i>. Wiley, 2018. <a href="https://doi.org/10.1111/mec.14950">https://doi.org/10.1111/mec.14950</a>.
  ieee: N. H. Barton, “The consequences of an introgression event,” <i>Molecular Ecology</i>,
    vol. 27, no. 24. Wiley, pp. 4973–4975, 2018.
  ista: Barton NH. 2018. The consequences of an introgression event. Molecular Ecology.
    27(24), 4973–4975.
  mla: Barton, Nicholas H. “The Consequences of an Introgression Event.” <i>Molecular
    Ecology</i>, vol. 27, no. 24, Wiley, 2018, pp. 4973–75, doi:<a href="https://doi.org/10.1111/mec.14950">10.1111/mec.14950</a>.
  short: N.H. Barton, Molecular Ecology 27 (2018) 4973–4975.
corr_author: '1'
date_created: 2018-12-11T11:44:18Z
date_published: 2018-12-31T00:00:00Z
date_updated: 2025-07-10T11:52:34Z
day: '31'
ddc:
- '576'
department:
- _id: NiBa
doi: 10.1111/mec.14950
external_id:
  isi:
  - '000454600500001'
  pmid:
  - '30599087'
file:
- access_level: open_access
  content_type: application/pdf
  creator: apreinsp
  date_created: 2019-07-19T06:54:46Z
  date_updated: 2020-07-14T12:46:22Z
  file_id: '6652'
  file_name: 2018_MolecularEcology_BartonNick.pdf
  file_size: 295452
  relation: main_file
file_date_updated: 2020-07-14T12:46:22Z
has_accepted_license: '1'
intvolume: '        27'
isi: 1
issue: '24'
language:
- iso: eng
license: https://creativecommons.org/licenses/by/4.0/
month: '12'
oa: 1
oa_version: Published Version
page: 4973-4975
pmid: 1
publication: Molecular Ecology
publication_identifier:
  issn:
  - 1365-294X
publication_status: published
publisher: Wiley
publist_id: '8014'
quality_controlled: '1'
related_material:
  record:
  - id: '9805'
    relation: research_data
    status: public
scopus_import: '1'
status: public
title: The consequences of an introgression event
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 27
year: '2018'
...
---
_id: '423'
abstract:
- lang: eng
  text: Herd immunity, a process in which resistant individuals limit the spread of
    a pathogen among susceptible hosts has been extensively studied in eukaryotes.
    Even though bacteria have evolved multiple immune systems against their phage
    pathogens, herd immunity in bacteria remains unexplored. Here we experimentally
    demonstrate that herd immunity arises during phage epidemics in structured and
    unstructured Escherichia coli populations consisting of differing frequencies
    of susceptible and resistant cells harboring CRISPR immunity. In addition, we
    develop a mathematical model that quantifies how herd immunity is affected by
    spatial population structure, bacterial growth rate, and phage replication rate.
    Using our model we infer a general epidemiological rule describing the relative
    speed of an epidemic in partially resistant spatially structured populations.
    Our experimental and theoretical findings indicate that herd immunity may be important
    in bacterial communities, allowing for stable coexistence of bacteria and their
    phages and the maintenance of polymorphism in bacterial immunity.
acknowledgement: "We are grateful to Remy Chait for his help and assistance with establishing
  our experimental setups and to Tobias Bergmiller for valuable insights into some
  specific experimental details. We thank Luciano Marraffini for donating us the pCas9
  plasmid used in this study. We also want to express our gratitude to Seth Barribeau,
  Andrea Betancourt, Călin Guet, Mato Lagator, Tiago Paixão and Maroš Pleška for valuable
  discussions on the manuscript. Finally, we would like to thank the \r\neditors and
  reviewers for their helpful comments and suggestions."
article_number: e32035
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
- first_name: Lukas
  full_name: Geyrhofer, Lukas
  last_name: Geyrhofer
- 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
citation:
  ama: Payne P, Geyrhofer L, Barton NH, Bollback JP. CRISPR-based herd immunity can
    limit phage epidemics in bacterial populations. <i>eLife</i>. 2018;7. doi:<a href="https://doi.org/10.7554/eLife.32035">10.7554/eLife.32035</a>
  apa: Payne, P., Geyrhofer, L., Barton, N. H., &#38; Bollback, J. P. (2018). CRISPR-based
    herd immunity can limit phage epidemics in bacterial populations. <i>ELife</i>.
    eLife Sciences Publications. <a href="https://doi.org/10.7554/eLife.32035">https://doi.org/10.7554/eLife.32035</a>
  chicago: Payne, Pavel, Lukas Geyrhofer, Nicholas H Barton, and Jonathan P Bollback.
    “CRISPR-Based Herd Immunity Can Limit Phage Epidemics in Bacterial Populations.”
