---
_id: '10736'
abstract:
- lang: eng
text: Predicting function from sequence is a central problem of biology. Currently,
this is possible only locally in a narrow mutational neighborhood around a wildtype
sequence rather than globally from any sequence. Using random mutant libraries,
we developed a biophysical model that accounts for multiple features of σ70 binding
bacterial promoters to predict constitutive gene expression levels from any sequence.
We experimentally and theoretically estimated that 10–20% of random sequences
lead to expression and ~80% of non-expressing sequences are one mutation away
from a functional promoter. The potential for generating expression from random
sequences is so pervasive that selection acts against σ70-RNA polymerase binding
sites even within inter-genic, promoter-containing regions. This pervasiveness
of σ70-binding sites implies that emergence of promoters is not the limiting step
in gene regulatory evolution. Ultimately, the inclusion of novel features of promoter
function into a mechanistic model enabled not only more accurate predictions of
gene expression levels, but also identified that promoters evolve more rapidly
than previously thought.
acknowledgement: 'We thank Hande Acar, Nicholas H Barton, Rok Grah, Tiago Paixao,
Maros Pleska, Anna Staron, and Murat Tugrul for insightful comments and input on
the manuscript. This work was supported by: Sir Henry Dale Fellowship jointly funded
by the Wellcome Trust and the Royal Society (grant number 216779/Z/19/Z) to ML;
IPC Grant from IST Austria to ML and SS; European Research Council Funding Programme
7 (2007–2013, grant agreement number 648440) to JPB.'
article_number: e64543
article_processing_charge: No
article_type: original
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: Magdalena
full_name: Steinrueck, Magdalena
last_name: Steinrueck
- first_name: David
full_name: Toledo-Aparicio, David
last_name: Toledo-Aparicio
- 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
- first_name: Gašper
full_name: Tkačik, Gašper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkačik
orcid: 0000-0002-6699-1455
citation:
ama: Lagator M, Sarikas S, Steinrueck M, et al. Predicting bacterial promoter function
and evolution from random sequences. eLife. 2022;11. doi:10.7554/eLife.64543
apa: Lagator, M., Sarikas, S., Steinrueck, M., Toledo-Aparicio, D., Bollback, J.
P., Guet, C. C., & Tkačik, G. (2022). Predicting bacterial promoter function
and evolution from random sequences. ELife. eLife Sciences Publications.
https://doi.org/10.7554/eLife.64543
chicago: Lagator, Mato, Srdjan Sarikas, Magdalena Steinrueck, David Toledo-Aparicio,
Jonathan P Bollback, Calin C Guet, and Gašper Tkačik. “Predicting Bacterial Promoter
Function and Evolution from Random Sequences.” ELife. eLife Sciences Publications,
2022. https://doi.org/10.7554/eLife.64543.
ieee: M. Lagator et al., “Predicting bacterial promoter function and evolution
from random sequences,” eLife, vol. 11. eLife Sciences Publications, 2022.
ista: Lagator M, Sarikas S, Steinrueck M, Toledo-Aparicio D, Bollback JP, Guet CC,
Tkačik G. 2022. Predicting bacterial promoter function and evolution from random
sequences. eLife. 11, e64543.
mla: Lagator, Mato, et al. “Predicting Bacterial Promoter Function and Evolution
from Random Sequences.” ELife, vol. 11, e64543, eLife Sciences Publications,
2022, doi:10.7554/eLife.64543.
short: M. Lagator, S. Sarikas, M. Steinrueck, D. Toledo-Aparicio, J.P. Bollback,
C.C. Guet, G. Tkačik, ELife 11 (2022).
date_created: 2022-02-06T23:01:32Z
date_published: 2022-01-26T00:00:00Z
date_updated: 2023-08-02T14:09:02Z
day: '26'
ddc:
- '576'
department:
- _id: CaGu
- _id: GaTk
- _id: NiBa
doi: 10.7554/eLife.64543
ec_funded: 1
external_id:
isi:
- '000751104400001'
pmid:
- '35080492'
file:
- access_level: open_access
checksum: decdcdf600ff51e9a9703b49ca114170
content_type: application/pdf
creator: cchlebak
date_created: 2022-02-07T07:14:09Z
date_updated: 2022-02-07T07:14:09Z
file_id: '10739'
file_name: 2022_ELife_Lagator.pdf
file_size: 5604343
relation: main_file
success: 1
file_date_updated: 2022-02-07T07:14:09Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 2578D616-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '648440'
name: Selective Barriers to Horizontal Gene Transfer
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Predicting bacterial promoter function and evolution from random sequences
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 11
year: '2022'
...
---
_id: '7652'
abstract:
- lang: eng
text: Organisms cope with change by taking advantage of transcriptional regulators.
However, when faced with rare environments, the evolution of transcriptional regulators
and their promoters may be too slow. Here, we investigate whether the intrinsic
instability of gene duplication and amplification provides a generic alternative
to canonical gene regulation. Using real-time monitoring of gene-copy-number mutations
in Escherichia coli, we show that gene duplications and amplifications enable
adaptation to fluctuating environments by rapidly generating copy-number and,
therefore, expression-level polymorphisms. This amplification-mediated gene expression
tuning (AMGET) occurs on timescales that are similar to canonical gene regulation
and can respond to rapid environmental changes. Mathematical modelling shows that
amplifications also tune gene expression in stochastic environments in which transcription-factor-based
schemes are hard to evolve or maintain. The fleeting nature of gene amplifications
gives rise to a generic population-level mechanism that relies on genetic heterogeneity
to rapidly tune the expression of any gene, without leaving any genomic signature.
acknowledgement: We thank L. Hurst, N. Barton, M. Pleska, M. Steinrück, B. Kavcic
and A. Staron for input on the manuscript, and To. Bergmiller and R. Chait for help
with microfluidics experiments. I.T. is a recipient the OMV fellowship. R.G. is
a recipient of a DOC (Doctoral Fellowship Programme of the Austrian Academy of Sciences)
Fellowship of the Austrian Academy of Sciences.
article_processing_charge: No
article_type: original
author:
- first_name: Isabella
full_name: Tomanek, Isabella
id: 3981F020-F248-11E8-B48F-1D18A9856A87
last_name: Tomanek
orcid: 0000-0001-6197-363X
- first_name: Rok
full_name: Grah, Rok
id: 483E70DE-F248-11E8-B48F-1D18A9856A87
last_name: Grah
orcid: 0000-0003-2539-3560
- first_name: M.
full_name: Lagator, M.
last_name: Lagator
- first_name: A. M. C.
full_name: Andersson, A. M. C.
last_name: Andersson
- first_name: Jonathan P
full_name: Bollback, Jonathan P
id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
last_name: Bollback
orcid: 0000-0002-4624-4612
- first_name: Gašper
full_name: Tkačik, Gašper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkačik
orcid: 0000-0002-6699-1455
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Tomanek I, Grah R, Lagator M, et al. Gene amplification as a form of population-level
gene expression regulation. Nature Ecology & Evolution. 2020;4(4):612-625.
doi:10.1038/s41559-020-1132-7
apa: Tomanek, I., Grah, R., Lagator, M., Andersson, A. M. C., Bollback, J. P., Tkačik,
G., & Guet, C. C. (2020). Gene amplification as a form of population-level
gene expression regulation. Nature Ecology & Evolution. Springer Nature.
https://doi.org/10.1038/s41559-020-1132-7
chicago: Tomanek, Isabella, Rok Grah, M. Lagator, A. M. C. Andersson, Jonathan P
Bollback, Gašper Tkačik, and Calin C Guet. “Gene Amplification as a Form of Population-Level
Gene Expression Regulation.” Nature Ecology & Evolution. Springer Nature,
2020. https://doi.org/10.1038/s41559-020-1132-7.
ieee: I. Tomanek et al., “Gene amplification as a form of population-level
gene expression regulation,” Nature Ecology & Evolution, vol. 4, no.
4. Springer Nature, pp. 612–625, 2020.
ista: Tomanek I, Grah R, Lagator M, Andersson AMC, Bollback JP, Tkačik G, Guet CC.
2020. Gene amplification as a form of population-level gene expression regulation.
Nature Ecology & Evolution. 4(4), 612–625.
mla: Tomanek, Isabella, et al. “Gene Amplification as a Form of Population-Level
Gene Expression Regulation.” Nature Ecology & Evolution, vol. 4, no.
4, Springer Nature, 2020, pp. 612–25, doi:10.1038/s41559-020-1132-7.
short: I. Tomanek, R. Grah, M. Lagator, A.M.C. Andersson, J.P. Bollback, G. Tkačik,
C.C. Guet, Nature Ecology & Evolution 4 (2020) 612–625.
date_created: 2020-04-08T15:20:53Z
date_published: 2020-04-01T00:00:00Z
date_updated: 2024-03-25T23:30:20Z
day: '01'
ddc:
- '570'
department:
- _id: GaTk
- _id: CaGu
doi: 10.1038/s41559-020-1132-7
external_id:
isi:
- '000519008300005'
file:
- access_level: open_access
checksum: ef3bbf42023e30b2c24a6278025d2040
content_type: application/pdf
creator: dernst
date_created: 2020-10-09T09:56:01Z
date_updated: 2020-10-09T09:56:01Z
file_id: '8640'
file_name: 2020_NatureEcolEvo_Tomanek.pdf
file_size: 745242
relation: main_file
success: 1
file_date_updated: 2020-10-09T09:56:01Z
has_accepted_license: '1'
intvolume: ' 4'
isi: 1
issue: '4'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Submitted Version
page: 612-625
project:
- _id: 267C84F4-B435-11E9-9278-68D0E5697425
name: Biophysically realistic genotype-phenotype maps for regulatory networks
publication: Nature Ecology & Evolution
publication_identifier:
issn:
- 2397-334X
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/how-to-thrive-without-gene-regulation/
record:
- id: '8155'
relation: dissertation_contains
status: public
- id: '7383'
relation: research_data
status: public
- id: '7016'
relation: research_data
status: public
- id: '8653'
relation: used_in_publication
status: public
scopus_import: '1'
status: public
title: Gene amplification as a form of population-level gene expression regulation
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 4
year: '2020'
...
