---
_id: '9712'
article_processing_charge: No
author:
- first_name: Murat
full_name: Tugrul, Murat
id: 37C323C6-F248-11E8-B48F-1D18A9856A87
last_name: Tugrul
orcid: 0000-0002-8523-0758
- 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: Gašper
full_name: Tkačik, Gašper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkačik
orcid: 0000-0002-6699-1455
citation:
ama: Tugrul M, Paixao T, Barton NH, Tkačik G. Other fitness models for comparison
& for interacting TFBSs. 2015. doi:10.1371/journal.pgen.1005639.s001
apa: Tugrul, M., Paixao, T., Barton, N. H., & Tkačik, G. (2015). Other fitness
models for comparison & for interacting TFBSs. Public Library of Science.
https://doi.org/10.1371/journal.pgen.1005639.s001
chicago: Tugrul, Murat, Tiago Paixao, Nicholas H Barton, and Gašper Tkačik. “Other
Fitness Models for Comparison & for Interacting TFBSs.” Public Library of
Science, 2015. https://doi.org/10.1371/journal.pgen.1005639.s001.
ieee: M. Tugrul, T. Paixao, N. H. Barton, and G. Tkačik, “Other fitness models for
comparison & for interacting TFBSs.” Public Library of Science, 2015.
ista: Tugrul M, Paixao T, Barton NH, Tkačik G. 2015. Other fitness models for comparison
& for interacting TFBSs, Public Library of Science, 10.1371/journal.pgen.1005639.s001.
mla: Tugrul, Murat, et al. Other Fitness Models for Comparison & for Interacting
TFBSs. Public Library of Science, 2015, doi:10.1371/journal.pgen.1005639.s001.
short: M. Tugrul, T. Paixao, N.H. Barton, G. Tkačik, (2015).
date_created: 2021-07-23T12:00:37Z
date_published: 2015-11-06T00:00:00Z
date_updated: 2025-05-28T11:57:04Z
day: '06'
department:
- _id: NiBa
- _id: CaGu
- _id: GaTk
doi: 10.1371/journal.pgen.1005639.s001
month: '11'
oa_version: Published Version
publisher: Public Library of Science
related_material:
record:
- id: '1666'
relation: used_in_publication
status: public
status: public
title: Other fitness models for comparison & for interacting TFBSs
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2015'
...
---
_id: '9719'
abstract:
- lang: eng
text: Parasitism creates selection for resistance mechanisms in host populations
and is hypothesized to promote increased host evolvability. However, the influence
of these traits on host evolution when parasites are no longer present is unclear.
We used experimental evolution and whole-genome sequencing of Escherichia coli
to determine the effects of past and present exposure to parasitic viruses (phages)
on the spread of mutator alleles, resistance, and bacterial competitive fitness.
We found that mutator alleles spread rapidly during adaptation to any of four
different phage species, and this pattern was even more pronounced with multiple
phages present simultaneously. However, hypermutability did not detectably accelerate
adaptation in the absence of phages and recovery of fitness costs associated with
resistance. Several lineages evolved phage resistance through elevated mucoidy,
and during subsequent evolution in phage-free conditions they rapidly reverted
to nonmucoid, phage-susceptible phenotypes. Genome sequencing revealed that this
phenotypic reversion was achieved by additional genetic changes rather than by
genotypic reversion of the initial resistance mutations. Insertion sequence (IS)
elements played a key role in both the acquisition of resistance and adaptation
in the absence of parasites; unlike single nucleotide polymorphisms, IS insertions
were not more frequent in mutator lineages. Our results provide a genetic explanation
for rapid reversion of mucoidy, a phenotype observed in other bacterial species
including human pathogens. Moreover, this demonstrates that the types of genetic
change underlying adaptation to fitness costs, and consequently the impact of
evolvability mechanisms such as increased point-mutation rates, depend critically
on the mechanism of resistance.
article_processing_charge: No
author:
- first_name: Sébastien
full_name: Wielgoss, Sébastien
last_name: Wielgoss
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Anna M.
full_name: Bischofberger, Anna M.
last_name: Bischofberger
- first_name: Alex R.
full_name: Hall, Alex R.
last_name: Hall
citation:
ama: 'Wielgoss S, Bergmiller T, Bischofberger AM, Hall AR. Data from: Adaptation
to parasites and costs of parasite resistance in mutator and non-mutator bacteria.
2015. doi:10.5061/dryad.cj910'
apa: 'Wielgoss, S., Bergmiller, T., Bischofberger, A. M., & Hall, A. R. (2015).
Data from: Adaptation to parasites and costs of parasite resistance in mutator
and non-mutator bacteria. Dryad. https://doi.org/10.5061/dryad.cj910'
chicago: 'Wielgoss, Sébastien, Tobias Bergmiller, Anna M. Bischofberger, and Alex
R. Hall. “Data from: Adaptation to Parasites and Costs of Parasite Resistance
in Mutator and Non-Mutator Bacteria.” Dryad, 2015. https://doi.org/10.5061/dryad.cj910.'
ieee: 'S. Wielgoss, T. Bergmiller, A. M. Bischofberger, and A. R. Hall, “Data from:
Adaptation to parasites and costs of parasite resistance in mutator and non-mutator
bacteria.” Dryad, 2015.'
ista: 'Wielgoss S, Bergmiller T, Bischofberger AM, Hall AR. 2015. Data from: Adaptation
to parasites and costs of parasite resistance in mutator and non-mutator bacteria,
Dryad, 10.5061/dryad.cj910.'
mla: 'Wielgoss, Sébastien, et al. Data from: Adaptation to Parasites and Costs
of Parasite Resistance in Mutator and Non-Mutator Bacteria. Dryad, 2015, doi:10.5061/dryad.cj910.'
short: S. Wielgoss, T. Bergmiller, A.M. Bischofberger, A.R. Hall, (2015).
date_created: 2021-07-26T08:44:04Z
date_published: 2015-12-21T00:00:00Z
date_updated: 2023-09-05T13:46:04Z
day: '21'
department:
- _id: CaGu
doi: 10.5061/dryad.cj910
main_file_link:
- open_access: '1'
url: https://doi.org/10.5061/dryad.cj910
month: '12'
oa: 1
oa_version: Published Version
publisher: Dryad
related_material:
record:
- id: '5749'
relation: used_in_publication
status: public
status: public
title: 'Data from: Adaptation to parasites and costs of parasite resistance in mutator
and non-mutator bacteria'
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2015'
...
---
_id: '1894'
abstract:
- lang: eng
text: 'Background: Bacterial Dsb enzymes are involved in the oxidative folding of
many proteins, through the formation of disulfide bonds between their cysteine
residues. The Dsb protein network has been well characterized in cells of the
model microorganism Escherichia coli. To gain insight into the functioning of
the Dsb system in epsilon-Proteobacteria, where it plays an important role in
the colonization process, we studied two homologs of the main Escherichia coli
Dsb oxidase (EcDsbA) that are present in the cells of the enteric pathogen Campylobacter
jejuni, the most frequently reported bacterial cause of human enteritis in the
world. Methods and Results: Phylogenetic analysis suggests the horizontal transfer
of the epsilon-Proteobacterial DsbAs from a common ancestor to gamma-Proteobacteria,
which then gave rise to the DsbL lineage. Phenotype and enzymatic assays suggest
that the two C. jejuni DsbAs play different roles in bacterial cells and have
divergent substrate spectra. CjDsbA1 is essential for the motility and autoagglutination
phenotypes, while CjDsbA2 has no impact on those processes. CjDsbA1 plays a critical
role in the oxidative folding that ensures the activity of alkaline phosphatase
CjPhoX, whereas CjDsbA2 is crucial for the activity of arylsulfotransferase CjAstA,
encoded within the dsbA2-dsbB-astA operon. Conclusions: Our results show that
CjDsbA1 is the primary thiol-oxidoreductase affecting life processes associated
with bacterial spread and host colonization, as well as ensuring the oxidative
folding of particular protein substrates. In contrast, CjDsbA2 activity does not
affect the same processes and so far its oxidative folding activity has been demonstrated
for one substrate, arylsulfotransferase CjAstA. The results suggest the cooperation
between CjDsbA2 and CjDsbB. In the case of the CjDsbA1, this cooperation is not
exclusive and there is probably another protein to be identified in C. jejuni
cells that acts to re-oxidize CjDsbA1. Altogether the data presented here constitute
the considerable insight to the Epsilonproteobacterial Dsb systems, which have
been poorly understood so far.'