    <i>ELife</i>. eLife Sciences Publications, 2018. <a href="https://doi.org/10.7554/eLife.32035">https://doi.org/10.7554/eLife.32035</a>.
  ieee: P. Payne, L. Geyrhofer, N. H. Barton, and J. P. Bollback, “CRISPR-based herd
    immunity can limit phage epidemics in bacterial populations,” <i>eLife</i>, vol.
    7. eLife Sciences Publications, 2018.
  ista: Payne P, Geyrhofer L, Barton NH, Bollback JP. 2018. CRISPR-based herd immunity
    can limit phage epidemics in bacterial populations. eLife. 7, e32035.
  mla: Payne, Pavel, et al. “CRISPR-Based Herd Immunity Can Limit Phage Epidemics
    in Bacterial Populations.” <i>ELife</i>, vol. 7, e32035, eLife Sciences Publications,
    2018, doi:<a href="https://doi.org/10.7554/eLife.32035">10.7554/eLife.32035</a>.
  short: P. Payne, L. Geyrhofer, N.H. Barton, J.P. Bollback, ELife 7 (2018).
date_created: 2018-12-11T11:46:23Z
date_published: 2018-03-09T00:00:00Z
date_updated: 2025-03-31T16:00:24Z
day: '09'
ddc:
- '576'
department:
- _id: NiBa
- _id: JoBo
doi: 10.7554/eLife.32035
ec_funded: 1
external_id:
  isi:
  - '000431035800001'
file:
- access_level: open_access
  checksum: 447cf6e680bdc3c01062a8737d876569
  content_type: application/pdf
  creator: dernst
  date_created: 2018-12-17T10:36:07Z
  date_updated: 2020-07-14T12:46:25Z
  file_id: '5689'
  file_name: 2018_eLife_Payne.pdf
  file_size: 3533881
  relation: main_file
file_date_updated: 2020-07-14T12:46:25Z
has_accepted_license: '1'
intvolume: '         7'
isi: 1
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
project:
- _id: 2578D616-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '648440'
  name: Selective Barriers to Horizontal Gene Transfer
publication: eLife
publication_status: published
publisher: eLife Sciences Publications
publist_id: '7400'
quality_controlled: '1'
related_material:
  record:
  - id: '9840'
    relation: research_data
    status: public
scopus_import: '1'
status: public
title: CRISPR-based herd immunity can limit phage epidemics in bacterial populations
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 7
year: '2018'
...
---
_id: '430'
abstract:
- lang: eng
  text: In this issue of GENETICS, a new method for detecting natural selection on
    polygenic traits is developed and applied to sev- eral human examples ( Racimo
    et al. 2018 ). By de fi nition, many loci contribute to variation in polygenic
    traits, and a challenge for evolutionary ge neticists has been that these traits
    can evolve by small, nearly undetectable shifts in allele frequencies across each
    of many, typically unknown, loci. Recently, a helpful remedy has arisen. Genome-wide
    associ- ation studies (GWAS) have been illuminating sets of loci that can be interrogated
    jointly for c hanges in allele frequencies. By aggregating small signal s of change
    across many such loci, directional natural selection is now in principle detect-
    able using genetic data, even for highly polygenic traits. This is an exciting
    arena of progress – with these methods, tests can be made for selection associated
    with traits, and we can now study selection in what may be its most prevalent
    mode. The continuing fast pace of GWAS publications suggest there will be many
    more polygenic tests of selection in the near future, as every new GWAS is an
    opportunity for an accom- panying test of polygenic selection. However, it is
    important to be aware of complications th at arise in interpretation, especially
    given that these studies may easily be misinter- preted both in and outside the
    evolutionary genetics commu- nity. Here, we provide context for understanding
    polygenic tests and urge caution regarding how these results are inter- preted
    and reported upon more broadly.
article_processing_charge: No
author:
- first_name: John
  full_name: Novembre, John
  last_name: Novembre
- 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: Novembre J, Barton NH. Tread lightly interpreting polygenic tests of selection.