---
_id: '67'
abstract:
- lang: eng
text: 'Gene regulatory networks evolve through rewiring of individual components—that
is, through changes in regulatory connections. However, the mechanistic basis
of regulatory rewiring is poorly understood. Using a canonical gene regulatory
system, we quantify the properties of transcription factors that determine the
evolutionary potential for rewiring of regulatory connections: robustness, tunability
and evolvability. In vivo repression measurements of two repressors at mutated
operator sites reveal their contrasting evolutionary potential: while robustness
and evolvability were positively correlated, both were in trade-off with tunability.
Epistatic interactions between adjacent operators alleviated this trade-off. A
thermodynamic model explains how the differences in robustness, tunability and
evolvability arise from biophysical characteristics of repressor–DNA binding.
The model also uncovers that the energy matrix, which describes how mutations
affect repressor–DNA binding, encodes crucial information about the evolutionary
potential of a repressor. The biophysical determinants of evolutionary potential
for regulatory rewiring constitute a mechanistic framework for understanding network
evolution.'
article_processing_charge: No
article_type: original
author:
- first_name: Claudia
full_name: Igler, Claudia
id: 46613666-F248-11E8-B48F-1D18A9856A87
last_name: Igler
- first_name: Mato
full_name: Lagator, Mato
id: 345D25EC-F248-11E8-B48F-1D18A9856A87
last_name: Lagator
- first_name: Gasper
full_name: Tkacik, Gasper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkacik
orcid: 0000-0002-6699-1455
- 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: Igler C, Lagator M, Tkačik G, Bollback JP, Guet CC. Evolutionary potential
of transcription factors for gene regulatory rewiring. Nature Ecology and Evolution.
2018;2(10):1633-1643. doi:10.1038/s41559-018-0651-y
apa: Igler, C., Lagator, M., Tkačik, G., Bollback, J. P., & Guet, C. C. (2018).
Evolutionary potential of transcription factors for gene regulatory rewiring.
Nature Ecology and Evolution. Nature Publishing Group. https://doi.org/10.1038/s41559-018-0651-y
chicago: Igler, Claudia, Mato Lagator, Gašper Tkačik, Jonathan P Bollback, and Calin
C Guet. “Evolutionary Potential of Transcription Factors for Gene Regulatory Rewiring.”
Nature Ecology and Evolution. Nature Publishing Group, 2018. https://doi.org/10.1038/s41559-018-0651-y.
ieee: C. Igler, M. Lagator, G. Tkačik, J. P. Bollback, and C. C. Guet, “Evolutionary
potential of transcription factors for gene regulatory rewiring,” Nature Ecology
and Evolution, vol. 2, no. 10. Nature Publishing Group, pp. 1633–1643, 2018.
ista: Igler C, Lagator M, Tkačik G, Bollback JP, Guet CC. 2018. Evolutionary potential
of transcription factors for gene regulatory rewiring. Nature Ecology and Evolution.
2(10), 1633–1643.
mla: Igler, Claudia, et al. “Evolutionary Potential of Transcription Factors for
Gene Regulatory Rewiring.” Nature Ecology and Evolution, vol. 2, no. 10,
Nature Publishing Group, 2018, pp. 1633–43, doi:10.1038/s41559-018-0651-y.
short: C. Igler, M. Lagator, G. Tkačik, J.P. Bollback, C.C. Guet, Nature Ecology
and Evolution 2 (2018) 1633–1643.
date_created: 2018-12-11T11:44:27Z
date_published: 2018-09-10T00:00:00Z
date_updated: 2024-03-25T23:30:27Z
day: '10'
ddc:
- '570'
department:
- _id: CaGu
- _id: GaTk
- _id: JoBo
doi: 10.1038/s41559-018-0651-y
ec_funded: 1
external_id:
isi:
- '000447947600021'
file:
- access_level: open_access
checksum: 383a2e2c944a856e2e821ec8e7bf71b6
content_type: application/pdf
creator: dernst
date_created: 2020-05-14T11:28:52Z
date_updated: 2020-07-14T12:47:37Z
file_id: '7830'
file_name: 2018_NatureEcology_Igler.pdf
file_size: 1135973
relation: main_file
file_date_updated: 2020-07-14T12:47:37Z
has_accepted_license: '1'
intvolume: ' 2'
isi: 1
issue: '10'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Submitted Version
page: 1633 - 1643
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
- _id: 251EE76E-B435-11E9-9278-68D0E5697425
grant_number: '24573'
name: Design principles underlying genetic switch architecture (DOC Fellowship)
publication: Nature Ecology and Evolution
publication_status: published
publisher: Nature Publishing Group
publist_id: '7987'
quality_controlled: '1'
related_material:
record:
- id: '5585'
relation: popular_science
status: public
- id: '6371'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Evolutionary potential of transcription factors for gene regulatory rewiring
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 2
year: '2018'
...
---
_id: '5585'
abstract:
- lang: eng
text: Mean repression values and standard error of the mean are given for all operator
mutant libraries.
article_processing_charge: No
author:
- first_name: Claudia
full_name: Igler, Claudia
id: 46613666-F248-11E8-B48F-1D18A9856A87
last_name: Igler
- first_name: Mato
full_name: Lagator, Mato
id: 345D25EC-F248-11E8-B48F-1D18A9856A87
last_name: Lagator
- first_name: Gasper
full_name: Tkacik, Gasper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkacik
orcid: 0000-0002-6699-1455
- 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: Igler C, Lagator M, Tkačik G, Bollback JP, Guet CC. Data for the paper Evolutionary
potential of transcription factors for gene regulatory rewiring. 2018. doi:10.15479/AT:ISTA:108
apa: Igler, C., Lagator, M., Tkačik, G., Bollback, J. P., & Guet, C. C. (2018).
Data for the paper Evolutionary potential of transcription factors for gene regulatory
rewiring. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:108
chicago: Igler, Claudia, Mato Lagator, Gašper Tkačik, Jonathan P Bollback, and Calin
C Guet. “Data for the Paper Evolutionary Potential of Transcription Factors for
Gene Regulatory Rewiring.” Institute of Science and Technology Austria, 2018.
https://doi.org/10.15479/AT:ISTA:108.
ieee: C. Igler, M. Lagator, G. Tkačik, J. P. Bollback, and C. C. Guet, “Data for
the paper Evolutionary potential of transcription factors for gene regulatory
rewiring.” Institute of Science and Technology Austria, 2018.
ista: Igler C, Lagator M, Tkačik G, Bollback JP, Guet CC. 2018. Data for the paper
Evolutionary potential of transcription factors for gene regulatory rewiring,
Institute of Science and Technology Austria, 10.15479/AT:ISTA:108.
mla: Igler, Claudia, et al. Data for the Paper Evolutionary Potential of Transcription
Factors for Gene Regulatory Rewiring. Institute of Science and Technology
Austria, 2018, doi:10.15479/AT:ISTA:108.
short: C. Igler, M. Lagator, G. Tkačik, J.P. Bollback, C.C. Guet, (2018).
datarep_id: '108'
date_created: 2018-12-12T12:31:40Z
date_published: 2018-07-20T00:00:00Z
date_updated: 2024-03-25T23:30:27Z
day: '20'
ddc:
- '576'
department:
- _id: CaGu
- _id: GaTk
doi: 10.15479/AT:ISTA:108
ec_funded: 1
file:
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checksum: 1435781526c77413802adee0d4583cce
content_type: application/vnd.openxmlformats-officedocument.spreadsheetml.sheet
creator: system
date_created: 2018-12-12T13:02:45Z
date_updated: 2020-07-14T12:47:07Z
file_id: '5611'
file_name: IST-2018-108-v1+1_data_figures.xlsx
file_size: 16507
relation: main_file
file_date_updated: 2020-07-14T12:47:07Z
has_accepted_license: '1'
month: '07'
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
- _id: 251EE76E-B435-11E9-9278-68D0E5697425
grant_number: '24573'
name: Design principles underlying genetic switch architecture (DOC Fellowship)
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '67'
relation: research_paper
status: public
- id: '6371'
relation: research_paper
status: public
status: public
title: Data for the paper Evolutionary potential of transcription factors for gene
regulatory rewiring
tmp:
image: /images/cc_0.png
legal_code_url: https://creativecommons.org/publicdomain/zero/1.0/legalcode
name: Creative Commons Public Domain Dedication (CC0 1.0)
short: CC0 (1.0)
type: research_data
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2018'
...
---
_id: '9840'
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.
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. Data from: CRISPR-based herd
immunity limits phage epidemics in bacterial populations. 2018. doi:10.5061/dryad.42n44'
apa: 'Payne, P., Geyrhofer, L., Barton, N. H., & Bollback, J. P. (2018). Data
from: CRISPR-based herd immunity limits phage epidemics in bacterial populations.
Dryad. https://doi.org/10.5061/dryad.42n44'
chicago: 'Payne, Pavel, Lukas Geyrhofer, Nicholas H Barton, and Jonathan P Bollback.
“Data from: CRISPR-Based Herd Immunity Limits Phage Epidemics in Bacterial Populations.”
Dryad, 2018. https://doi.org/10.5061/dryad.42n44.'
ieee: 'P. Payne, L. Geyrhofer, N. H. Barton, and J. P. Bollback, “Data from: CRISPR-based
herd immunity limits phage epidemics in bacterial populations.” Dryad, 2018.'
ista: 'Payne P, Geyrhofer L, Barton NH, Bollback JP. 2018. Data from: CRISPR-based
herd immunity limits phage epidemics in bacterial populations, Dryad, 10.5061/dryad.42n44.'
mla: 'Payne, Pavel, et al. Data from: CRISPR-Based Herd Immunity Limits Phage
Epidemics in Bacterial Populations. Dryad, 2018, doi:10.5061/dryad.42n44.'
short: P. Payne, L. Geyrhofer, N.H. Barton, J.P. Bollback, (2018).
date_created: 2021-08-09T13:10:02Z
date_published: 2018-03-12T00:00:00Z
date_updated: 2023-09-11T12:49:17Z
day: '12'
department:
- _id: NiBa
- _id: JoBo
doi: 10.5061/dryad.42n44
main_file_link:
- open_access: '1'
url: https://doi.org/10.5061/dryad.42n44
month: '03'
oa: 1
oa_version: Published Version
publisher: Dryad
related_material:
record:
- id: '423'
relation: used_in_publication
status: public
status: public
title: 'Data from: CRISPR-based herd immunity limits phage epidemics in bacterial
populations'
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
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. eLife. 2018;7. doi:10.7554/eLife.32035
apa: Payne, P., Geyrhofer, L., Barton, N. H., & Bollback, J. P. (2018). CRISPR-based
herd immunity can limit phage epidemics in bacterial populations. ELife.
eLife Sciences Publications. https://doi.org/10.7554/eLife.32035
chicago: Payne, Pavel, Lukas Geyrhofer, Nicholas H Barton, and Jonathan P Bollback.