article_number: e106247
author:
- first_name: Anna
full_name: Grabowska, Anna
last_name: Grabowska
- first_name: Ewa
full_name: Wywiał, Ewa
last_name: Wywiał
- first_name: Stanislaw
full_name: Dunin Horkawicz, Stanislaw
last_name: Dunin Horkawicz
- first_name: Anna
full_name: Łasica, Anna
last_name: Łasica
- first_name: Marc
full_name: Wösten, Marc
last_name: Wösten
- first_name: Anna A
full_name: Nagy-Staron, Anna A
id: 3ABC5BA6-F248-11E8-B48F-1D18A9856A87
last_name: Nagy-Staron
- first_name: Renata
full_name: Godlewska, Renata
last_name: Godlewska
- first_name: Katarzyna
full_name: Bocian Ostrzycka, Katarzyna
last_name: Bocian Ostrzycka
- first_name: Katarzyna
full_name: Pieńkowska, Katarzyna
last_name: Pieńkowska
- first_name: Paweł
full_name: Łaniewski, Paweł
last_name: Łaniewski
- first_name: Janusz
full_name: Bujnicki, Janusz
last_name: Bujnicki
- first_name: Jos
full_name: Van Putten, Jos
last_name: Van Putten
- first_name: Elzbieta
full_name: Jagusztyn Krynicka, Elzbieta
last_name: Jagusztyn Krynicka
citation:
ama: Grabowska A, Wywiał E, Dunin Horkawicz S, et al. Functional and bioinformatics
analysis of two Campylobacter jejuni homologs of the thiol-disulfide oxidoreductase,
DsbA. PLoS One. 2014;9(9). doi:10.1371/journal.pone.0106247
apa: Grabowska, A., Wywiał, E., Dunin Horkawicz, S., Łasica, A., Wösten, M., Nagy-Staron,
A. A., … Jagusztyn Krynicka, E. (2014). Functional and bioinformatics analysis
of two Campylobacter jejuni homologs of the thiol-disulfide oxidoreductase, DsbA.
PLoS One. Public Library of Science. https://doi.org/10.1371/journal.pone.0106247
chicago: Grabowska, Anna, Ewa Wywiał, Stanislaw Dunin Horkawicz, Anna Łasica, Marc
Wösten, Anna A Nagy-Staron, Renata Godlewska, et al. “Functional and Bioinformatics
Analysis of Two Campylobacter Jejuni Homologs of the Thiol-Disulfide Oxidoreductase,
DsbA.” PLoS One. Public Library of Science, 2014. https://doi.org/10.1371/journal.pone.0106247.
ieee: A. Grabowska et al., “Functional and bioinformatics analysis of two
Campylobacter jejuni homologs of the thiol-disulfide oxidoreductase, DsbA,” PLoS
One, vol. 9, no. 9. Public Library of Science, 2014.
ista: Grabowska A, Wywiał E, Dunin Horkawicz S, Łasica A, Wösten M, Nagy-Staron
AA, Godlewska R, Bocian Ostrzycka K, Pieńkowska K, Łaniewski P, Bujnicki J, Van
Putten J, Jagusztyn Krynicka E. 2014. Functional and bioinformatics analysis of
two Campylobacter jejuni homologs of the thiol-disulfide oxidoreductase, DsbA.
PLoS One. 9(9), e106247.
mla: Grabowska, Anna, et al. “Functional and Bioinformatics Analysis of Two Campylobacter
Jejuni Homologs of the Thiol-Disulfide Oxidoreductase, DsbA.” PLoS One,
vol. 9, no. 9, e106247, Public Library of Science, 2014, doi:10.1371/journal.pone.0106247.
short: A. Grabowska, E. Wywiał, S. Dunin Horkawicz, A. Łasica, M. Wösten, A.A. Nagy-Staron,
R. Godlewska, K. Bocian Ostrzycka, K. Pieńkowska, P. Łaniewski, J. Bujnicki, J.
Van Putten, E. Jagusztyn Krynicka, PLoS One 9 (2014).
date_created: 2018-12-11T11:54:35Z
date_published: 2014-09-02T00:00:00Z
date_updated: 2021-01-12T06:53:54Z
day: '02'
ddc:
- '570'
department:
- _id: CaGu
doi: 10.1371/journal.pone.0106247
file:
- access_level: open_access
checksum: 7d02c3da7f72b82bb5d7932d80c3251f
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:16:19Z
date_updated: 2020-07-14T12:45:20Z
file_id: '5205'
file_name: IST-2016-438-v1+1_journal.pone.0106247.pdf
file_size: 4248801
relation: main_file
file_date_updated: 2020-07-14T12:45:20Z
has_accepted_license: '1'
intvolume: ' 9'
issue: '9'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
publication: PLoS One
publication_status: published
publisher: Public Library of Science
publist_id: '5201'
pubrep_id: '438'
quality_controlled: '1'
scopus_import: 1
status: public
title: Functional and bioinformatics analysis of two Campylobacter jejuni homologs
of the thiol-disulfide oxidoreductase, DsbA
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: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 9
year: '2014'
...
---
_id: '1913'
abstract:
- lang: eng
text: 'Deposits of phosphorylated tau protein and convergence of pathology in the
hippocampus are the hallmarks of neurodegenerative tauopathies. Thus we aimed
to evaluate whether regional and cellular vulnerability patterns in the hippocampus
distinguish tauopathies or are influenced by their concomitant presence. Methods:
We created a heat map of phospho-tau (AT8) immunoreactivity patterns in 24 hippocampal
subregions/layers in individuals with Alzheimer''s disease (AD)-related neurofibrillary
degeneration (n = 40), Pick''s disease (n = 8), progressive supranuclear palsy
(n = 7), corticobasal degeneration (n = 6), argyrophilic grain disease (AGD, n
= 18), globular glial tauopathy (n = 5), and tau-astrogliopathy of the elderly
(n = 10). AT8 immunoreactivity patterns were compared by mathematical analysis.
Results: Our study reveals disease-specific hot spots and regional selective vulnerability
for these disorders. The pattern of hippocampal AD-related tau pathology is strongly
influenced by concomitant AGD. Mathematical analysis reveals that hippocampal
involvement in primary tauopathies is distinguishable from early-stage AD-related
neurofibrillary degeneration. Conclusion: Our data demonstrate disease-specific
AT8 immunoreactivity patterns and hot spots in the hippocampus even in tauopathies,
which primarily do not affect the hippocampus. These hot spots can be shifted
to other regions by the co-occurrence of tauopathies like AGD. Our observations
support the notion that globular glial tauopathies and tau-astrogliopathy of the
elderly are distinct entities.'
acknowledgement: This study was supported by the European Commission’s 7th Framework
Programme under GA No. 278486, ‘DEVELAGE’.
article_processing_charge: No
article_type: original
author:
- first_name: Ivan
full_name: Milenković, Ivan
last_name: Milenković
- first_name: Tatjana
full_name: Petrov, Tatjana
id: 3D5811FC-F248-11E8-B48F-1D18A9856A87
last_name: Petrov
orcid: 0000-0002-9041-0905
- first_name: Gábor
full_name: Kovács, Gábor
last_name: Kovács
citation:
ama: Milenković I, Petrov T, Kovács G. Patterns of hippocampal tau pathology differentiate
neurodegenerative dementias. Dementia and Geriatric Cognitive Disorders.