    <i>Genetics</i>. 2018;208(4):1351-1355. doi:<a href="https://doi.org/10.1534/genetics.118.300786">10.1534/genetics.118.300786</a>
  apa: Novembre, J., &#38; Barton, N. H. (2018). Tread lightly interpreting polygenic
    tests of selection. <i>Genetics</i>. Genetics Society of America. <a href="https://doi.org/10.1534/genetics.118.300786">https://doi.org/10.1534/genetics.118.300786</a>
  chicago: Novembre, John, and Nicholas H Barton. “Tread Lightly Interpreting Polygenic
    Tests of Selection.” <i>Genetics</i>. Genetics Society of America, 2018. <a href="https://doi.org/10.1534/genetics.118.300786">https://doi.org/10.1534/genetics.118.300786</a>.
  ieee: J. Novembre and N. H. Barton, “Tread lightly interpreting polygenic tests
    of selection,” <i>Genetics</i>, vol. 208, no. 4. Genetics Society of America,
    pp. 1351–1355, 2018.
  ista: Novembre J, Barton NH. 2018. Tread lightly interpreting polygenic tests of
    selection. Genetics. 208(4), 1351–1355.
  mla: Novembre, John, and Nicholas H. Barton. “Tread Lightly Interpreting Polygenic
    Tests of Selection.” <i>Genetics</i>, vol. 208, no. 4, Genetics Society of America,
    2018, pp. 1351–55, doi:<a href="https://doi.org/10.1534/genetics.118.300786">10.1534/genetics.118.300786</a>.
  short: J. Novembre, N.H. Barton, Genetics 208 (2018) 1351–1355.
date_created: 2018-12-11T11:46:26Z
date_published: 2018-04-01T00:00:00Z
date_updated: 2023-09-19T10:17:30Z
day: '01'
ddc:
- '576'
department:
- _id: NiBa
doi: 10.1534/genetics.118.300786
external_id:
  isi:
  - '000429094400005'
file:
- access_level: open_access
  checksum: 3d838dc285df394376555b794b6a5ad1
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:12:40Z
  date_updated: 2020-07-14T12:46:26Z
  file_id: '4958'
  file_name: IST-2018-1012-v1+1_2018_Barton_Tread.pdf
  file_size: 500129
  relation: main_file
file_date_updated: 2020-07-14T12:46:26Z
has_accepted_license: '1'
intvolume: '       208'
isi: 1
issue: '4'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 1351 - 1355
publication: Genetics
publication_status: published
publisher: Genetics Society of America
publist_id: '7393'
pubrep_id: '1012'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Tread lightly interpreting polygenic tests of selection
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 208
year: '2018'
...
---
_id: '1111'
abstract:
- lang: eng
  text: Adaptation depends critically on the effects of new mutations and their dependency
    on the genetic background in which they occur. These two factors can be summarized
    by the fitness landscape. However, it would require testing all mutations in all
    backgrounds, making the definition and analysis of fitness landscapes mostly inaccessible.
    Instead of postulating a particular fitness landscape, we address this problem
    by considering general classes of landscapes and calculating an upper limit for
    the time it takes for a population to reach a fitness peak, circumventing the
    need to have full knowledge about the fitness landscape. We analyze populations
    in the weak-mutation regime and characterize the conditions that enable them to
    quickly reach the fitness peak as a function of the number of sites under selection.
    We show that for additive landscapes there is a critical selection strength enabling
    populations to reach high-fitness genotypes, regardless of the distribution of
    effects. This threshold scales with the number of sites under selection, effectively
    setting a limit to adaptation, and results from the inevitable increase in deleterious
    mutational pressure as the population adapts in a space of discrete genotypes.
    Furthermore, we show that for the class of all unimodal landscapes this condition
    is sufficient but not necessary for rapid adaptation, as in some highly epistatic
    landscapes the critical strength does not depend on the number of sites under
    selection; effectively removing this barrier to adaptation.
article_processing_charge: No
article_type: original
author:
- first_name: Jorge
  full_name: Heredia, Jorge
  last_name: Heredia
- first_name: Barbora
  full_name: Trubenova, Barbora
  id: 42302D54-F248-11E8-B48F-1D18A9856A87
  last_name: Trubenova
  orcid: 0000-0002-6873-2967
- first_name: Dirk
  full_name: Sudholt, Dirk
  last_name: Sudholt
- first_name: Tiago
  full_name: Paixao, Tiago
  id: 2C5658E6-F248-11E8-B48F-1D18A9856A87
  last_name: Paixao
  orcid: 0000-0003-2361-3953
citation:
  ama: Heredia J, Trubenova B, Sudholt D, Paixao T. Selection limits to adaptive walks
    on correlated landscapes. <i>Genetics</i>. 2017;205(2):803-825. doi:<a href="https://doi.org/10.1534/genetics.116.189340">10.1534/genetics.116.189340</a>
  apa: Heredia, J., Trubenova, B., Sudholt, D., &#38; Paixao, T. (2017). Selection
    limits to adaptive walks on correlated landscapes. <i>Genetics</i>. Genetics Society
    of America. <a href="https://doi.org/10.1534/genetics.116.189340">https://doi.org/10.1534/genetics.116.189340</a>
  chicago: Heredia, Jorge, Barbora Trubenova, Dirk Sudholt, and Tiago Paixao. “Selection
    Limits to Adaptive Walks on Correlated Landscapes.” <i>Genetics</i>. Genetics
    Society of America, 2017. <a href="https://doi.org/10.1534/genetics.116.189340">https://doi.org/10.1534/genetics.116.189340</a>.