“CRISPR-Based Herd Immunity Can Limit Phage Epidemics in Bacterial Populations.”
ELife. eLife Sciences Publications, 2018. https://doi.org/10.7554/eLife.32035.
ieee: P. Payne, L. Geyrhofer, N. H. Barton, and J. P. Bollback, “CRISPR-based herd
immunity can limit phage epidemics in bacterial populations,” eLife, 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.” ELife, vol. 7, e32035, eLife Sciences Publications,
2018, doi:10.7554/eLife.32035.
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: 2023-09-11T12:49:17Z
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: '1077'
abstract:
- lang: eng
text: Viral capsids are structurally constrained by interactions among the amino
acids (AAs) of their constituent proteins. Therefore, epistasis is expected to
evolve among physically interacting sites and to influence the rates of substitution.
To study the evolution of epistasis, we focused on the major structural protein
of the fX174 phage family by first reconstructing the ancestral protein sequences
of 18 species using a Bayesian statistical framework. The inferred ancestral reconstruction
differed at eight AAs, for a total of 256 possible ancestral haplotypes. For each
ancestral haplotype and the extant species, we estimated, in silico, the distribution
of free energies and epistasis of the capsid structure. We found that free energy
has not significantly increased but epistasis has. We decomposed epistasis up
to fifth order and found that higher-order epistasis sometimes compensates pairwise
interactions making the free energy seem additive. The dN/dS ratio is low, suggesting
strong purifying selection, and that structure is under stabilizing selection.
We synthesized phages carrying ancestral haplotypes of the coat protein gene and
measured their fitness experimentally. Our findings indicate that stabilizing
mutations can have higher fitness, and that fitness optima do not necessarily
coincide with energy minima.
article_number: '20160139'
article_processing_charge: Yes (in subscription journal)
author:
- first_name: Rodrigo A
full_name: Fernandes Redondo, Rodrigo A
id: 409D5C96-F248-11E8-B48F-1D18A9856A87
last_name: Fernandes Redondo
orcid: 0000-0002-5837-2793
- first_name: Harold
full_name: Vladar, Harold
id: 2A181218-F248-11E8-B48F-1D18A9856A87
last_name: Vladar
orcid: 0000-0002-5985-7653
- first_name: Tomasz
full_name: Włodarski, Tomasz
last_name: Włodarski
- first_name: Jonathan P
full_name: Bollback, Jonathan P
id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
last_name: Bollback
orcid: 0000-0002-4624-4612
citation:
ama: Fernandes Redondo RA, de Vladar H, Włodarski T, Bollback JP. Evolutionary interplay
between structure, energy and epistasis in the coat protein of the ϕX174 phage
family. Journal of the Royal Society Interface. 2017;14(126). doi:10.1098/rsif.2016.0139
apa: Fernandes Redondo, R. A., de Vladar, H., Włodarski, T., & Bollback, J.
P. (2017). Evolutionary interplay between structure, energy and epistasis in the
coat protein of the ϕX174 phage family. Journal of the Royal Society Interface.
Royal Society of London. https://doi.org/10.1098/rsif.2016.0139
chicago: Fernandes Redondo, Rodrigo A, Harold de Vladar, Tomasz Włodarski, and Jonathan
P Bollback. “Evolutionary Interplay between Structure, Energy and Epistasis in
the Coat Protein of the ΦX174 Phage Family.” Journal of the Royal Society Interface.
Royal Society of London, 2017. https://doi.org/10.1098/rsif.2016.0139.
ieee: R. A. Fernandes Redondo, H. de Vladar, T. Włodarski, and J. P. Bollback, “Evolutionary
interplay between structure, energy and epistasis in the coat protein of the ϕX174
phage family,” Journal of the Royal Society Interface, vol. 14, no. 126.
Royal Society of London, 2017.
ista: Fernandes Redondo RA, de Vladar H, Włodarski T, Bollback JP. 2017. Evolutionary
interplay between structure, energy and epistasis in the coat protein of the ϕX174
phage family. Journal of the Royal Society Interface. 14(126), 20160139.
mla: Fernandes Redondo, Rodrigo A., et al. “Evolutionary Interplay between Structure,
Energy and Epistasis in the Coat Protein of the ΦX174 Phage Family.” Journal
of the Royal Society Interface, vol. 14, no. 126, 20160139, Royal Society
of London, 2017, doi:10.1098/rsif.2016.0139.
short: R.A. Fernandes Redondo, H. de Vladar, T. Włodarski, J.P. Bollback, Journal
of the Royal Society Interface 14 (2017).
date_created: 2018-12-11T11:50:01Z
date_published: 2017-01-04T00:00:00Z
date_updated: 2025-05-28T11:42:51Z
day: '04'
ddc:
- '570'
department:
- _id: NiBa
- _id: JoBo
doi: 10.1098/rsif.2016.0139
ec_funded: 1
external_id:
isi:
- '000393380400001'
file:
- access_level: open_access
content_type: application/pdf
creator: dernst
date_created: 2019-01-18T09:14:02Z
date_updated: 2019-01-18T09:14:02Z
file_id: '5843'
file_name: 2017_JRSI_Redondo.pdf
file_size: 1092015
relation: main_file
success: 1
file_date_updated: 2019-01-18T09:14:02Z
has_accepted_license: '1'
intvolume: ' 14'
isi: 1
issue: '126'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
project:
- _id: 25B07788-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '250152'
name: Limits to selection in biology and in evolutionary computation
- _id: 2578D616-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '648440'
name: Selective Barriers to Horizontal Gene Transfer
publication: Journal of the Royal Society Interface
publication_identifier:
issn:
- '17425689'
publication_status: published
publisher: Royal Society of London
publist_id: '6303'
quality_controlled: '1'
related_material:
record:
- id: '9864'
relation: research_data
status: public
scopus_import: '1'
status: public
title: Evolutionary interplay between structure, energy and epistasis in the coat
protein of the ϕX174 phage family
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 14
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
author:
- first_name: Mato
full_name: Lagator, Mato
id: 345D25EC-F248-11E8-B48F-1D18A9856A87
last_name: Lagator
- first_name: Srdjan
full_name: Sarikas, Srdjan
id: 35F0286E-F248-11E8-B48F-1D18A9856A87
last_name: Sarikas
- first_name: Hande
full_name: Acar, Hande
id: 2DDF136A-F248-11E8-B48F-1D18A9856A87
last_name: Acar
orcid: 0000-0003-1986-9753
- first_name: Jonathan P
full_name: Bollback, Jonathan P
id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
last_name: Bollback
orcid: 0000-0002-4624-4612
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Lagator M, Sarikas S, Acar H, Bollback JP, Guet CC. Regulatory network structure
determines patterns of intermolecular epistasis. eLife. 2017;6. doi:10.7554/eLife.28921
apa: Lagator, M., Sarikas, S., Acar, H., Bollback, J. P., & Guet, C. C. (2017).
Regulatory network structure determines patterns of intermolecular epistasis.
ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.28921
chicago: Lagator, Mato, Srdjan Sarikas, Hande Acar, Jonathan P Bollback, and Calin
C Guet. “Regulatory Network Structure Determines Patterns of Intermolecular Epistasis.”
ELife. eLife Sciences Publications, 2017. https://doi.org/10.7554/eLife.28921.
ieee: M. Lagator, S. Sarikas, H. Acar, J. P. Bollback, and C. C. Guet, “Regulatory
network structure determines patterns of intermolecular epistasis,” eLife,
vol. 6. eLife Sciences Publications, 2017.
ista: Lagator M, Sarikas S, Acar H, Bollback JP, Guet CC. 2017. Regulatory network
structure determines patterns of intermolecular epistasis. eLife. 6, e28921.
mla: Lagator, Mato, et al. “Regulatory Network Structure Determines Patterns of
Intermolecular Epistasis.” ELife, vol. 6, e28921, eLife Sciences Publications,
2017, doi:10.7554/eLife.28921.
short: M. Lagator, S. Sarikas, H. Acar, J.P. Bollback, C.C. Guet, ELife 6 (2017).
date_created: 2018-12-11T11:47:14Z
date_published: 2017-11-13T00:00:00Z
date_updated: 2021-01-12T08:03:15Z
day: '13'
ddc:
- '576'
department:
- _id: CaGu
- _id: JoBo
- _id: NiBa
doi: 10.7554/eLife.28921
ec_funded: 1
file:
- access_level: open_access
checksum: 273ab17f33305e4eaafd911ff88e7c5b
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:42Z
date_updated: 2020-07-14T12:47:10Z
file_id: '5096'
file_name: IST-2017-918-v1+1_elife-28921-figures-v3.pdf
file_size: 8453470
relation: main_file
- access_level: open_access
checksum: b433f90576c7be597cd43367946f8e7f
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:43Z
date_updated: 2020-07-14T12:47:10Z
file_id: '5097'
file_name: IST-2017-918-v1+2_elife-28921-v3.pdf
file_size: 1953221
relation: main_file
file_date_updated: 2020-07-14T12:47:10Z
has_accepted_license: '1'
intvolume: ' 6'
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:
- 2050084X
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: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 6
year: '2017'
...
---
_id: '954'
abstract:
- lang: eng
text: Understanding the relation between genotype and phenotype remains a major
challenge. The difficulty of predicting individual mutation effects, and particularly
the interactions between them, has prevented the development of a comprehensive
theory that links genotypic changes to their phenotypic effects. We show that
a general thermodynamic framework for gene regulation, based on a biophysical
understanding of protein-DNA binding, accurately predicts the sign of epistasis
in a canonical cis-regulatory element consisting of overlapping RNA polymerase
and repressor binding sites. Sign and magnitude of individual mutation effects
are sufficient to predict the sign of epistasis and its environmental dependence.