2014;38(5-6):375-388. doi:10.1159/000365548
apa: Milenković, I., Petrov, T., & Kovács, G. (2014). Patterns of hippocampal
tau pathology differentiate neurodegenerative dementias. Dementia and Geriatric
Cognitive Disorders. Karger Publishers. https://doi.org/10.1159/000365548
chicago: Milenković, Ivan, Tatjana Petrov, and Gábor Kovács. “Patterns of Hippocampal
Tau Pathology Differentiate Neurodegenerative Dementias.” Dementia and Geriatric
Cognitive Disorders. Karger Publishers, 2014. https://doi.org/10.1159/000365548.
ieee: I. Milenković, T. Petrov, and G. Kovács, “Patterns of hippocampal tau pathology
differentiate neurodegenerative dementias,” Dementia and Geriatric Cognitive
Disorders, vol. 38, no. 5–6. Karger Publishers, pp. 375–388, 2014.
ista: Milenković I, Petrov T, Kovács G. 2014. Patterns of hippocampal tau pathology
differentiate neurodegenerative dementias. Dementia and Geriatric Cognitive Disorders.
38(5–6), 375–388.
mla: Milenković, Ivan, et al. “Patterns of Hippocampal Tau Pathology Differentiate
Neurodegenerative Dementias.” Dementia and Geriatric Cognitive Disorders,
vol. 38, no. 5–6, Karger Publishers, 2014, pp. 375–88, doi:10.1159/000365548.
short: I. Milenković, T. Petrov, G. Kovács, Dementia and Geriatric Cognitive Disorders
38 (2014) 375–388.
date_created: 2018-12-11T11:54:41Z
date_published: 2014-11-07T00:00:00Z
date_updated: 2023-10-17T10:21:17Z
day: '07'
department:
- _id: CaGu
doi: 10.1159/000365548
external_id:
pmid:
- '25195847'
intvolume: ' 38'
issue: 5-6
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://kops.uni-konstanz.de/bitstream/123456789/42127/1/Milenkovic_2-17ivylo2up0798.pdf
month: '11'
oa: 1
oa_version: Published Version
page: 375 - 388
pmid: 1
publication: Dementia and Geriatric Cognitive Disorders
publication_identifier:
issn:
- 1420-8008
publication_status: published
publisher: Karger Publishers
publist_id: '5181'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Patterns of hippocampal tau pathology differentiate neurodegenerative dementias
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 38
year: '2014'
...
---
_id: '2036'
abstract:
- lang: eng
text: ' In rapidly changing environments, selection history may impact the dynamics
of adaptation. Mutations selected in one environment may result in pleiotropic
fitness trade-offs in subsequent novel environments, slowing the rates of adaptation.
Epistatic interactions between mutations selected in sequential stressful environments
may slow or accelerate subsequent rates of adaptation, depending on the nature
of that interaction. We explored the dynamics of adaptation during sequential
exposure to herbicides with different modes of action in Chlamydomonas reinhardtii.
Evolution of resistance to two of the herbicides was largely independent of selection
history. For carbetamide, previous adaptation to other herbicide modes of action
positively impacted the likelihood of adaptation to this herbicide. Furthermore,
while adaptation to all individual herbicides was associated with pleiotropic
fitness costs in stress-free environments, we observed that accumulation of resistance
mechanisms was accompanied by a reduction in overall fitness costs. We suggest
that antagonistic epistasis may be a driving mechanism that enables populations
to more readily adapt in novel environments. These findings highlight the potential
for sequences of xenobiotics to facilitate the rapid evolution of multiple-drug
and -pesticide resistance, as well as the potential for epistatic interactions
between adaptive mutations to facilitate evolutionary rescue in rapidly changing
environments. '
acknowledgement: The project was supported by Leverhulme Trust.
article_number: '20141679'
author:
- first_name: Mato
full_name: Lagator, Mato
id: 345D25EC-F248-11E8-B48F-1D18A9856A87
last_name: Lagator
- first_name: Nick
full_name: Colegrave, Nick
last_name: Colegrave
- first_name: Paul
full_name: Neve, Paul
last_name: Neve
citation:
ama: Lagator M, Colegrave N, Neve P. Selection history and epistatic interactions
impact dynamics of adaptation to novel environmental stresses. Proceedings
of the Royal Society of London Series B Biological Sciences. 2014;281(1794).
doi:10.1098/rspb.2014.1679
apa: Lagator, M., Colegrave, N., & Neve, P. (2014). Selection history and epistatic
interactions impact dynamics of adaptation to novel environmental stresses. Proceedings
of the Royal Society of London Series B Biological Sciences. Royal Society,
The. https://doi.org/10.1098/rspb.2014.1679
chicago: Lagator, Mato, Nick Colegrave, and Paul Neve. “Selection History and Epistatic
Interactions Impact Dynamics of Adaptation to Novel Environmental Stresses.” Proceedings
of the Royal Society of London Series B Biological Sciences. Royal Society,
The, 2014. https://doi.org/10.1098/rspb.2014.1679.
ieee: M. Lagator, N. Colegrave, and P. Neve, “Selection history and epistatic interactions
impact dynamics of adaptation to novel environmental stresses,” Proceedings
of the Royal Society of London Series B Biological Sciences, vol. 281, no.
1794. Royal Society, The, 2014.
ista: Lagator M, Colegrave N, Neve P. 2014. Selection history and epistatic interactions
impact dynamics of adaptation to novel environmental stresses. Proceedings of
the Royal Society of London Series B Biological Sciences. 281(1794), 20141679.
mla: Lagator, Mato, et al. “Selection History and Epistatic Interactions Impact
Dynamics of Adaptation to Novel Environmental Stresses.” Proceedings of the
Royal Society of London Series B Biological Sciences, vol. 281, no. 1794,
20141679, Royal Society, The, 2014, doi:10.1098/rspb.2014.1679.
short: M. Lagator, N. Colegrave, P. Neve, Proceedings of the Royal Society of London
Series B Biological Sciences 281 (2014).
date_created: 2018-12-11T11:55:21Z
date_published: 2014-09-17T00:00:00Z
date_updated: 2023-02-23T14:06:44Z
day: '17'
department:
- _id: CaGu
doi: 10.1098/rspb.2014.1679
intvolume: ' 281'
issue: '1794'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4211454/
month: '09'
oa: 1
oa_version: Submitted Version
publication: Proceedings of the Royal Society of London Series B Biological Sciences
publication_status: published
publisher: Royal Society, The
publist_id: '5019'
quality_controlled: '1'
related_material:
record:
- id: '9741'
relation: research_data
status: public
scopus_import: 1
status: public
title: Selection history and epistatic interactions impact dynamics of adaptation
to novel environmental stresses
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 281
year: '2014'
...