  ieee: J. Heredia, B. Trubenova, D. Sudholt, and T. Paixao, “Selection limits to
    adaptive walks on correlated landscapes,” <i>Genetics</i>, vol. 205, no. 2. Genetics
    Society of America, pp. 803–825, 2017.
  ista: Heredia J, Trubenova B, Sudholt D, Paixao T. 2017. Selection limits to adaptive
    walks on correlated landscapes. Genetics. 205(2), 803–825.
  mla: Heredia, Jorge, et al. “Selection Limits to Adaptive Walks on Correlated Landscapes.”
    <i>Genetics</i>, vol. 205, no. 2, Genetics Society of America, 2017, pp. 803–25,
    doi:<a href="https://doi.org/10.1534/genetics.116.189340">10.1534/genetics.116.189340</a>.
  short: J. Heredia, B. Trubenova, D. Sudholt, T. Paixao, Genetics 205 (2017) 803–825.
date_created: 2018-12-11T11:50:12Z
date_published: 2017-02-01T00:00:00Z
date_updated: 2026-06-18T10:46:55Z
day: '01'
ddc:
- '570'
department:
- _id: NiBa
doi: 10.1534/genetics.116.189340
ec_funded: 1
external_id:
  isi:
  - '000394144900025'
  pmid:
  - '27881471'
intvolume: '       205'
isi: 1
issue: '2'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1534/genetics.116.189340
month: '02'
oa: 1
oa_version: Published Version
page: 803 - 825
pmid: 1
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_identifier:
  issn:
  - 0016-6731
publication_status: published
publisher: Genetics Society of America
publist_id: '6256'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Selection limits to adaptive walks on correlated landscapes
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 205
year: '2017'
...
---
_id: '1112'
abstract:
- lang: eng
  text: There has been renewed interest in modelling the behaviour of evolutionary
    algorithms by more traditional mathematical objects, such as ordinary differential
    equations or Markov chains. The advantage is that the analysis becomes greatly
    facilitated due to the existence of well established methods. However, this typically
    comes at the cost of disregarding information about the process. Here, we introduce
    the use of stochastic differential equations (SDEs) for the study of EAs. SDEs
    can produce simple analytical results for the dynamics of stochastic processes,
    unlike Markov chains which can produce rigorous but unwieldy expressions about
    the dynamics. On the other hand, unlike ordinary differential equations (ODEs),
    they do not discard information about the stochasticity of the process. We show
    that these are especially suitable for the analysis of fixed budget scenarios
    and present analogs of the additive and multiplicative drift theorems for SDEs.
    We exemplify the use of these methods for two model algorithms ((1+1) EA and RLS)
    on two canonical problems(OneMax and LeadingOnes).
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
citation:
  ama: 'Paixao T, Pérez Heredia J. An application of stochastic differential equations
    to evolutionary algorithms. In: <i>Proceedings of the 14th ACM/SIGEVO Conference
    on Foundations of Genetic Algorithms</i>. ACM; 2017:3-11. doi:<a href="https://doi.org/10.1145/3040718.3040729">10.1145/3040718.3040729</a>'
  apa: 'Paixao, T., &#38; Pérez Heredia, J. (2017). An application of stochastic differential
    equations to evolutionary algorithms. In <i>Proceedings of the 14th ACM/SIGEVO
    Conference on Foundations of Genetic Algorithms</i> (pp. 3–11). Copenhagen, Denmark:
    ACM. <a href="https://doi.org/10.1145/3040718.3040729">https://doi.org/10.1145/3040718.3040729</a>'
  chicago: Paixao, Tiago, and Jorge Pérez Heredia. “An Application of Stochastic Differential
    Equations to Evolutionary Algorithms.” In <i>Proceedings of the 14th ACM/SIGEVO
    Conference on Foundations of Genetic Algorithms</i>, 3–11. ACM, 2017. <a href="https://doi.org/10.1145/3040718.3040729">https://doi.org/10.1145/3040718.3040729</a>.
  ieee: T. Paixao and J. Pérez Heredia, “An application of stochastic differential
    equations to evolutionary algorithms,” in <i>Proceedings of the 14th ACM/SIGEVO
    Conference on Foundations of Genetic Algorithms</i>, Copenhagen, Denmark, 2017,
    pp. 3–11.
  ista: 'Paixao T, Pérez Heredia J. 2017. An application of stochastic differential
    equations to evolutionary algorithms. Proceedings of the 14th ACM/SIGEVO Conference
    on Foundations of Genetic Algorithms. FOGA: Foundations of Genetic Algorithms,
    3–11.'