Thus, the thermodynamic model offers the correct null prediction for epistasis
between mutations across DNA-binding sites. Our results indicate that a predictive
theory for the effects of cis-regulatory mutations is possible from first principles,
as long as the essential molecular mechanisms and the constraints these impose
on a biological system are accounted for.
article_number: e25192
article_processing_charge: Yes
author:
- first_name: Mato
full_name: Lagator, Mato
id: 345D25EC-F248-11E8-B48F-1D18A9856A87
last_name: Lagator
- first_name: Tiago
full_name: Paixao, Tiago
id: 2C5658E6-F248-11E8-B48F-1D18A9856A87
last_name: Paixao
orcid: 0000-0003-2361-3953
- first_name: Nicholas H
full_name: Barton, Nicholas H
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
orcid: 0000-0002-8548-5240
- first_name: Jonathan P
full_name: Bollback, Jonathan P
id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
last_name: Bollback
orcid: 0000-0002-4624-4612
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Lagator M, Paixao T, Barton NH, Bollback JP, Guet CC. On the mechanistic nature
of epistasis in a canonical cis-regulatory element. eLife. 2017;6. doi:10.7554/eLife.25192
apa: Lagator, M., Paixao, T., Barton, N. H., Bollback, J. P., & Guet, C. C.
(2017). On the mechanistic nature of epistasis in a canonical cis-regulatory element.
ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.25192
chicago: Lagator, Mato, Tiago Paixao, Nicholas H Barton, Jonathan P Bollback, and
Calin C Guet. “On the Mechanistic Nature of Epistasis in a Canonical Cis-Regulatory
Element.” ELife. eLife Sciences Publications, 2017. https://doi.org/10.7554/eLife.25192.
ieee: M. Lagator, T. Paixao, N. H. Barton, J. P. Bollback, and C. C. Guet, “On the
mechanistic nature of epistasis in a canonical cis-regulatory element,” eLife,
vol. 6. eLife Sciences Publications, 2017.
ista: Lagator M, Paixao T, Barton NH, Bollback JP, Guet CC. 2017. On the mechanistic
nature of epistasis in a canonical cis-regulatory element. eLife. 6, e25192.
mla: Lagator, Mato, et al. “On the Mechanistic Nature of Epistasis in a Canonical
Cis-Regulatory Element.” ELife, vol. 6, e25192, eLife Sciences Publications,
2017, doi:10.7554/eLife.25192.
short: M. Lagator, T. Paixao, N.H. Barton, J.P. Bollback, C.C. Guet, ELife 6 (2017).
date_created: 2018-12-11T11:49:23Z
date_published: 2017-05-18T00:00:00Z
date_updated: 2023-09-22T10:01:17Z
day: '18'
ddc:
- '576'
department:
- _id: CaGu
- _id: NiBa
- _id: JoBo
doi: 10.7554/eLife.25192
ec_funded: 1
external_id:
isi:
- '000404024800001'
file:
- access_level: open_access
checksum: 59cdd4400fb41280122d414fea971546
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:17:49Z
date_updated: 2020-07-14T12:48:16Z
file_id: '5306'
file_name: IST-2017-841-v1+1_elife-25192-v2.pdf
file_size: 2441529
relation: main_file
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checksum: b69024880558b858eb8c5d47a92b6377
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:17:50Z
date_updated: 2020-07-14T12:48:16Z
file_id: '5307'
file_name: IST-2017-841-v1+2_elife-25192-figures-v2.pdf
file_size: 3752660
relation: main_file
file_date_updated: 2020-07-14T12:48:16Z
has_accepted_license: '1'
intvolume: ' 6'
isi: 1
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
project:
- _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: 2578D616-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '648440'
name: Selective Barriers to Horizontal Gene Transfer
publication: eLife
publication_identifier:
issn:
- 2050084X
publication_status: published
publisher: eLife Sciences Publications
publist_id: '6460'
pubrep_id: '841'
quality_controlled: '1'
scopus_import: '1'
status: public
title: On the mechanistic nature of epistasis in a canonical cis-regulatory element
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: 6
year: '2017'
...
---
_id: '1427'
abstract:
- lang: eng
text: Changes in gene expression are an important mode of evolution; however, the
proximate mechanism of these changes is poorly understood. In particular, little
is known about the effects of mutations within cis binding sites for transcription
factors, or the nature of epistatic interactions between these mutations. Here,
we tested the effects of single and double mutants in two cis binding sites involved
in the transcriptional regulation of the Escherichia coli araBAD operon, a component
of arabinose metabolism, using a synthetic system. This system decouples transcriptional
control from any posttranslational effects on fitness, allowing a precise estimate
of the effect of single and double mutations, and hence epistasis, on gene expression.
We found that epistatic interactions between mutations in the araBAD cis-regulatory
element are common, and that the predominant form of epistasis is negative. The
magnitude of the interactions depended on whether the mutations are located in
the same or in different operator sites. Importantly, these epistatic interactions
were dependent on the presence of arabinose, a native inducer of the araBAD operon
in vivo, with some interactions changing in sign (e.g., from negative to positive)
in its presence. This study thus reveals that mutations in even relatively simple
cis-regulatory elements interact in complex ways such that selection on the level
of gene expression in one environment might perturb regulation in the other environment
in an unpredictable and uncorrelated manner.
author:
- first_name: Mato
full_name: Lagator, Mato
id: 345D25EC-F248-11E8-B48F-1D18A9856A87
last_name: Lagator
- first_name: Claudia
full_name: Igler, Claudia
id: 46613666-F248-11E8-B48F-1D18A9856A87
last_name: Igler
- first_name: Anaisa
full_name: Moreno, Anaisa
last_name: Moreno
- 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: Jonathan P
full_name: Bollback, Jonathan P
id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
last_name: Bollback
orcid: 0000-0002-4624-4612
citation:
ama: Lagator M, Igler C, Moreno A, Guet CC, Bollback JP. Epistatic interactions
in the arabinose cis-regulatory element. Molecular Biology and Evolution.
2016;33(3):761-769. doi:10.1093/molbev/msv269
apa: Lagator, M., Igler, C., Moreno, A., Guet, C. C., & Bollback, J. P. (2016).
Epistatic interactions in the arabinose cis-regulatory element. Molecular Biology
and Evolution. Oxford University Press. https://doi.org/10.1093/molbev/msv269
chicago: Lagator, Mato, Claudia Igler, Anaisa Moreno, Calin C Guet, and Jonathan
P Bollback. “Epistatic Interactions in the Arabinose Cis-Regulatory Element.”
Molecular Biology and Evolution. Oxford University Press, 2016. https://doi.org/10.1093/molbev/msv269.
ieee: M. Lagator, C. Igler, A. Moreno, C. C. Guet, and J. P. Bollback, “Epistatic
interactions in the arabinose cis-regulatory element,” Molecular Biology and
Evolution, vol. 33, no. 3. Oxford University Press, pp. 761–769, 2016.
ista: Lagator M, Igler C, Moreno A, Guet CC, Bollback JP. 2016. Epistatic interactions
in the arabinose cis-regulatory element. Molecular Biology and Evolution. 33(3),
761–769.
mla: Lagator, Mato, et al. “Epistatic Interactions in the Arabinose Cis-Regulatory
Element.” Molecular Biology and Evolution, vol. 33, no. 3, Oxford University
Press, 2016, pp. 761–69, doi:10.1093/molbev/msv269.
short: M. Lagator, C. Igler, A. Moreno, C.C. Guet, J.P. Bollback, Molecular Biology
and Evolution 33 (2016) 761–769.
date_created: 2018-12-11T11:51:57Z
date_published: 2016-03-01T00:00:00Z
date_updated: 2021-01-12T06:50:39Z
day: '01'
ddc:
- '570'
- '576'
department:
- _id: CaGu
- _id: JoBo
doi: 10.1093/molbev/msv269
ec_funded: 1
file:
- access_level: open_access
checksum: 1f456ce1d2aa2f67176a1709f9702ecf
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:09:27Z
date_updated: 2020-07-14T12:44:53Z
file_id: '4751'
file_name: IST-2016-588-v1+1_Mol_Biol_Evol-2016-Lagator-761-9.pdf
file_size: 648115
relation: main_file
file_date_updated: 2020-07-14T12:44:53Z
has_accepted_license: '1'
intvolume: ' 33'
issue: '3'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
page: 761 - 769
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
publication: Molecular Biology and Evolution
publication_status: published
publisher: Oxford University Press
publist_id: '5772'
pubrep_id: '588'
quality_controlled: '1'
scopus_import: 1
status: public
title: Epistatic interactions in the arabinose cis-regulatory element
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 33
year: '2016'
...
---
_id: '9864'
abstract:
- lang: eng
text: Viral capsids are structurally constrained by interactions among the amino
acids (AAs) of their constituent proteins. Therefore, epistasis is expected to
evolve among physically interacting sites and to influence the rates of substitution.
To study the evolution of epistasis, we focused on the major structural protein
of the ϕX174 phage family by, first, reconstructing the ancestral protein sequences
of 18 species using a Bayesian statistical framework. The inferred ancestral reconstruction
differed at eight AAs, for a total of 256 possible ancestral haplotypes. For each
ancestral haplotype and the extant species, we estimated, in silico, the distribution
of free energies and epistasis of the capsid structure. We found that free energy
has not significantly increased but epistasis has. We decomposed epistasis up
to fifth order and found that higher-order epistasis sometimes compensates pairwise
interactions making the free energy seem additive. The dN/dS ratio is low, suggesting
strong purifying selection, and that structure is under stabilizing selection.
We synthesized phages carrying ancestral haplotypes of the coat protein gene and
measured their fitness experimentally. Our findings indicate that stabilizing
mutations can have higher fitness, and that fitness optima do not necessarily
coincide with energy minima.
article_processing_charge: No
author:
- first_name: Rodrigo A
full_name: Fernandes Redondo, Rodrigo A
id: 409D5C96-F248-11E8-B48F-1D18A9856A87
last_name: Fernandes Redondo
orcid: 0000-0002-5837-2793
- first_name: Harold
full_name: de Vladar, Harold
id: 2A181218-F248-11E8-B48F-1D18A9856A87
last_name: de Vladar
orcid: 0000-0002-5985-7653
- first_name: Tomasz
full_name: Włodarski, Tomasz
last_name: Włodarski
- first_name: Jonathan P
full_name: Bollback, Jonathan P
id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
last_name: Bollback
orcid: 0000-0002-4624-4612
citation:
ama: Fernandes Redondo RA, de Vladar H, Włodarski T, Bollback JP. Data from evolutionary
interplay between structure, energy and epistasis in the coat protein of the ϕX174
phage family. 2016. doi:10.6084/m9.figshare.4315652.v1
apa: Fernandes Redondo, R. A., de Vladar, H., Włodarski, T., & Bollback, J.