---
_id: '2056'
abstract:
- lang: eng
text: 'We consider a continuous-time Markov chain (CTMC) whose state space is partitioned
into aggregates, and each aggregate is assigned a probability measure. A sufficient
condition for defining a CTMC over the aggregates is presented as a variant of
weak lumpability, which also characterizes that the measure over the original
process can be recovered from that of the aggregated one. We show how the applicability
of de-aggregation depends on the initial distribution. The application section
is devoted to illustrate how the developed theory aids in reducing CTMC models
of biochemical systems particularly in connection to protein-protein interactions.
We assume that the model is written by a biologist in form of site-graph-rewrite
rules. Site-graph-rewrite rules compactly express that, often, only a local context
of a protein (instead of a full molecular species) needs to be in a certain configuration
in order to trigger a reaction event. This observation leads to suitable aggregate
Markov chains with smaller state spaces, thereby providing sufficient reduction
in computational complexity. This is further exemplified in two case studies:
simple unbounded polymerization and early EGFR/insulin crosstalk.'
acknowledgement: T. Petrov is supported by SystemsX.ch—the Swiss Inititative for Systems
Biology.
author:
- first_name: Arnab
full_name: Ganguly, Arnab
last_name: Ganguly
- first_name: Tatjana
full_name: Petrov, Tatjana
id: 3D5811FC-F248-11E8-B48F-1D18A9856A87
last_name: Petrov
orcid: 0000-0002-9041-0905
- first_name: Heinz
full_name: Koeppl, Heinz
last_name: Koeppl
citation:
ama: Ganguly A, Petrov T, Koeppl H. Markov chain aggregation and its applications
to combinatorial reaction networks. Journal of Mathematical Biology. 2014;69(3):767-797.
doi:10.1007/s00285-013-0738-7
apa: Ganguly, A., Petrov, T., & Koeppl, H. (2014). Markov chain aggregation
and its applications to combinatorial reaction networks. Journal of Mathematical
Biology. Springer. https://doi.org/10.1007/s00285-013-0738-7
chicago: Ganguly, Arnab, Tatjana Petrov, and Heinz Koeppl. “Markov Chain Aggregation
and Its Applications to Combinatorial Reaction Networks.” Journal of Mathematical
Biology. Springer, 2014. https://doi.org/10.1007/s00285-013-0738-7.
ieee: A. Ganguly, T. Petrov, and H. Koeppl, “Markov chain aggregation and its applications
to combinatorial reaction networks,” Journal of Mathematical Biology, vol.
69, no. 3. Springer, pp. 767–797, 2014.
ista: Ganguly A, Petrov T, Koeppl H. 2014. Markov chain aggregation and its applications
to combinatorial reaction networks. Journal of Mathematical Biology. 69(3), 767–797.
mla: Ganguly, Arnab, et al. “Markov Chain Aggregation and Its Applications to Combinatorial
Reaction Networks.” Journal of Mathematical Biology, vol. 69, no. 3, Springer,
2014, pp. 767–97, doi:10.1007/s00285-013-0738-7.
short: A. Ganguly, T. Petrov, H. Koeppl, Journal of Mathematical Biology 69 (2014)
767–797.
date_created: 2018-12-11T11:55:28Z
date_published: 2014-11-20T00:00:00Z
date_updated: 2021-01-12T06:55:01Z
day: '20'
department:
- _id: CaGu
- _id: ToHe
doi: 10.1007/s00285-013-0738-7
intvolume: ' 69'
issue: '3'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://arxiv.org/abs/1303.4532
month: '11'
oa: 1
oa_version: Submitted Version
page: 767 - 797
publication: Journal of Mathematical Biology
publication_status: published
publisher: Springer
publist_id: '4990'
quality_controlled: '1'
scopus_import: 1
status: public
title: Markov chain aggregation and its applications to combinatorial reaction networks
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 69
year: '2014'
...
---
_id: '2083'
abstract:
- lang: eng
text: Understanding the effects of sex and migration on adaptation to novel environments
remains a key problem in evolutionary biology. Using a single-cell alga Chlamydomonas
reinhardtii, we investigated how sex and migration affected rates of evolutionary
rescue in a sink environment, and subsequent changes in fitness following evolutionary
rescue. We show that sex and migration affect both the rate of evolutionary rescue
and subsequent adaptation. However, their combined effects change as the populations
adapt to a sink habitat. Both sex and migration independently increased rates
of evolutionary rescue, but the effect of sex on subsequent fitness improvements,
following initial rescue, changed with migration, as sex was beneficial in the
absence of migration but constraining adaptation when combined with migration.
These results suggest that sex and migration are beneficial during the initial
stages of adaptation, but can become detrimental as the population adapts to its
environment.
acknowledgement: The authors are grateful to the Leverhulme Trust (F/00 215/AW) for
funding this work.
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: Andrew
full_name: Morgan, Andrew
last_name: Morgan
- first_name: Paul
full_name: Neve, Paul
last_name: Neve
- first_name: Nick
full_name: Colegrave, Nick
last_name: Colegrave
citation:
ama: Lagator M, Morgan A, Neve P, Colegrave N. Role of sex and migration in adaptation
to sink environments. Evolution. 2014;68(8):2296-2305. doi:10.1111/evo.12440
apa: Lagator, M., Morgan, A., Neve, P., & Colegrave, N. (2014). Role of sex
and migration in adaptation to sink environments. Evolution. Wiley. https://doi.org/10.1111/evo.12440
chicago: Lagator, Mato, Andrew Morgan, Paul Neve, and Nick Colegrave. “Role of Sex
and Migration in Adaptation to Sink Environments.” Evolution. Wiley, 2014.
https://doi.org/10.1111/evo.12440.
ieee: M. Lagator, A. Morgan, P. Neve, and N. Colegrave, “Role of sex and migration
in adaptation to sink environments,” Evolution, vol. 68, no. 8. Wiley,
pp. 2296–2305, 2014.
ista: Lagator M, Morgan A, Neve P, Colegrave N. 2014. Role of sex and migration
in adaptation to sink environments. Evolution. 68(8), 2296–2305.
mla: Lagator, Mato, et al. “Role of Sex and Migration in Adaptation to Sink Environments.”
Evolution, vol. 68, no. 8, Wiley, 2014, pp. 2296–305, doi:10.1111/evo.12440.
short: M. Lagator, A. Morgan, P. Neve, N. Colegrave, Evolution 68 (2014) 2296–2305.
date_created: 2018-12-11T11:55:36Z
date_published: 2014-04-25T00:00:00Z
date_updated: 2023-02-23T14:06:51Z
day: '25'
ddc:
- '570'
department:
- _id: CaGu
doi: 10.1111/evo.12440
file:
- access_level: open_access
checksum: 8d459b07e4a11bb5fde92d969184fe48
content_type: application/pdf
creator: dernst
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date_updated: 2020-07-14T12:45:28Z
file_id: '7845'
file_name: 2014_Evolution_Lagator.pdf
file_size: 467254
relation: main_file
file_date_updated: 2020-07-14T12:45:28Z
has_accepted_license: '1'
intvolume: ' 68'
issue: '8'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 2296 - 2305
publication: Evolution
publication_status: published
publisher: Wiley
publist_id: '4954'
quality_controlled: '1'
related_material:
record:
- id: '9747'
relation: research_data
status: public
scopus_import: 1
status: public
title: Role of sex and migration in adaptation to sink environments
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 68
year: '2014'
...
---
_id: '9741'
abstract:
- lang: eng
text: In rapidly changing environments, selection history may impact the dynamics
of adaptation. Mutations selected in one environment may result in pleiotropic
fitness trade-offs in subsequent novel environments, slowing the rates of adaptation.
Epistatic interactions between mutations selected in sequential stressful environments
may slow or accelerate subsequent rates of adaptation, depending on the nature
of that interaction. We explored the dynamics of adaptation during sequential
exposure to herbicides with different modes of action in Chlamydomonas reinhardtii.