  mla: Paixao, Tiago, and Jorge Pérez Heredia. “An Application of Stochastic Differential
    Equations to Evolutionary Algorithms.” <i>Proceedings of the 14th ACM/SIGEVO Conference
    on Foundations of Genetic Algorithms</i>, ACM, 2017, pp. 3–11, doi:<a href="https://doi.org/10.1145/3040718.3040729">10.1145/3040718.3040729</a>.
  short: T. Paixao, J. Pérez Heredia, in:, Proceedings of the 14th ACM/SIGEVO Conference
    on Foundations of Genetic Algorithms, ACM, 2017, pp. 3–11.
conference:
  end_date: 2017-01-15
  location: Copenhagen, Denmark
  name: 'FOGA: Foundations of Genetic Algorithms'
  start_date: 2017-01-12
date_created: 2018-12-11T11:50:12Z
date_published: 2017-01-12T00:00:00Z
date_updated: 2021-01-12T06:48:22Z
day: '12'
department:
- _id: NiBa
doi: 10.1145/3040718.3040729
language:
- iso: eng
month: '01'
oa_version: None
page: 3 - 11
publication: Proceedings of the 14th ACM/SIGEVO Conference on Foundations of Genetic
  Algorithms
publication_identifier:
  isbn:
  - 978-145034651-1
publication_status: published
publisher: ACM
publist_id: '6255'
quality_controlled: '1'
scopus_import: 1
status: public
title: An application of stochastic differential equations to evolutionary algorithms
type: conference
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2017'
...
---
_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.
    <i>Genetics</i>. 2017;205(1):367-374. doi:<a href="https://doi.org/10.1534/genetics.116.193946">10.1534/genetics.116.193946</a>
  apa: Novak, S., &#38; Kollár, R. (2017). Spatial gene frequency waves under genotype
    dependent dispersal. <i>Genetics</i>. Genetics Society of America. <a href="https://doi.org/10.1534/genetics.116.193946">https://doi.org/10.1534/genetics.116.193946</a>
  chicago: Novak, Sebastian, and Richard Kollár. “Spatial Gene Frequency Waves under
    Genotype Dependent Dispersal.” <i>Genetics</i>. Genetics Society of America, 2017.
    <a href="https://doi.org/10.1534/genetics.116.193946">https://doi.org/10.1534/genetics.116.193946</a>.
  ieee: S. Novak and R. Kollár, “Spatial gene frequency waves under genotype dependent
    dispersal,” <i>Genetics</i>, 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.” <i>Genetics</i>, vol. 205, no. 1, Genetics Society of America,
    2017, pp. 367–74, doi:<a href="https://doi.org/10.1534/genetics.116.193946">10.1534/genetics.116.193946</a>.
  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.
    <i>Bulletin of Mathematical Biology</i>. 2017;79(3):525-559. doi:<a href="https://doi.org/10.1007/s11538-016-0244-3">10.1007/s11538-016-0244-3</a>
  apa: Kollár, R., &#38; Novak, S. (2017). Existence of traveling waves for the generalized
    F–KPP equation. <i>Bulletin of Mathematical Biology</i>. Springer. <a href="https://doi.org/10.1007/s11538-016-0244-3">https://doi.org/10.1007/s11538-016-0244-3</a>
  chicago: Kollár, Richard, and Sebastian Novak. “Existence of Traveling Waves for
    the Generalized F–KPP Equation.” <i>Bulletin of Mathematical Biology</i>. Springer,
    2017. <a href="https://doi.org/10.1007/s11538-016-0244-3">https://doi.org/10.1007/s11538-016-0244-3</a>.
  ieee: R. Kollár and S. Novak, “Existence of traveling waves for the generalized
    F–KPP equation,” <i>Bulletin of Mathematical Biology</i>, 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.” <i>Bulletin of Mathematical Biology</i>, vol. 79,
    no. 3, Springer, 2017, pp. 525–59, doi:<a href="https://doi.org/10.1007/s11538-016-0244-3">10.1007/s11538-016-0244-3</a>.
  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? <i>Heredity</i>.
    2017;118:96-109. doi:<a href="https://doi.org/10.1038/hdy.2016.109">10.1038/hdy.2016.109</a>
  apa: Barton, N. H. (2017). How does epistasis influence the response to selection?
    <i>Heredity</i>. Nature Publishing Group. <a href="https://doi.org/10.1038/hdy.2016.109">https://doi.org/10.1038/hdy.2016.109</a>
  chicago: Barton, Nicholas H. “How Does Epistasis Influence the Response to Selection?”
    <i>Heredity</i>. Nature Publishing Group, 2017. <a href="https://doi.org/10.1038/hdy.2016.109">https://doi.org/10.1038/hdy.2016.109</a>.
  ieee: N. H. Barton, “How does epistasis influence the response to selection?,” <i>Heredity</i>,
    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?”