P. (2016). Data from evolutionary interplay between structure, energy and epistasis
in the coat protein of the ϕX174 phage family. The Royal Society. https://doi.org/10.6084/m9.figshare.4315652.v1
chicago: Fernandes Redondo, Rodrigo A, Harold de Vladar, Tomasz Włodarski, and Jonathan
P Bollback. “Data from Evolutionary Interplay between Structure, Energy and Epistasis
in the Coat Protein of the ΦX174 Phage Family.” The Royal Society, 2016. https://doi.org/10.6084/m9.figshare.4315652.v1.
ieee: R. A. Fernandes Redondo, H. de Vladar, T. Włodarski, and J. P. Bollback, “Data
from evolutionary interplay between structure, energy and epistasis in the coat
protein of the ϕX174 phage family.” The Royal Society, 2016.
ista: Fernandes Redondo RA, de Vladar H, Włodarski T, Bollback JP. 2016. Data from
evolutionary interplay between structure, energy and epistasis in the coat protein
of the ϕX174 phage family, The Royal Society, 10.6084/m9.figshare.4315652.v1.
mla: Fernandes Redondo, Rodrigo A., et al. Data from Evolutionary Interplay between
Structure, Energy and Epistasis in the Coat Protein of the ΦX174 Phage Family.
The Royal Society, 2016, doi:10.6084/m9.figshare.4315652.v1.
short: R.A. Fernandes Redondo, H. de Vladar, T. Włodarski, J.P. Bollback, (2016).
date_created: 2021-08-10T08:29:47Z
date_published: 2016-12-14T00:00:00Z
date_updated: 2025-05-28T11:57:06Z
day: '14'
department:
- _id: NiBa
- _id: JoBo
doi: 10.6084/m9.figshare.4315652.v1
main_file_link:
- open_access: '1'
url: https://doi.org/10.6084/m9.figshare.4315652.v1
month: '12'
oa: 1
oa_version: Published Version
publisher: The Royal Society
related_material:
record:
- id: '1077'
relation: used_in_publication
status: public
status: public
title: Data from evolutionary interplay between structure, energy and epistasis in
the coat protein of the ϕX174 phage family
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2016'
...
---
_id: '2042'
abstract:
- lang: eng
text: 'Background: CRISPR is a microbial immune system likely to be involved in
host-parasite coevolution. It functions using target sequences encoded by the
bacterial genome, which interfere with invading nucleic acids using a homology-dependent
system. The system also requires protospacer associated motifs (PAMs), short motifs
close to the target sequence that are required for interference in CRISPR types
I and II. Here, we investigate whether PAMs are depleted in phage genomes due
to selection pressure to escape recognition.Results: To this end, we analyzed
two data sets. Phages infecting all bacterial hosts were analyzed first, followed
by a detailed analysis of phages infecting the genus Streptococcus, where PAMs
are best understood. We use two different measures of motif underrepresentation
that control for codon bias and the frequency of submotifs. We compare phages
infecting species with a particular CRISPR type to those infecting species without
that type. Since only known PAMs were investigated, the analysis is restricted
to CRISPR types I-C and I-E and in Streptococcus to types I-C and II. We found
evidence for PAM depletion in Streptococcus phages infecting hosts with CRISPR
type I-C, in Vibrio phages infecting hosts with CRISPR type I-E and in Streptococcus
thermopilus phages infecting hosts with type II-A, known as CRISPR3.Conclusions:
The observed motif depletion in phages with hosts having CRISPR can be attributed
to selection rather than to mutational bias, as mutational bias should affect
the phages of all hosts. This observation implies that the CRISPR system has been
efficient in the groups discussed here.'
article_number: '663'
author:
- first_name: Anne
full_name: Kupczok, Anne
id: 2BB22BC2-F248-11E8-B48F-1D18A9856A87
last_name: Kupczok
- 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: Kupczok A, Bollback JP. Motif depletion in bacteriophages infecting hosts with
CRISPR systems. BMC Genomics. 2014;15(1). doi:10.1186/1471-2164-15-663
apa: Kupczok, A., & Bollback, J. P. (2014). Motif depletion in bacteriophages
infecting hosts with CRISPR systems. BMC Genomics. BioMed Central. https://doi.org/10.1186/1471-2164-15-663
chicago: Kupczok, Anne, and Jonathan P Bollback. “Motif Depletion in Bacteriophages
Infecting Hosts with CRISPR Systems.” BMC Genomics. BioMed Central, 2014.
https://doi.org/10.1186/1471-2164-15-663.
ieee: A. Kupczok and J. P. Bollback, “Motif depletion in bacteriophages infecting
hosts with CRISPR systems,” BMC Genomics, vol. 15, no. 1. BioMed Central,
2014.
ista: Kupczok A, Bollback JP. 2014. Motif depletion in bacteriophages infecting
hosts with CRISPR systems. BMC Genomics. 15(1), 663.
mla: Kupczok, Anne, and Jonathan P. Bollback. “Motif Depletion in Bacteriophages
Infecting Hosts with CRISPR Systems.” BMC Genomics, vol. 15, no. 1, 663,
BioMed Central, 2014, doi:10.1186/1471-2164-15-663.
short: A. Kupczok, J.P. Bollback, BMC Genomics 15 (2014).
date_created: 2018-12-11T11:55:23Z
date_published: 2014-08-08T00:00:00Z
date_updated: 2021-01-12T06:54:56Z
day: '08'
ddc:
- '570'
department:
- _id: JoBo
doi: 10.1186/1471-2164-15-663
file:
- access_level: open_access
checksum: 3f6d2776b90a842a28359cc957d3d04b
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:11:24Z
date_updated: 2020-07-14T12:45:26Z
file_id: '4878'
file_name: IST-2015-396-v1+1_1471-2164-15-663.pdf
file_size: 1489769
relation: main_file
file_date_updated: 2020-07-14T12:45:26Z
has_accepted_license: '1'
intvolume: ' 15'
issue: '1'
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
publication: BMC Genomics
publication_status: published
publisher: BioMed Central
publist_id: '5009'
pubrep_id: '396'
quality_controlled: '1'
scopus_import: 1
status: public
title: Motif depletion in bacteriophages infecting hosts with CRISPR systems
tmp:
image: /images/cc_0.png
legal_code_url: https://creativecommons.org/publicdomain/zero/1.0/legalcode
name: Creative Commons Public Domain Dedication (CC0 1.0)
short: CC0 (1.0)
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 15
year: '2014'
...
---
_id: '2410'
abstract:
- lang: eng
text: 'Here, we describe a novel virulent bacteriophage that infects Bacillus weihenstephanensis,
isolated from soil in Austria. It is the first phage to be discovered that infects
this species. Here, we present the complete genome sequence of this podovirus. '
author:
- first_name: Rodrigo A
full_name: Fernandes Redondo, Rodrigo A
id: 409D5C96-F248-11E8-B48F-1D18A9856A87
last_name: Fernandes Redondo
orcid: 0000-0002-5837-2793
- first_name: Anne
full_name: Kupczok, Anne
id: 2BB22BC2-F248-11E8-B48F-1D18A9856A87
last_name: Kupczok
- first_name: Gertraud
full_name: Stift, Gertraud
id: 2DB195CA-F248-11E8-B48F-1D18A9856A87
last_name: Stift
- first_name: Jonathan P
full_name: Bollback, Jonathan P
id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
last_name: Bollback
orcid: 0000-0002-4624-4612
citation:
ama: Fernandes Redondo RA, Kupczok A, Stift G, Bollback JP. Complete genome sequence
of the novel phage MG-B1 infecting bacillus weihenstephanensis. Genome Announcements.
2013;1(3). doi:10.1128/genomeA.00216-13
apa: Fernandes Redondo, R. A., Kupczok, A., Stift, G., & Bollback, J. P. (2013).
Complete genome sequence of the novel phage MG-B1 infecting bacillus weihenstephanensis.
Genome Announcements. American Society for Microbiology. https://doi.org/10.1128/genomeA.00216-13
chicago: Fernandes Redondo, Rodrigo A, Anne Kupczok, Gertraud Stift, and Jonathan
P Bollback. “Complete Genome Sequence of the Novel Phage MG-B1 Infecting Bacillus
Weihenstephanensis.” Genome Announcements. American Society for Microbiology,
2013. https://doi.org/10.1128/genomeA.00216-13.
ieee: R. A. Fernandes Redondo, A. Kupczok, G. Stift, and J. P. Bollback, “Complete
genome sequence of the novel phage MG-B1 infecting bacillus weihenstephanensis,”
Genome Announcements, vol. 1, no. 3. American Society for Microbiology,
2013.
ista: Fernandes Redondo RA, Kupczok A, Stift G, Bollback JP. 2013. Complete genome
sequence of the novel phage MG-B1 infecting bacillus weihenstephanensis. Genome
Announcements. 1(3).
mla: Fernandes Redondo, Rodrigo A., et al. “Complete Genome Sequence of the Novel
Phage MG-B1 Infecting Bacillus Weihenstephanensis.” Genome Announcements,
vol. 1, no. 3, American Society for Microbiology, 2013, doi:10.1128/genomeA.00216-13.
short: R.A. Fernandes Redondo, A. Kupczok, G. Stift, J.P. Bollback, Genome Announcements
1 (2013).
date_created: 2018-12-11T11:57:30Z
date_published: 2013-06-13T00:00:00Z
date_updated: 2021-01-12T06:57:19Z
day: '13'
ddc:
- '576'
department:
- _id: JoBo
- _id: LifeSc
doi: 10.1128/genomeA.00216-13
file:
- access_level: open_access
checksum: 0751ec74b695567e0cdf02aaf9c26829
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:17:36Z
date_updated: 2020-07-14T12:45:40Z
file_id: '5291'
file_name: IST-2015-398-v1+1_Genome_Announc.-2013-Redondo-.pdf
file_size: 130026
relation: main_file
file_date_updated: 2020-07-14T12:45:40Z
has_accepted_license: '1'
intvolume: ' 1'
issue: '3'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
publication: Genome Announcements
publication_status: published
publisher: American Society for Microbiology
publist_id: '4516'
pubrep_id: '398'
quality_controlled: '1'
scopus_import: 1
status: public
title: Complete genome sequence of the novel phage MG-B1 infecting bacillus weihenstephanensis
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 1
year: '2013'
...