Evolution of resistance to two of the herbicides was largely independent of selection
history. For carbetamide, previous adaptation to other herbicide modes of action
positively impacted the likelihood of adaptation to this herbicide. Furthermore,
while adaptation to all individual herbicides was associated with pleiotropic
fitness costs in stress-free environments, we observed that accumulation of resistance
mechanisms was accompanied by a reduction in overall fitness costs. We suggest
that antagonistic epistasis may be a driving mechanism that enables populations
to more readily adapt in novel environments. These findings highlight the potential
for sequences of xenobiotics to facilitate the rapid evolution of multiple-drug
and -pesticide resistance, as well as the potential for epistatic interactions
between adaptive mutations to facilitate evolutionary rescue in rapidly changing
environments.
article_processing_charge: No
author:
- first_name: Mato
full_name: Lagator, Mato
id: 345D25EC-F248-11E8-B48F-1D18A9856A87
last_name: Lagator
- first_name: Nick
full_name: Colegrave, Nick
last_name: Colegrave
- first_name: Paul
full_name: Neve, Paul
last_name: Neve
citation:
ama: 'Lagator M, Colegrave N, Neve P. Data from: Selection history and epistatic
interactions impact dynamics of adaptation to novel environmental stresses. 2014.
doi:10.5061/dryad.85dn7'
apa: 'Lagator, M., Colegrave, N., & Neve, P. (2014). Data from: Selection history
and epistatic interactions impact dynamics of adaptation to novel environmental
stresses. Dryad. https://doi.org/10.5061/dryad.85dn7'
chicago: 'Lagator, Mato, Nick Colegrave, and Paul Neve. “Data from: Selection History
and Epistatic Interactions Impact Dynamics of Adaptation to Novel Environmental
Stresses.” Dryad, 2014. https://doi.org/10.5061/dryad.85dn7.'
ieee: 'M. Lagator, N. Colegrave, and P. Neve, “Data from: Selection history and
epistatic interactions impact dynamics of adaptation to novel environmental stresses.”
Dryad, 2014.'
ista: 'Lagator M, Colegrave N, Neve P. 2014. Data from: Selection history and epistatic
interactions impact dynamics of adaptation to novel environmental stresses, Dryad,
10.5061/dryad.85dn7.'
mla: 'Lagator, Mato, et al. Data from: Selection History and Epistatic Interactions
Impact Dynamics of Adaptation to Novel Environmental Stresses. Dryad, 2014,
doi:10.5061/dryad.85dn7.'
short: M. Lagator, N. Colegrave, P. Neve, (2014).
date_created: 2021-07-28T08:48:06Z
date_published: 2014-08-21T00:00:00Z
date_updated: 2023-02-23T10:25:31Z
day: '21'
department:
- _id: CaGu
doi: 10.5061/dryad.85dn7
main_file_link:
- open_access: '1'
url: https://doi.org/10.5061/dryad.85dn7
month: '08'
oa: 1
oa_version: Published Version
publisher: Dryad
related_material:
record:
- id: '2036'
relation: used_in_publication
status: public
status: public
title: 'Data from: Selection history and epistatic interactions impact dynamics of
adaptation to novel environmental stresses'
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2014'
...
---
_id: '9747'
abstract:
- lang: eng
text: Understanding the effects of sex and migration on adaptation to novel environments
remains a key problem in evolutionary biology. Using a single-cell alga Chlamydomonas
reinhardtii, we investigated how sex and migration affected rates of evolutionary
rescue in a sink environment, and subsequent changes in fitness following evolutionary
rescue. We show that sex and migration affect both the rate of evolutionary rescue
and subsequent adaptation. However, their combined effects change as the populations
adapt to a sink habitat. Both sex and migration independently increased rates
of evolutionary rescue, but the effect of sex on subsequent fitness improvements,
following initial rescue, changed with migration, as sex was beneficial in the
absence of migration but constraining adaptation when combined with migration.
These results suggest that sex and migration are beneficial during the initial
stages of adaptation, but can become detrimental as the population adapts to its
environment.
article_processing_charge: No
author:
- first_name: Mato
full_name: Lagator, Mato
id: 345D25EC-F248-11E8-B48F-1D18A9856A87
last_name: Lagator
- first_name: Andrew
full_name: Morgan, Andrew
last_name: Morgan
- first_name: Paul
full_name: Neve, Paul
last_name: Neve
- first_name: Nick
full_name: Colegrave, Nick
last_name: Colegrave
citation:
ama: 'Lagator M, Morgan A, Neve P, Colegrave N. Data from: Role of sex and migration
in adaptation to sink environments. 2014. doi:10.5061/dryad.s42n1'
apa: 'Lagator, M., Morgan, A., Neve, P., & Colegrave, N. (2014). Data from:
Role of sex and migration in adaptation to sink environments. Dryad. https://doi.org/10.5061/dryad.s42n1'
chicago: 'Lagator, Mato, Andrew Morgan, Paul Neve, and Nick Colegrave. “Data from:
Role of Sex and Migration in Adaptation to Sink Environments.” Dryad, 2014. https://doi.org/10.5061/dryad.s42n1.'
ieee: 'M. Lagator, A. Morgan, P. Neve, and N. Colegrave, “Data from: Role of sex
and migration in adaptation to sink environments.” Dryad, 2014.'
ista: 'Lagator M, Morgan A, Neve P, Colegrave N. 2014. Data from: Role of sex and
migration in adaptation to sink environments, Dryad, 10.5061/dryad.s42n1.'
mla: 'Lagator, Mato, et al. Data from: Role of Sex and Migration in Adaptation
to Sink Environments. Dryad, 2014, doi:10.5061/dryad.s42n1.'
short: M. Lagator, A. Morgan, P. Neve, N. Colegrave, (2014).
date_created: 2021-07-28T15:32:55Z
date_published: 2014-04-17T00:00:00Z
date_updated: 2023-02-23T10:27:31Z
day: '17'
department:
- _id: CaGu
doi: 10.5061/dryad.s42n1
main_file_link:
- open_access: '1'
url: https://doi.org/10.5061/dryad.s42n1
month: '04'
oa: 1
oa_version: Published Version
publisher: Dryad
related_material:
record:
- id: '2083'
relation: used_in_publication
status: public
status: public
title: 'Data from: Role of sex and migration in adaptation to sink environments'
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2014'
...
---
_id: '9931'
abstract:
- lang: eng
text: Gene duplication is important in evolution, because it provides new raw material
for evolutionary adaptations. Several existing hypotheses about the causes of
duplicate retention and diversification differ in their emphasis on gene dosage,
subfunctionalization, and neofunctionalization. Little experimental data exist
on the relative importance of gene expression changes and changes in coding regions
for the evolution of duplicate genes. Furthermore, we do not know how strongly
the environment could affect this importance. To address these questions, we performed
evolution experiments with the TEM-1 beta lactamase gene in Escherichia coli to
study the initial stages of duplicate gene evolution in the laboratory. We mimicked
tandem duplication by inserting two copies of the TEM-1 gene on the same plasmid.