    <i>Heredity</i>, vol. 118, Nature Publishing Group, 2017, pp. 96–109, doi:<a href="https://doi.org/10.1038/hdy.2016.109">10.1038/hdy.2016.109</a>.
  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. <i>Algorithmica</i>. 2017;78(2):681-713.
    doi:<a href="https://doi.org/10.1007/s00453-016-0212-1">10.1007/s00453-016-0212-1</a>
  apa: Paixao, T., Pérez Heredia, J., Sudholt, D., &#38; Trubenova, B. (2017). Towards
    a runtime comparison of natural and artificial evolution. <i>Algorithmica</i>.
    Springer. <a href="https://doi.org/10.1007/s00453-016-0212-1">https://doi.org/10.1007/s00453-016-0212-1</a>
  chicago: Paixao, Tiago, Jorge Pérez Heredia, Dirk Sudholt, and Barbora Trubenova.
    “Towards a Runtime Comparison of Natural and Artificial Evolution.” <i>Algorithmica</i>.
    Springer, 2017. <a href="https://doi.org/10.1007/s00453-016-0212-1">https://doi.org/10.1007/s00453-016-0212-1</a>.
  ieee: T. Paixao, J. Pérez Heredia, D. Sudholt, and B. Trubenova, “Towards a runtime
    comparison of natural and artificial evolution,” <i>Algorithmica</i>, 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.” <i>Algorithmica</i>, vol. 78, no. 2, Springer, 2017, pp. 681–713,
    doi:<a href="https://doi.org/10.1007/s00453-016-0212-1">10.1007/s00453-016-0212-1</a>.
  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. <i>Acta Informatica</i>. 2017;54(8):765-787.
    doi:<a href="https://doi.org/10.1007/s00236-016-0278-x">10.1007/s00236-016-0278-x</a>
  apa: Giacobbe, M., Guet, C. C., Gupta, A., Henzinger, T. A., Paixao, T., &#38; Petrov,
    T. (2017). Model checking the evolution of gene regulatory networks. <i>Acta Informatica</i>.
    Springer. <a href="https://doi.org/10.1007/s00236-016-0278-x">https://doi.org/10.1007/s00236-016-0278-x</a>
  chicago: Giacobbe, Mirco, Calin C Guet, Ashutosh Gupta, Thomas A Henzinger, Tiago
    Paixao, and Tatjana Petrov. “Model Checking the Evolution of Gene Regulatory Networks.”
    <i>Acta Informatica</i>. Springer, 2017. <a href="https://doi.org/10.1007/s00236-016-0278-x">https://doi.org/10.1007/s00236-016-0278-x</a>.
  ieee: M. Giacobbe, C. C. Guet, A. Gupta, T. A. Henzinger, T. Paixao, and T. Petrov,
    “Model checking the evolution of gene regulatory networks,” <i>Acta Informatica</i>,
    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.”
    <i>Acta Informatica</i>, vol. 54, no. 8, Springer, 2017, pp. 765–87, doi:<a href="https://doi.org/10.1007/s00236-016-0278-x">10.1007/s00236-016-0278-x</a>.
  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:
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  checksum: 4e661d9135d7f8c342e8e258dee76f3e
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  creator: dernst
  date_created: 2019-01-17T15:57:29Z
  date_updated: 2020-07-14T12:44:46Z
  file_id: '5841'
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file_date_updated: 2020-07-14T12:44:46Z
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intvolume: '        54'
isi: 1
issue: '8'
language:
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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. <i>eLife</i>. 2017;6. doi:<a
    href="https://doi.org/10.7554/eLife.28921">10.7554/eLife.28921</a>
  apa: Lagator, M., Sarikas, S., Acar, H., Bollback, J. P., &#38; Guet, C. C. (2017).
    Regulatory network structure determines patterns of intermolecular epistasis.
    <i>ELife</i>. eLife Sciences Publications. <a href="https://doi.org/10.7554/eLife.28921">https://doi.org/10.7554/eLife.28921</a>
  chicago: Lagator, Mato, Srdjan Sarikas, Hande Acar, Jonathan P Bollback, and Calin
    C Guet. “Regulatory Network Structure Determines Patterns of Intermolecular Epistasis.”
    <i>ELife</i>. eLife Sciences Publications, 2017. <a href="https://doi.org/10.7554/eLife.28921">https://doi.org/10.7554/eLife.28921</a>.
  ieee: M. Lagator, S. Sarikas, H. Acar, J. P. Bollback, and C. C. Guet, “Regulatory
    network structure determines patterns of intermolecular epistasis,” <i>eLife</i>,
    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.” <i>ELife</i>, vol. 6, e28921, eLife Sciences Publications,
    2017, doi:<a href="https://doi.org/10.7554/eLife.28921">10.7554/eLife.28921</a>.