---
_id: '2412'
abstract:
- lang: eng
text: 'Background: The CRISPR/Cas system is known to act as an adaptive and heritable
immune system in Eubacteria and Archaea. Immunity is encoded in an array of spacer
sequences. Each spacer can provide specific immunity to invasive elements that
carry the same or a similar sequence. Even in closely related strains, spacer
content is very dynamic and evolves quickly. Standard models of nucleotide evolutioncannot
be applied to quantify its rate of change since processes other than single nucleotide
changes determine its evolution.Methods We present probabilistic models that are
specific for spacer content evolution. They account for the different processes
of insertion and deletion. Insertions can be constrained to occur on one end only
or are allowed to occur throughout the array. One deletion event can affect one
spacer or a whole fragment of adjacent spacers. Parameters of the underlying models
are estimated for a pair of arrays by maximum likelihood using explicit ancestor
enumeration.Results Simulations show that parameters are well estimated on average
under the models presented here. There is a bias in the rate estimation when including
fragment deletions. The models also estimate times between pairs of strains. But
with increasing time, spacer overlap goes to zero, and thus there is an upper
bound on the distance that can be estimated. Spacer content similarities are displayed
in a distance based phylogeny using the estimated times.We use the presented models
to analyze different Yersinia pestis data sets and find that the results among
them are largely congruent. The models also capture the variation in diversity
of spacers among the data sets. A comparison of spacer-based phylogenies and Cas
gene phylogenies shows that they resolve very different time scales for this data
set.Conclusions The simulations and data analyses show that the presented models
are useful for quantifying spacer content evolution and for displaying spacer
content similarities of closely related strains in a phylogeny. This allows for
comparisons of different CRISPR arrays or for comparisons between CRISPR arrays
and nucleotide substitution rates.'
author:
- first_name: Anne
full_name: Kupczok, Anne
id: 2BB22BC2-F248-11E8-B48F-1D18A9856A87
last_name: Kupczok
- 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: Kupczok A, Bollback JP. Probabilistic models for CRISPR spacer content evolution
. BMC Evolutionary Biology. 2013;13(1):54-54. doi:10.1186/1471-2148-13-54
apa: Kupczok, A., & Bollback, J. P. (2013). Probabilistic models for CRISPR
spacer content evolution . BMC Evolutionary Biology. BioMed Central. https://doi.org/10.1186/1471-2148-13-54
chicago: Kupczok, Anne, and Jonathan P Bollback. “Probabilistic Models for CRISPR
Spacer Content Evolution .” BMC Evolutionary Biology. BioMed Central, 2013.
https://doi.org/10.1186/1471-2148-13-54.
ieee: A. Kupczok and J. P. Bollback, “Probabilistic models for CRISPR spacer content
evolution ,” BMC Evolutionary Biology, vol. 13, no. 1. BioMed Central,
pp. 54–54, 2013.
ista: Kupczok A, Bollback JP. 2013. Probabilistic models for CRISPR spacer content
evolution . BMC Evolutionary Biology. 13(1), 54–54.
mla: Kupczok, Anne, and Jonathan P. Bollback. “Probabilistic Models for CRISPR Spacer
Content Evolution .” BMC Evolutionary Biology, vol. 13, no. 1, BioMed Central,
2013, pp. 54–54, doi:10.1186/1471-2148-13-54.
short: A. Kupczok, J.P. Bollback, BMC Evolutionary Biology 13 (2013) 54–54.
date_created: 2018-12-11T11:57:31Z
date_published: 2013-02-26T00:00:00Z
date_updated: 2021-01-12T06:57:20Z
day: '26'
ddc:
- '576'
department:
- _id: JoBo
doi: 10.1186/1471-2148-13-54
file:
- access_level: open_access
checksum: 029c7e0b198c19312b66ecce3cabb22f
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:17:15Z
date_updated: 2020-07-14T12:45:40Z
file_id: '5268'
file_name: IST-2015-397-v1+1_1471-2148-13-54.pdf
file_size: 518729
relation: main_file
file_date_updated: 2020-07-14T12:45:40Z
has_accepted_license: '1'
intvolume: ' 13'
issue: '1'
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
page: 54 - 54
publication: BMC Evolutionary Biology
publication_status: published
publisher: BioMed Central
publist_id: '4514'
pubrep_id: '397'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'Probabilistic models for CRISPR spacer content evolution '
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 13
year: '2013'
...
---
_id: '500'
abstract:
- lang: eng
text: 'Background: Reassortment between the RNA segments encoding haemagglutinin
(HA) and neuraminidase (NA), the major antigenic influenza proteins, produces
viruses with novel HA and NA subtype combinations and has preceded the emergence
of pandemic strains. It has been suggested that productive viral infection requires
a balance in the level of functional activity of HA and NA, arising from their
closely interacting roles in the viral life cycle, and that this functional balance
could be mediated by genetic changes in the HA and NA. Here, we investigate how
the selective pressure varies for H7 avian influenza HA on different NA subtype
backgrounds. Results: By extending Bayesian stochastic mutational mapping methods
to calculate the ratio of the rate of non-synonymous change to the rate of synonymous
change (d N/d S), we found the average d N/d S across the avian influenza H7 HA1
region to be significantly greater on an N2 NA subtype background than on an N1,
N3 or N7 background. Observed differences in evolutionary rates of H7 HA on different
NA subtype backgrounds could not be attributed to underlying differences between
avian host species or virus pathogenicity. Examination of d N/d S values for each
subtype on a site-by-site basis indicated that the elevated d N/d S on the N2
NA background was a result of increased selection, rather than a relaxation of
selective constraint. Conclusions: Our results are consistent with the hypothesis
that reassortment exposes influenza HA to significant changes in selective pressure
through genetic interactions with NA. Such epistatic effects might be explicitly
accounted for in future models of influenza evolution.'
acknowledgement: "This work was supported by the Biotechnology and Biological Sciences
Research Council, the Government of the Republic of Panama, the Interdisciplinary
Centre for Human and Avian Influenza Research (www.ichair-flu.org) funded by the
Scottish Funding Council, and the Institute for Science and Technology Austria.\r\nCC
BY 2.0\r\n"
article_number: '222'
author:
- first_name: Melissa
full_name: Ward, Melissa
last_name: Ward
- first_name: Samantha
full_name: Lycett, Samantha
last_name: Lycett
- first_name: Dorita
full_name: Avila, Dorita
last_name: Avila
- 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: Andrew
full_name: Leigh Brown, Andrew
last_name: Leigh Brown
citation:
ama: Ward M, Lycett S, Avila D, Bollback JP, Leigh Brown A. Evolutionary interactions
between haemagglutinin and neuraminidase in avian influenza. BMC Evolutionary
Biology. 2013;13(1). doi:10.1186/1471-2148-13-222
apa: Ward, M., Lycett, S., Avila, D., Bollback, J. P., & Leigh Brown, A. (2013).
Evolutionary interactions between haemagglutinin and neuraminidase in avian influenza.
BMC Evolutionary Biology. BioMed Central. https://doi.org/10.1186/1471-2148-13-222
chicago: Ward, Melissa, Samantha Lycett, Dorita Avila, Jonathan P Bollback, and
Andrew Leigh Brown. “Evolutionary Interactions between Haemagglutinin and Neuraminidase
in Avian Influenza.” BMC Evolutionary Biology. BioMed Central, 2013. https://doi.org/10.1186/1471-2148-13-222.
ieee: M. Ward, S. Lycett, D. Avila, J. P. Bollback, and A. Leigh Brown, “Evolutionary
interactions between haemagglutinin and neuraminidase in avian influenza,” BMC
Evolutionary Biology, vol. 13, no. 1. BioMed Central, 2013.
ista: Ward M, Lycett S, Avila D, Bollback JP, Leigh Brown A. 2013. Evolutionary
interactions between haemagglutinin and neuraminidase in avian influenza. BMC
Evolutionary Biology. 13(1), 222.
mla: Ward, Melissa, et al. “Evolutionary Interactions between Haemagglutinin and
Neuraminidase in Avian Influenza.” BMC Evolutionary Biology, vol. 13, no.
1, 222, BioMed Central, 2013, doi:10.1186/1471-2148-13-222.
short: M. Ward, S. Lycett, D. Avila, J.P. Bollback, A. Leigh Brown, BMC Evolutionary
Biology 13 (2013).
date_created: 2018-12-11T11:46:49Z
date_published: 2013-10-09T00:00:00Z
date_updated: 2021-01-12T08:01:08Z
day: '09'
ddc:
- '576'
department:
- _id: JoBo
doi: 10.1186/1471-2148-13-222
file:
- access_level: open_access
checksum: 52cf48a7c1794676ae8b0029573a84a9
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:08:59Z
date_updated: 2020-07-14T12:46:36Z
file_id: '4722'
file_name: IST-2018-941-v1+1_2013_Bollback_Evolutionary_interactionspdf.pdf
file_size: 1150052
relation: main_file
file_date_updated: 2020-07-14T12:46:36Z
has_accepted_license: '1'
intvolume: ' 13'
issue: '1'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
publication: BMC Evolutionary Biology
publication_status: published
publisher: BioMed Central
publist_id: '7320'
pubrep_id: '941'
quality_controlled: '1'
scopus_import: 1
status: public
title: Evolutionary interactions between haemagglutinin and neuraminidase in avian
influenza
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 13
year: '2013'
...
---
_id: '4358'
abstract:
- lang: eng
text: Phenotypic biotyping has traditionally been used to differentiate bacteria
occupying distinct ecological niches such as host species. For example, the capacity
of Staphylococcus aureus from sheep to coagulate ruminant plasma, reported over
60 years ago, led to the description of small ruminant and bovine S. aureus ecovars.