We then subjected these copies to repeated cycles of mutagenesis and selection
in various environments that contained antibiotics in different combinations and
concentrations. Our experiments showed that gene dosage is the most important
factor in the initial stages of duplicate gene evolution, and overshadows the
importance of point mutations in the coding region.
acknowledgement: We thank the Functional Genomics Center Zurich for its service in
generating sequencing data, M. Ackermann and E. Hayden for helpful discussions,
A. de Visser for comments on earlier versions of this manuscript, and M. Moser for
help with quantitative PCR. This work was supported by Swiss National Science Foundation
(grant 315230–129708), as well as through the YeastX project of SystemsX.ch, and
the University Priority Research Program in Systems Biology at the University of
Zurich. RD acknowledges support from the Forschungskredit program of the University
of Zurich. The authors declare no conflict of interest.
article_processing_charge: No
article_type: original
author:
- first_name: Riddhiman
full_name: Dhar, Riddhiman
last_name: Dhar
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Andreas
full_name: Wagner, Andreas
last_name: Wagner
citation:
ama: Dhar R, Bergmiller T, Wagner A. Increased gene dosage plays a predominant role
in the initial stages of evolution of duplicate TEM-1 beta lactamase genes. Evolution.
2014;68(6):1775-1791. doi:10.1111/evo.12373
apa: Dhar, R., Bergmiller, T., & Wagner, A. (2014). Increased gene dosage plays
a predominant role in the initial stages of evolution of duplicate TEM-1 beta
lactamase genes. Evolution. Wiley. https://doi.org/10.1111/evo.12373
chicago: Dhar, Riddhiman, Tobias Bergmiller, and Andreas Wagner. “Increased Gene
Dosage Plays a Predominant Role in the Initial Stages of Evolution of Duplicate
TEM-1 Beta Lactamase Genes.” Evolution. Wiley, 2014. https://doi.org/10.1111/evo.12373.
ieee: R. Dhar, T. Bergmiller, and A. Wagner, “Increased gene dosage plays a predominant
role in the initial stages of evolution of duplicate TEM-1 beta lactamase genes,”
Evolution, vol. 68, no. 6. Wiley, pp. 1775–1791, 2014.
ista: Dhar R, Bergmiller T, Wagner A. 2014. Increased gene dosage plays a predominant
role in the initial stages of evolution of duplicate TEM-1 beta lactamase genes.
Evolution. 68(6), 1775–1791.
mla: Dhar, Riddhiman, et al. “Increased Gene Dosage Plays a Predominant Role in
the Initial Stages of Evolution of Duplicate TEM-1 Beta Lactamase Genes.” Evolution,
vol. 68, no. 6, Wiley, 2014, pp. 1775–91, doi:10.1111/evo.12373.
short: R. Dhar, T. Bergmiller, A. Wagner, Evolution 68 (2014) 1775–1791.
date_created: 2021-08-17T09:03:09Z
date_published: 2014-06-03T00:00:00Z
date_updated: 2023-02-23T14:13:27Z
day: '03'
department:
- _id: CaGu
doi: 10.1111/evo.12373
external_id:
pmid:
- '24495000'
intvolume: ' 68'
issue: '6'
language:
- iso: eng
month: '06'
oa_version: None
page: 1775-1791
pmid: 1
publication: Evolution
publication_identifier:
eissn:
- 1558-5646
issn:
- 0014-3820
publication_status: published
publisher: Wiley
quality_controlled: '1'
related_material:
record:
- id: '9932'
relation: research_data
status: public
scopus_import: '1'
status: public
title: Increased gene dosage plays a predominant role in the initial stages of evolution
of duplicate TEM-1 beta lactamase genes
type: journal_article
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
volume: 68
year: '2014'
...
---
_id: '9932'
abstract:
- lang: eng
text: Gene duplication is important in evolution, because it provides new raw material
for evolutionary adaptations. Several existing hypotheses about the causes of
duplicate retention and diversification differ in their emphasis on gene dosage,
sub-functionalization, and neo-functionalization. Little experimental data exists
on the relative importance of gene expression changes and changes in coding regions
for the evolution of duplicate genes. Furthermore, we do not know how strongly
the environment could affect this importance. To address these questions, we performed
evolution experiments with the TEM-1 beta lactamase gene in E. coli to study the
initial stages of duplicate gene evolution in the laboratory. We mimicked tandem
duplication by inserting two copies of the TEM-1 gene on the same plasmid. We
then subjected these copies to repeated cycles of mutagenesis and selection in
various environments that contained antibiotics in different combinations and
concentrations. Our experiments showed that gene dosage is the most important
factor in the initial stages of duplicate gene evolution, and overshadows the
importance of point mutations in the coding region.
article_processing_charge: No
author:
- first_name: Riddhiman
full_name: Dhar, Riddhiman
last_name: Dhar
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Andreas
full_name: Wagner, Andreas
last_name: Wagner
citation:
ama: 'Dhar R, Bergmiller T, Wagner A. Data from: Increased gene dosage plays a predominant
role in the initial stages of evolution of duplicate TEM-1 beta lactamase genes.
2014. doi:10.5061/dryad.jc402'
apa: 'Dhar, R., Bergmiller, T., & Wagner, A. (2014). Data from: Increased gene
dosage plays a predominant role in the initial stages of evolution of duplicate
TEM-1 beta lactamase genes. Dryad. https://doi.org/10.5061/dryad.jc402'
chicago: 'Dhar, Riddhiman, Tobias Bergmiller, and Andreas Wagner. “Data from: Increased
Gene Dosage Plays a Predominant Role in the Initial Stages of Evolution of Duplicate
TEM-1 Beta Lactamase Genes.” Dryad, 2014. https://doi.org/10.5061/dryad.jc402.'
ieee: 'R. Dhar, T. Bergmiller, and A. Wagner, “Data from: Increased gene dosage
plays a predominant role in the initial stages of evolution of duplicate TEM-1
beta lactamase genes.” Dryad, 2014.'
ista: 'Dhar R, Bergmiller T, Wagner A. 2014. Data from: Increased gene dosage plays
a predominant role in the initial stages of evolution of duplicate TEM-1 beta
lactamase genes, Dryad, 10.5061/dryad.jc402.'
mla: 'Dhar, Riddhiman, et al. Data from: Increased Gene Dosage Plays a Predominant
Role in the Initial Stages of Evolution of Duplicate TEM-1 Beta Lactamase Genes.
Dryad, 2014, doi:10.5061/dryad.jc402.'
short: R. Dhar, T. Bergmiller, A. Wagner, (2014).
date_created: 2021-08-17T09:11:40Z
date_published: 2014-01-27T00:00:00Z
date_updated: 2023-02-23T14:13:24Z
day: '27'
department:
- _id: CaGu
doi: 10.5061/dryad.jc402
main_file_link:
- open_access: '1'
url: https://doi.org/10.5061/dryad.jc402
month: '01'
oa: 1
oa_version: Published Version
publisher: Dryad
related_material:
record:
- id: '9931'
relation: used_in_publication
status: public
status: public
title: 'Data from: Increased gene dosage plays a predominant role in the initial stages
of evolution of duplicate TEM-1 beta lactamase genes'
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2014'
...
---
_id: '2718'
abstract:
- lang: eng
text: Even though both population and quantitative genetics, and evolutionary computation,
deal with the same questions, they have developed largely independently of each
other. I review key results from each field, emphasising those that apply independently
of the (usually unknown) relation between genotype and phenotype. The infinitesimal
model provides a simple framework for predicting the response of complex traits
to selection, which in biology has proved remarkably successful. This allows one
to choose the schedule of population sizes and selection intensities that will
maximise the response to selection, given that the total number of individuals
realised, C = ∑t Nt, is constrained. This argument shows that for an additive
trait (i.e., determined by the sum of effects of the genes), the optimum population
size and the maximum possible response (i.e., the total change in trait mean)
are both proportional to √C.