  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:
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  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. <i>Science</i>. 2017;358(6365):925-928. doi:<a
    href="https://doi.org/10.1126/science.aao3526">10.1126/science.aao3526</a>
  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. <i>Science</i>. American Association for the Advancement of Science.
    <a href="https://doi.org/10.1126/science.aao3526">https://doi.org/10.1126/science.aao3526</a>
  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.” <i>Science</i>. American Association for
    the Advancement of Science, 2017. <a href="https://doi.org/10.1126/science.aao3526">https://doi.org/10.1126/science.aao3526</a>.
  ieee: D. Bradley <i>et al.</i>, “Evolution of flower color pattern through selection
    on regulatory small RNAs,” <i>Science</i>, 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.” <i>Science</i>, vol. 358, no. 6365, American Association
    for the Advancement of Science, 2017, pp. 925–28, doi:<a href="https://doi.org/10.1126/science.aao3526">10.1126/science.aao3526</a>.
  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. <i>Nature Communications</i>.
    2017;8(1). doi:<a href="https://doi.org/10.1038/s41467-017-01663-5">10.1038/s41467-017-01663-5</a>
  apa: Fraisse, C., Picard, M. A. L., &#38; Vicoso, B. (2017). The deep conservation
    of the Lepidoptera Z chromosome suggests a non canonical origin of the W. <i>Nature
    Communications</i>. Nature Publishing Group. <a href="https://doi.org/10.1038/s41467-017-01663-5">https://doi.org/10.1038/s41467-017-01663-5</a>
  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.” <i>Nature
    Communications</i>. Nature Publishing Group, 2017. <a href="https://doi.org/10.1038/s41467-017-01663-5">https://doi.org/10.1038/s41467-017-01663-5</a>.
  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,” <i>Nature
    Communications</i>, 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.” <i>Nature Communications</i>, vol.
    8, no. 1, 1486, Nature Publishing Group, 2017, doi:<a href="https://doi.org/10.1038/s41467-017-01663-5">10.1038/s41467-017-01663-5</a>.
  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:
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  checksum: 4da2651303c8afc2f7fc419be42a2433
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  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. <i>Theoretical Population Biology</i>. 2017;118:50-73. doi:<a
    href="https://doi.org/10.1016/j.tpb.2017.06.001">10.1016/j.tpb.2017.06.001</a>'
  apa: 'Barton, N. H., Etheridge, A., &#38; Véber, A. (2017). The infinitesimal model:
    Definition derivation and implications. <i>Theoretical Population Biology</i>.
    Academic Press. <a href="https://doi.org/10.1016/j.tpb.2017.06.001">https://doi.org/10.1016/j.tpb.2017.06.001</a>'
  chicago: 'Barton, Nicholas H, Alison Etheridge, and Amandine Véber. “The Infinitesimal
    Model: Definition Derivation and Implications.” <i>Theoretical Population Biology</i>.
    Academic Press, 2017. <a href="https://doi.org/10.1016/j.tpb.2017.06.001">https://doi.org/10.1016/j.tpb.2017.06.001</a>.'
  ieee: 'N. H. Barton, A. Etheridge, and A. Véber, “The infinitesimal model: Definition
    derivation and implications,” <i>Theoretical Population Biology</i>, 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.” <i>Theoretical Population Biology</i>, vol. 118, Academic Press,
    2017, pp. 50–73, doi:<a href="https://doi.org/10.1016/j.tpb.2017.06.001">10.1016/j.tpb.2017.06.001</a>.'
  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
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  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
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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). <i>Bacterial herd and social immunity to phages</i>. 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. <i>Bacterial Herd and Social Immunity to Phages</i>. 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
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  date_updated: 2020-07-14T12:47:27Z
  file_id: '6292'
  file_name: thesis_pavel_payne_final_w_signature_page.pdf
  file_size: 3025175
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- 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.
    <i>Evolution</i>. 2017;71(4):845-858. doi:<a href="https://doi.org/10.1111/evo.13191">10.1111/evo.13191</a>
  apa: Uecker, H. (2017). Evolutionary rescue in randomly mating, selfing, and clonal
    populations. <i>Evolution</i>. Wiley. <a href="https://doi.org/10.1111/evo.13191">https://doi.org/10.1111/evo.13191</a>
  chicago: Uecker, Hildegard. “Evolutionary Rescue in Randomly Mating, Selfing, and
    Clonal Populations.” <i>Evolution</i>. Wiley, 2017. <a href="https://doi.org/10.1111/evo.13191">https://doi.org/10.1111/evo.13191</a>.
  ieee: H. Uecker, “Evolutionary rescue in randomly mating, selfing, and clonal populations,”
    <i>Evolution</i>, 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.” <i>Evolution</i>, vol. 71, no. 4, Wiley, 2017, pp. 845–58, doi:<a
    href="https://doi.org/10.1111/evo.13191">10.1111/evo.13191</a>.