The great majority of small ruminant isolates are represented by a single, widespread
clonal complex (CC133) of S. aureus, but its evolutionary origin and the molecular
basis for its host tropism remain unknown. Here, we provide evidence that the
CC133 clone evolved as the result of a human to ruminant host jump followed by
adaptive genome diversification. Comparative whole-genome sequencing revealed
molecular evidence for host adaptation including gene decay and diversification
of proteins involved in host-pathogen interactions. Importantly, several novel
mobile genetic elements encoding virulence proteins with attenuated or enhanced
activity in ruminants were widely distributed in CC133 isolates, suggesting a
key role in its host-specific interactions. To investigate this further, we examined
the activity of a novel staphylococcal pathogenicity island (SaPIov2) found in
the great majority of CC133 isolates which encodes a variant of the chromosomally
encoded von Willebrand-binding protein (vWbp(Sov2)), previously demonstrated to
have coagulase activity for human plasma. Remarkably, we discovered that SaPIov2
confers the ability to coagulate ruminant plasma suggesting an important role
in ruminant disease pathogenesis and revealing the origin of a defining phenotype
of the classical S. aureus biotyping scheme. Taken together, these data provide
broad new insights into the origin and molecular basis of S. aureus ruminant host
specificity.
author:
- first_name: Caitriona
full_name: Guinane, Caitriona M
last_name: Guinane
- first_name: Nouri
full_name: Ben Zakour, Nouri L
last_name: Ben Zakour
- first_name: Maria
full_name: Tormo-Mas, Maria A
last_name: Tormo Mas
- first_name: Lucy
full_name: Weinert, Lucy A
last_name: Weinert
- first_name: Bethan
full_name: Lowder, Bethan V
last_name: Lowder
- first_name: Robyn
full_name: Cartwright, Robyn A
last_name: Cartwright
- first_name: Davida
full_name: Smyth, Davida S
last_name: Smyth
- first_name: Cyril
full_name: Smyth, Cyril J
last_name: Smyth
- first_name: Jodi
full_name: Lindsay, Jodi A
last_name: Lindsay
- first_name: Katherine
full_name: Gould, Katherine A
last_name: Gould
- first_name: Adam
full_name: Witney, Adam
last_name: Witney
- first_name: Jason
full_name: Hinds, Jason
last_name: Hinds
- first_name: Jonathan P
full_name: Jonathan Bollback
id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
last_name: Bollback
orcid: 0000-0002-4624-4612
- first_name: Andrew
full_name: Rambaut, Andrew
last_name: Rambaut
- first_name: Jose
full_name: Penades, Jose R
last_name: Penades
- first_name: J Ross
full_name: Fitzgerald, J Ross
last_name: Fitzgerald
citation:
ama: Guinane C, Ben Zakour N, Tormo Mas M, et al. Evolutionary genomics of Staphylococcus
aureus reveals insights into the origin and molecular basis of ruminant host adaptation.
Genome Biology and Evolution. 2010;2:454-466. doi:10.1093/gbe/evq031
apa: Guinane, C., Ben Zakour, N., Tormo Mas, M., Weinert, L., Lowder, B., Cartwright,
R., … Fitzgerald, J. R. (2010). Evolutionary genomics of Staphylococcus aureus
reveals insights into the origin and molecular basis of ruminant host adaptation.
Genome Biology and Evolution. Oxford University Press. https://doi.org/10.1093/gbe/evq031
chicago: Guinane, Caitriona, Nouri Ben Zakour, Maria Tormo Mas, Lucy Weinert, Bethan
Lowder, Robyn Cartwright, Davida Smyth, et al. “Evolutionary Genomics of Staphylococcus
Aureus Reveals Insights into the Origin and Molecular Basis of Ruminant Host Adaptation.”
Genome Biology and Evolution. Oxford University Press, 2010. https://doi.org/10.1093/gbe/evq031.
ieee: C. Guinane et al., “Evolutionary genomics of Staphylococcus aureus
reveals insights into the origin and molecular basis of ruminant host adaptation,”
Genome Biology and Evolution, vol. 2. Oxford University Press, pp. 454–466,
2010.
ista: Guinane C, Ben Zakour N, Tormo Mas M, Weinert L, Lowder B, Cartwright R, Smyth
D, Smyth C, Lindsay J, Gould K, Witney A, Hinds J, Bollback JP, Rambaut A, Penades
J, Fitzgerald JR. 2010. Evolutionary genomics of Staphylococcus aureus reveals
insights into the origin and molecular basis of ruminant host adaptation. Genome
Biology and Evolution. 2, 454–466.
mla: Guinane, Caitriona, et al. “Evolutionary Genomics of Staphylococcus Aureus
Reveals Insights into the Origin and Molecular Basis of Ruminant Host Adaptation.”
Genome Biology and Evolution, vol. 2, Oxford University Press, 2010, pp.
454–66, doi:10.1093/gbe/evq031.
short: C. Guinane, N. Ben Zakour, M. Tormo Mas, L. Weinert, B. Lowder, R. Cartwright,
D. Smyth, C. Smyth, J. Lindsay, K. Gould, A. Witney, J. Hinds, J.P. Bollback,
A. Rambaut, J. Penades, J.R. Fitzgerald, Genome Biology and Evolution 2 (2010)
454–466.
date_created: 2018-12-11T12:08:27Z
date_published: 2010-06-09T00:00:00Z
date_updated: 2021-01-12T07:56:23Z
day: '09'
doi: 10.1093/gbe/evq031
extern: 1
intvolume: ' 2'
month: '06'
page: 454 - 466
publication: Genome Biology and Evolution
publication_status: published
publisher: Oxford University Press
publist_id: '1100'
quality_controlled: 0
status: public
title: Evolutionary genomics of Staphylococcus aureus reveals insights into the origin
and molecular basis of ruminant host adaptation
type: journal_article
volume: 2
year: '2010'
...
---
_id: '4357'
abstract:
- lang: eng
text: Parallel evolution is the acquisition of identical adaptive traits in independently
evolving populations. Understanding whether the genetic changes underlying adaptation
to a common selective environment are parallel within and between species is interesting
because it sheds light on the degree of evolutionary constraints. If parallel
evolution is perfect, then the implication is that forces such as functional constraints,
epistasis, and pleiotropy play an important role in shaping the outcomes of adaptive
evolution. In addition, population genetic theory predicts that the probability
of parallel evolution will decline with an increase in the number of adaptive
solutions-if a single adaptive solution exists, then parallel evolution will be
observed among highly divergent species. For this reason, it is predicted that
close relatives-which likely overlap more in the details of their adaptive solutions-will
show more parallel evolution. By adapting three related bacteriophage species
to a novel environment we find (1) a high rate of parallel genetic evolution at
orthologous nucleotide and amino acid residues within species, (2) parallel beneficial
mutations do not occur in a common order in which they fix or appear in an evolving
population, (3) low rates of parallel evolution and convergent evolution between
species, and (4) the probability of parallel and convergent evolution between
species is strongly effected by divergence.
author:
- first_name: Jonathan P
full_name: Jonathan Bollback
id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
last_name: Bollback
orcid: 0000-0002-4624-4612
- first_name: John
full_name: Huelsenbeck, John P
last_name: Huelsenbeck
citation:
ama: Bollback JP, Huelsenbeck J. Parallel genetic evolution within and between bacteriophage
species of varying degrees of divergence. Genetics. 2009;181(1):225-234.
doi:10.1534/genetics.107.085225
apa: Bollback, J. P., & Huelsenbeck, J. (2009). Parallel genetic evolution within
and between bacteriophage species of varying degrees of divergence. Genetics.
Genetics Society of America. https://doi.org/10.1534/genetics.107.085225
chicago: Bollback, Jonathan P, and John Huelsenbeck. “Parallel Genetic Evolution
within and between Bacteriophage Species of Varying Degrees of Divergence.” Genetics.
Genetics Society of America, 2009. https://doi.org/10.1534/genetics.107.085225.
ieee: J. P. Bollback and J. Huelsenbeck, “Parallel genetic evolution within and
between bacteriophage species of varying degrees of divergence,” Genetics,
vol. 181, no. 1. Genetics Society of America, pp. 225–234, 2009.
ista: Bollback JP, Huelsenbeck J. 2009. Parallel genetic evolution within and between
bacteriophage species of varying degrees of divergence. Genetics. 181(1), 225–234.
mla: Bollback, Jonathan P., and John Huelsenbeck. “Parallel Genetic Evolution within
and between Bacteriophage Species of Varying Degrees of Divergence.” Genetics,
vol. 181, no. 1, Genetics Society of America, 2009, pp. 225–34, doi:10.1534/genetics.107.085225.
short: J.P. Bollback, J. Huelsenbeck, Genetics 181 (2009) 225–234.
date_created: 2018-12-11T12:08:26Z
date_published: 2009-01-01T00:00:00Z
date_updated: 2021-01-12T07:56:22Z
day: '01'
doi: 10.1534/genetics.107.085225
extern: 1
intvolume: ' 181'
issue: '1'
month: '01'
page: 225 - 234
publication: Genetics
publication_status: published
publisher: Genetics Society of America
publist_id: '1101'
quality_controlled: 0
status: public
title: Parallel genetic evolution within and between bacteriophage species of varying
degrees of divergence
type: journal_article
volume: 181
year: '2009'
...