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: Tiago
full_name: Paixao, Tiago
id: 2C5658E6-F248-11E8-B48F-1D18A9856A87
last_name: Paixao
orcid: 0000-0003-2361-3953
citation:
ama: 'Barton NH, Paixao T. Can quantitative and population genetics help us understand
evolutionary computation? In: Proceedings of the 15th Annual Conference on
Genetic and Evolutionary Computation. ACM; 2013:1573-1580. doi:10.1145/2463372.2463568'
apa: 'Barton, N. H., & Paixao, T. (2013). Can quantitative and population genetics
help us understand evolutionary computation? In Proceedings of the 15th annual
conference on Genetic and evolutionary computation (pp. 1573–1580). Amsterdam,
Netherlands: ACM. https://doi.org/10.1145/2463372.2463568'
chicago: Barton, Nicholas H, and Tiago Paixao. “Can Quantitative and Population
Genetics Help Us Understand Evolutionary Computation?” In Proceedings of the
15th Annual Conference on Genetic and Evolutionary Computation, 1573–80. ACM,
2013. https://doi.org/10.1145/2463372.2463568.
ieee: N. H. Barton and T. Paixao, “Can quantitative and population genetics help
us understand evolutionary computation?,” in Proceedings of the 15th annual
conference on Genetic and evolutionary computation, Amsterdam, Netherlands,
2013, pp. 1573–1580.
ista: 'Barton NH, Paixao T. 2013. Can quantitative and population genetics help
us understand evolutionary computation? Proceedings of the 15th annual conference
on Genetic and evolutionary computation. GECCO: Genetic and evolutionary computation
conference, 1573–1580.'
mla: Barton, Nicholas H., and Tiago Paixao. “Can Quantitative and Population Genetics
Help Us Understand Evolutionary Computation?” Proceedings of the 15th Annual
Conference on Genetic and Evolutionary Computation, ACM, 2013, pp. 1573–80,
doi:10.1145/2463372.2463568.
short: N.H. Barton, T. Paixao, in:, Proceedings of the 15th Annual Conference on
Genetic and Evolutionary Computation, ACM, 2013, pp. 1573–1580.
conference:
end_date: 2013-07-10
location: Amsterdam, Netherlands
name: 'GECCO: Genetic and evolutionary computation conference'
start_date: 2013-07-06
date_created: 2018-12-11T11:59:14Z
date_published: 2013-07-01T00:00:00Z
date_updated: 2021-01-12T06:59:15Z
day: '01'
ddc:
- '570'
department:
- _id: NiBa
- _id: CaGu
doi: 10.1145/2463372.2463568
ec_funded: 1
file:
- access_level: open_access
checksum: 9d9be9090ce5c20766e0eb076ace5b98
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:15:38Z
date_updated: 2020-07-14T12:45:45Z
file_id: '5159'
file_name: IST-2016-564-v1+1_NickGECCO_2013_1_-1.pdf
file_size: 475844
relation: main_file
file_date_updated: 2020-07-14T12:45:45Z
has_accepted_license: '1'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Submitted Version
page: 1573 - 1580
project:
- _id: 25B07788-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '250152'
name: Limits to selection in biology and in evolutionary computation
publication: Proceedings of the 15th annual conference on Genetic and evolutionary
computation
publication_status: published
publisher: ACM
publist_id: '4174'
pubrep_id: '564'
quality_controlled: '1'
scopus_import: 1
status: public
title: Can quantitative and population genetics help us understand evolutionary computation?
type: conference
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2013'
...
---
_id: '2719'
abstract:
- lang: eng
text: Prediction of the evolutionary process is a long standing problem both in
the theory of evolutionary biology and evolutionary computation (EC). It has long
been realized that heritable variation is crucial to both the response to selection
and the success of genetic algorithms. However, not all variation contributes
in the same way to the response. Quantitative genetics has developed a large body
of work trying to estimate and understand how different components of the variance
in fitness in the population contribute to the response to selection. We illustrate
how to apply some concepts of quantitative genetics to the analysis of genetic
algorithms. In particular, we derive estimates for the short term prediction of
the response to selection and we use variance decomposition to gain insight on
local aspects of the landscape. Finally, we propose a new population based genetic
algorithm that uses these methods to improve its operation.
author:
- 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
citation:
ama: 'Paixao T, Barton NH. A variance decomposition approach to the analysis of
genetic algorithms. In: Proceedings of the 15th Annual Conference on Genetic
and Evolutionary Computation. ACM; 2013:845-852. doi:10.1145/2463372.2463470'
apa: 'Paixao, T., & Barton, N. H. (2013). A variance decomposition approach
to the analysis of genetic algorithms. In Proceedings of the 15th annual conference
on Genetic and evolutionary computation (pp. 845–852). Amsterdam, Netherlands:
ACM. https://doi.org/10.1145/2463372.2463470'
chicago: Paixao, Tiago, and Nicholas H Barton. “A Variance Decomposition Approach
to the Analysis of Genetic Algorithms.” In Proceedings of the 15th Annual Conference
on Genetic and Evolutionary Computation, 845–52. ACM, 2013. https://doi.org/10.1145/2463372.2463470.
ieee: T. Paixao and N. H. Barton, “A variance decomposition approach to the analysis
of genetic algorithms,” in Proceedings of the 15th annual conference on Genetic
and evolutionary computation, Amsterdam, Netherlands, 2013, pp. 845–852.
ista: 'Paixao T, Barton NH. 2013. A variance decomposition approach to the analysis
of genetic algorithms. Proceedings of the 15th annual conference on Genetic and
evolutionary computation. GECCO: Genetic and evolutionary computation conference,
845–852.'
mla: Paixao, Tiago, and Nicholas H. Barton. “A Variance Decomposition Approach to
the Analysis of Genetic Algorithms.” Proceedings of the 15th Annual Conference
on Genetic and Evolutionary Computation, ACM, 2013, pp. 845–52, doi:10.1145/2463372.2463470.
short: T. Paixao, N.H. Barton, in:, Proceedings of the 15th Annual Conference on
Genetic and Evolutionary Computation, ACM, 2013, pp. 845–852.
conference:
end_date: 2013-07-10
location: Amsterdam, Netherlands
name: 'GECCO: Genetic and evolutionary computation conference'
start_date: 2013-07-06
date_created: 2018-12-11T11:59:15Z
date_published: 2013-07-01T00:00:00Z
date_updated: 2021-01-12T06:59:15Z
day: '01'
department:
- _id: NiBa
- _id: CaGu
doi: 10.1145/2463372.2463470
ec_funded: 1
language:
- iso: eng
month: '07'
oa_version: None
page: 845 - 852
project:
- _id: 25B07788-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '250152'
name: Limits to selection in biology and in evolutionary computation
publication: Proceedings of the 15th annual conference on Genetic and evolutionary
computation
publication_status: published
publisher: ACM
publist_id: '4173'
quality_controlled: '1'
scopus_import: 1
status: public
title: A variance decomposition approach to the analysis of genetic algorithms
type: conference
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2013'
...