  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. <i>Genetics</i>. 2017;205(3):1335-1351.
    doi:<a href="https://doi.org/10.1534/genetics.116.196220">10.1534/genetics.116.196220</a>
  apa: Ringbauer, H., Coop, G., &#38; Barton, N. H. (2017). Inferring recent demography
    from isolation by distance of long shared sequence blocks. <i>Genetics</i>. Genetics
    Society of America. <a href="https://doi.org/10.1534/genetics.116.196220">https://doi.org/10.1534/genetics.116.196220</a>
  chicago: Ringbauer, Harald, Graham Coop, and Nicholas H Barton. “Inferring Recent
    Demography from Isolation by Distance of Long Shared Sequence Blocks.” <i>Genetics</i>.
    Genetics Society of America, 2017. <a href="https://doi.org/10.1534/genetics.116.196220">https://doi.org/10.1534/genetics.116.196220</a>.
  ieee: H. Ringbauer, G. Coop, and N. H. Barton, “Inferring recent demography from
    isolation by distance of long shared sequence blocks,” <i>Genetics</i>, 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.” <i>Genetics</i>, vol. 205, no. 3, Genetics Society
    of America, 2017, pp. 1335–51, doi:<a href="https://doi.org/10.1534/genetics.116.196220">10.1534/genetics.116.196220</a>.
  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: '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? <i>Genetics</i>. 2017;207(2):653-668. doi:<a href="https://doi.org/10.1534/genetics.117.300129">10.1534/genetics.117.300129</a>
  apa: Novak, S., &#38; Barton, N. H. (2017). When does frequency-independent selection
    maintain genetic variation? <i>Genetics</i>. Genetics Society of America. <a href="https://doi.org/10.1534/genetics.117.300129">https://doi.org/10.1534/genetics.117.300129</a>
  chicago: Novak, Sebastian, and Nicholas H Barton. “When Does Frequency-Independent
    Selection Maintain Genetic Variation?” <i>Genetics</i>. Genetics Society of America,
    2017. <a href="https://doi.org/10.1534/genetics.117.300129">https://doi.org/10.1534/genetics.117.300129</a>.
  ieee: S. Novak and N. H. Barton, “When does frequency-independent selection maintain
    genetic variation?,” <i>Genetics</i>, 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?” <i>Genetics</i>, vol. 207, no. 2, Genetics
    Society of America, 2017, pp. 653–68, doi:<a href="https://doi.org/10.1534/genetics.117.300129">10.1534/genetics.117.300129</a>.
  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. <i>Theoretical Population
    Biology</i>. 2017;115:45-60. doi:<a href="https://doi.org/10.1016/j.tpb.2017.03.003">10.1016/j.tpb.2017.03.003</a>'
  apa: 'Turelli, M., &#38; Barton, N. H. (2017). Deploying dengue-suppressing Wolbachia:
    Robust models predict slow but effective spatial spread in Aedes aegypti. <i>Theoretical
    Population Biology</i>. Elsevier. <a href="https://doi.org/10.1016/j.tpb.2017.03.003">https://doi.org/10.1016/j.tpb.2017.03.003</a>'
  chicago: 'Turelli, Michael, and Nicholas H Barton. “Deploying Dengue-Suppressing
    Wolbachia: Robust Models Predict Slow but Effective Spatial Spread in Aedes Aegypti.”
    <i>Theoretical Population Biology</i>. Elsevier, 2017. <a href="https://doi.org/10.1016/j.tpb.2017.03.003">https://doi.org/10.1016/j.tpb.2017.03.003</a>.'
  ieee: 'M. Turelli and N. H. Barton, “Deploying dengue-suppressing Wolbachia: Robust
    models predict slow but effective spatial spread in Aedes aegypti,” <i>Theoretical
    Population Biology</i>, 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.” <i>Theoretical
    Population Biology</i>, vol. 115, Elsevier, 2017, pp. 45–60, doi:<a href="https://doi.org/10.1016/j.tpb.2017.03.003">10.1016/j.tpb.2017.03.003</a>.'
  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
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month: '06'
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page: 45 - 60
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publication: Theoretical Population Biology
publication_identifier:
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publication_status: published
publisher: Elsevier
publist_id: '6463'
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title: 'Deploying dengue-suppressing Wolbachia: Robust models predict slow but effective
  spatial spread in Aedes aegypti'
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...