---
_id: '3435'
abstract:
- lang: eng
text: We develop a new method for estimating effective population sizes, Ne, and
selection coefficients, s, from time-series data of allele frequencies sampled
from a single diallelic locus. The method is based on calculating transition probabilities,
using a numerical solution of the diffusion process, and assuming independent
binomial sampling from this diffusion process at each time point. We apply the
method in two example applications. First, we estimate selection coefficients
acting on the CCR5-Δ32 mutation on the basis of published samples of contemporary
and ancient human DNA. We show that the data are compatible with the assumption
of s = 0, although moderate amounts of selection acting on this mutation cannot
be excluded. In our second example, we estimate the selection coefficient acting
on a mutation segregating in an experimental phage population. We show that the
selection coefficient acting on this mutation is ~0.43.
author:
- first_name: Jonathan P
full_name: Jonathan Bollback
id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
last_name: Bollback
orcid: 0000-0002-4624-4612
- first_name: Thomas
full_name: York, Thomas L
last_name: York
- first_name: Rasmus
full_name: Nielsen, Rasmus
last_name: Nielsen
citation:
ama: Bollback JP, York T, Nielsen R. Estimation of 2Nes From Temporal Allele Frequency
Data. Genetics. 2008;179(1):497-502. doi:10.1534/genetics.107.085019
apa: Bollback, J. P., York, T., & Nielsen, R. (2008). Estimation of 2Nes From
Temporal Allele Frequency Data. Genetics. Genetics Society of America.
https://doi.org/10.1534/genetics.107.085019
chicago: Bollback, Jonathan P, Thomas York, and Rasmus Nielsen. “Estimation of 2Nes
From Temporal Allele Frequency Data.” Genetics. Genetics Society of America,
2008. https://doi.org/10.1534/genetics.107.085019.
ieee: J. P. Bollback, T. York, and R. Nielsen, “Estimation of 2Nes From Temporal
Allele Frequency Data,” Genetics, vol. 179, no. 1. Genetics Society of
America, pp. 497–502, 2008.
ista: Bollback JP, York T, Nielsen R. 2008. Estimation of 2Nes From Temporal Allele
Frequency Data. Genetics. 179(1), 497–502.
mla: Bollback, Jonathan P., et al. “Estimation of 2Nes From Temporal Allele Frequency
Data.” Genetics, vol. 179, no. 1, Genetics Society of America, 2008, pp.
497–502, doi:10.1534/genetics.107.085019.
short: J.P. Bollback, T. York, R. Nielsen, Genetics 179 (2008) 497–502.
date_created: 2018-12-11T12:03:19Z
date_published: 2008-05-01T00:00:00Z
date_updated: 2021-01-12T07:43:27Z
day: '01'
doi: 10.1534/genetics.107.085019
extern: 1
intvolume: ' 179'
issue: '1'
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2390626
month: '05'
oa: 1
page: 497 - 502
publication: Genetics
publication_status: published
publisher: Genetics Society of America
publist_id: '2965'
quality_controlled: 0
status: public
title: Estimation of 2Nes From Temporal Allele Frequency Data
type: journal_article
volume: 179
year: '2008'
...
---
_id: '3432'
abstract:
- lang: eng
text: Evolution has left its signature on the molecules and morphology of living
organisms. Ancestral reconstruction offers an excellent tool for understanding
the process of evolution using comparative information. Methods for ancestral
reconstruction have generally focused on reconstructing the ancestral states at
the internal nodes of a phylogeny. Often, we are not interested in particular
nodes of the phylogeny but the whole history of a character. This chapter focuses
on a Bayesian method for estimating these histories, or mutational paths, on phylogenies.
Mutational path methods differ most notably from other approaches in their ability
to estimate not only the ancestral states at the internal nodes of a phylogeny,
but also the order and timing of mutational changes across the phylogeny. The
chapter provides a concise introduction to the statistical tools needed for sampling
mutational paths on a phylogeny.
author:
- first_name: Jonathan P
full_name: Jonathan Bollback
id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
last_name: Bollback
orcid: 0000-0002-4624-4612
- first_name: Paul
full_name: Gardner, Paul P
last_name: Gardner
- first_name: Rasmus
full_name: Nielsen, Rasmus
last_name: Nielsen
citation:
ama: 'Bollback JP, Gardner P, Nielsen R. Estimating the history of mutations on
a phylogeny. In: Liberles D, ed. Ancestral Sequence Reconstruction. Oxford
University Press; 2007:69-79. doi:10.1093/acprof:oso/9780199299188.003.0006'
apa: Bollback, J. P., Gardner, P., & Nielsen, R. (2007). Estimating the history
of mutations on a phylogeny. In D. Liberles (Ed.), Ancestral Sequence Reconstruction
(pp. 69–79). Oxford University Press. https://doi.org/10.1093/acprof:oso/9780199299188.003.0006
chicago: Bollback, Jonathan P, Paul Gardner, and Rasmus Nielsen. “Estimating the
History of Mutations on a Phylogeny.” In Ancestral Sequence Reconstruction,
edited by David Liberles, 69–79. Oxford University Press, 2007. https://doi.org/10.1093/acprof:oso/9780199299188.003.0006.
ieee: J. P. Bollback, P. Gardner, and R. Nielsen, “Estimating the history of mutations
on a phylogeny,” in Ancestral Sequence Reconstruction, D. Liberles, Ed.
Oxford University Press, 2007, pp. 69–79.
ista: 'Bollback JP, Gardner P, Nielsen R. 2007.Estimating the history of mutations
on a phylogeny. In: Ancestral Sequence Reconstruction. , 69–79.'
mla: Bollback, Jonathan P., et al. “Estimating the History of Mutations on a Phylogeny.”
Ancestral Sequence Reconstruction, edited by David Liberles, Oxford University
Press, 2007, pp. 69–79, doi:10.1093/acprof:oso/9780199299188.003.0006.
short: J.P. Bollback, P. Gardner, R. Nielsen, in:, D. Liberles (Ed.), Ancestral
Sequence Reconstruction, Oxford University Press, 2007, pp. 69–79.
date_created: 2018-12-11T12:03:18Z
date_published: 2007-01-01T00:00:00Z
date_updated: 2021-01-12T07:43:26Z
day: '01'
doi: 10.1093/acprof:oso/9780199299188.003.0006
editor:
- first_name: David
full_name: Liberles, David A
last_name: Liberles
extern: 1
month: '01'
page: 69 - 79
publication: Ancestral Sequence Reconstruction
publication_status: published
publisher: Oxford University Press
publist_id: '2968'
quality_controlled: 0
status: public
title: Estimating the history of mutations on a phylogeny
type: book_chapter
year: '2007'
...
---
_id: '3436'
abstract:
- lang: eng
text: 'he potential for di? erences between genetic paternity and paternity inferred
from behavioral observation has long been recognized. These di? erences are associated
with the challenge for females of seeking both genetic and material bene? ts;
this challenge is less severe in species with polygynous, non-resource-based mating
systems (such as leks) than in those with resource-based systems. We pres- ent
the ? rst study of paternity patt erns in a non-resource-based species that does
not form true leks. We compared paternity inferred from observed mating behavior
to genetically assigned paternity in the Satin Bowerbird (Ptilonorhynchus violaceus)
using eight microsatellite markers. Mating behavior was observed and recorded
via automated video-cameras positioned at all bowers (29?34 bowers each year)
in the study site throughout each mating season. We obtained blood samples and
identi- ? ed mothers for 11 chicks in 9 nests. For all chicks, the most likely
genetic father had been observed to mate with the mother in the year the chick
was sampled. All most likely genetic fathers were assigned with high con? dence
and all were bower- holding males. These results demonstrate that genetic paternity
can be inferred from observed mating behavior with reasonable con? dence in Satin
Bowerbirds. Observed male mating-success is therefore a reliable predictor of
reproductive success, and this suggests that high skew in observed male mating-success
translates directly to high skew in reproductive success. '
author:
- first_name: Sheila
full_name: Reynolds, Sheila M
last_name: Reynolds
- first_name: Katie
full_name: Dryer, Katie
last_name: Dryer
- first_name: Jonathan P
full_name: Jonathan Bollback
id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
last_name: Bollback
orcid: 0000-0002-4624-4612
- first_name: J Albert
full_name: Uy, J Albert
last_name: Uy
- first_name: Gail
full_name: Patricelli, Gail L
last_name: Patricelli
- first_name: Timothy
full_name: Robson, Timothy
last_name: Robson
- first_name: Gerald
full_name: Borgia, Gerald
last_name: Borgia
- first_name: Michael
full_name: Braun, Michael J
last_name: Braun
citation:
ama: Reynolds S, Dryer K, Bollback JP, et al. Behavioral paternity predicts genetic
paternity in satin bowerbirds, a species with a non-resource-based mating system.
The Auk. 2007;124(3):857-867. doi:10.1642/0004-8038(2007)124[857:BPPGPI]2.0.CO;2
apa: Reynolds, S., Dryer, K., Bollback, J. P., Uy, J. A., Patricelli, G., Robson,
T., … Braun, M. (2007). Behavioral paternity predicts genetic paternity in satin
bowerbirds, a species with a non-resource-based mating system. The Auk.
University of California Press. https://doi.org/10.1642/0004-8038(2007)124[857:BPPGPI]2.0.CO;2
chicago: Reynolds, Sheila, Katie Dryer, Jonathan P Bollback, J Albert Uy, Gail Patricelli,
Timothy Robson, Gerald Borgia, and Michael Braun. “Behavioral Paternity Predicts
Genetic Paternity in Satin Bowerbirds, a Species with a Non-Resource-Based Mating
System.” The Auk. University of California Press, 2007. https://doi.org/10.1642/0004-8038(2007)124[857:BPPGPI]2.0.CO;2.
ieee: S. Reynolds et al., “Behavioral paternity predicts genetic paternity
in satin bowerbirds, a species with a non-resource-based mating system,” The
Auk, vol. 124, no. 3. University of California Press, pp. 857–867, 2007.
ista: Reynolds S, Dryer K, Bollback JP, Uy JA, Patricelli G, Robson T, Borgia G,
Braun M. 2007. Behavioral paternity predicts genetic paternity in satin bowerbirds,
a species with a non-resource-based mating system. The Auk. 124(3), 857–867.
mla: Reynolds, Sheila, et al. “Behavioral Paternity Predicts Genetic Paternity in
Satin Bowerbirds, a Species with a Non-Resource-Based Mating System.” The Auk,
vol. 124, no. 3, University of California Press, 2007, pp. 857–67, doi:10.1642/0004-8038(2007)124[857:BPPGPI]2.0.CO;2.
short: S. Reynolds, K. Dryer, J.P. Bollback, J.A. Uy, G. Patricelli, T. Robson,
G. Borgia, M. Braun, The Auk 124 (2007) 857–867.
date_created: 2018-12-11T12:03:19Z
date_published: 2007-01-01T00:00:00Z
date_updated: 2021-01-12T07:43:27Z
day: '01'
doi: 10.1642/0004-8038(2007)124[857:BPPGPI]2.0.CO;2
extern: 1
intvolume: ' 124'
issue: '3'
month: '01'
page: 857 - 867
publication: The Auk
publication_status: published
publisher: University of California Press
publist_id: '2964'
quality_controlled: 0
status: public
title: Behavioral paternity predicts genetic paternity in satin bowerbirds, a species
with a non-resource-based mating system
type: journal_article
volume: 124
year: '2007'
...