---
_id: '2720'
abstract:
- lang: eng
text: 'Knowledge of the rate and fitness effects of mutations is essential for understanding
the process of evolution. Mutations are inherently difficult to study because
they are rare and are frequently eliminated by natural selection. In the ciliate
Tetrahymena thermophila, mutations can accumulate in the germline genome without
being exposed to selection. We have conducted a mutation accumulation (MA) experiment
in this species. Assuming that all mutations are deleterious and have the same
effect, we estimate that the deleterious mutation rate per haploid germline genome
per generation is U = 0.0047 (95% credible interval: 0.0015, 0.0125), and that
germline mutations decrease fitness by s = 11% when expressed in a homozygous
state (95% CI: 4.4%, 27%). We also estimate that deleterious mutations are partially
recessive on average (h = 0.26; 95% CI: –0.022, 0.62) and that the rate of lethal
mutations is <10% of the deleterious mutation rate. Comparisons between the
observed evolutionary responses in the germline and somatic genomes and the results
from individual-based simulations of MA suggest that the two genomes have similar
mutational parameters. These are the first estimates of the deleterious mutation
rate and fitness effects from the eukaryotic supergroup Chromalveolata and are
within the range of those of other eukaryotes.'
article_processing_charge: No
author:
- first_name: Hongan
full_name: Long, Hongan
last_name: Long
- first_name: Tiago
full_name: Paixao, Tiago
id: 2C5658E6-F248-11E8-B48F-1D18A9856A87
last_name: Paixao
orcid: 0000-0003-2361-3953
- first_name: Ricardo
full_name: Azevedo, Ricardo
last_name: Azevedo
- first_name: Rebecca
full_name: Zufall, Rebecca
last_name: Zufall
citation:
ama: Long H, Paixao T, Azevedo R, Zufall R. Accumulation of spontaneous mutations
in the ciliate Tetrahymena thermophila. Genetics. 2013;195(2):527-540.
doi:10.1534/genetics.113.153536
apa: Long, H., Paixao, T., Azevedo, R., & Zufall, R. (2013). Accumulation of
spontaneous mutations in the ciliate Tetrahymena thermophila. Genetics.
Genetics Society of America. https://doi.org/10.1534/genetics.113.153536
chicago: Long, Hongan, Tiago Paixao, Ricardo Azevedo, and Rebecca Zufall. “Accumulation
of Spontaneous Mutations in the Ciliate Tetrahymena Thermophila.” Genetics.
Genetics Society of America, 2013. https://doi.org/10.1534/genetics.113.153536.
ieee: H. Long, T. Paixao, R. Azevedo, and R. Zufall, “Accumulation of spontaneous
mutations in the ciliate Tetrahymena thermophila,” Genetics, vol. 195,
no. 2. Genetics Society of America, pp. 527–540, 2013.
ista: Long H, Paixao T, Azevedo R, Zufall R. 2013. Accumulation of spontaneous mutations
in the ciliate Tetrahymena thermophila. Genetics. 195(2), 527–540.
mla: Long, Hongan, et al. “Accumulation of Spontaneous Mutations in the Ciliate
Tetrahymena Thermophila.” Genetics, vol. 195, no. 2, Genetics Society of
America, 2013, pp. 527–40, doi:10.1534/genetics.113.153536.
short: H. Long, T. Paixao, R. Azevedo, R. Zufall, Genetics 195 (2013) 527–540.
date_created: 2018-12-11T11:59:15Z
date_published: 2013-10-01T00:00:00Z
date_updated: 2021-01-12T06:59:16Z
day: '01'
department:
- _id: NiBa
- _id: CaGu
doi: 10.1534/genetics.113.153536
ec_funded: 1
external_id:
pmid:
- '23934880'
intvolume: ' 195'
issue: '2'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3781978/
month: '10'
oa: 1
oa_version: Submitted Version
page: 527-540
pmid: 1
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_status: published
publisher: Genetics Society of America
publist_id: '4172'
quality_controlled: '1'
scopus_import: 1
status: public
title: Accumulation of spontaneous mutations in the ciliate Tetrahymena thermophila
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 195
year: '2013'
...
---
_id: '2853'
abstract:
- lang: eng
text: High relatedness among interacting individuals has generally been considered
a precondition for the evolution of altruism. However, kin-selection theory also
predicts the evolution of altruism when relatedness is low, as long as the cost
of the altruistic act is minor compared with its benefit. Here, we demonstrate
evidence for a low-cost altruistic act in bacteria. We investigated Escherichia
coli responding to the attack of an obligately lytic phage by committing suicide
in order to prevent parasite transmission to nearby relatives. We found that bacterial
suicide provides large benefits to survivors at marginal costs to committers.
The cost of suicide was low, because infected cells are moribund, rapidly dying
upon phage infection, such that no more opportunity for reproduction remains.
As a consequence of its marginal cost, host suicide was selectively favoured even
when relatedness between committers and survivors approached zero. Altogether,
our findings demonstrate that low-cost suicide can evolve with ease, represents
an effective host-defence strategy, and seems to be widespread among microbes.
Moreover, low-cost suicide might also occur in higher organisms as exemplified
by infected social insect workers leaving the colony to die in isolation.
article_processing_charge: No
article_type: original
author:
- first_name: Dominik
full_name: Refardt, Dominik
last_name: Refardt
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Rolf
full_name: Kümmerli, Rolf
last_name: Kümmerli
citation:
ama: 'Refardt D, Bergmiller T, Kümmerli R. Altruism can evolve when relatedness
is low: Evidence from bacteria committing suicide upon phage infection. Proceedings
of the Royal Society of London Series B Biological Sciences. 2013;280(1759).
doi:10.1098/rspb.2012.3035'
apa: 'Refardt, D., Bergmiller, T., & Kümmerli, R. (2013). Altruism can evolve
when relatedness is low: Evidence from bacteria committing suicide upon phage
infection. Proceedings of the Royal Society of London Series B Biological Sciences.
The Royal Society. https://doi.org/10.1098/rspb.2012.3035'
chicago: 'Refardt, Dominik, Tobias Bergmiller, and Rolf Kümmerli. “Altruism Can
Evolve When Relatedness Is Low: Evidence from Bacteria Committing Suicide upon
Phage Infection.” Proceedings of the Royal Society of London Series B Biological
Sciences. The Royal Society, 2013. https://doi.org/10.1098/rspb.2012.3035.'
ieee: 'D. Refardt, T. Bergmiller, and R. Kümmerli, “Altruism can evolve when relatedness
is low: Evidence from bacteria committing suicide upon phage infection,” Proceedings
of the Royal Society of London Series B Biological Sciences, vol. 280, no.
1759. The Royal Society, 2013.'
ista: 'Refardt D, Bergmiller T, Kümmerli R. 2013. Altruism can evolve when relatedness
is low: Evidence from bacteria committing suicide upon phage infection. Proceedings
of the Royal Society of London Series B Biological Sciences. 280(1759).'
mla: 'Refardt, Dominik, et al. “Altruism Can Evolve When Relatedness Is Low: Evidence
from Bacteria Committing Suicide upon Phage Infection.” Proceedings of the
Royal Society of London Series B Biological Sciences, vol. 280, no. 1759,
The Royal Society, 2013, doi:10.1098/rspb.2012.3035.'
short: D. Refardt, T. Bergmiller, R. Kümmerli, Proceedings of the Royal Society
of London Series B Biological Sciences 280 (2013).
date_created: 2018-12-11T11:59:56Z
date_published: 2013-05-22T00:00:00Z
date_updated: 2023-10-18T06:43:23Z
day: '22'
department:
- _id: CaGu
doi: 10.1098/rspb.2012.3035
external_id:
pmid:
- '23516238'
intvolume: ' 280'
issue: '1759'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3619501/
month: '05'
oa: 1
oa_version: Submitted Version
pmid: 1
publication: Proceedings of the Royal Society of London Series B Biological Sciences
publication_identifier:
eissn:
- 1471-2954
publication_status: published
publisher: The Royal Society
publist_id: '3939'
quality_controlled: '1'
related_material:
record:
- id: '9751'
relation: research_data
status: public
scopus_import: '1'
status: public
title: 'Altruism can evolve when relatedness is low: Evidence from bacteria committing
suicide upon phage infection'
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 280
year: '2013'
...
---
_id: '499'
abstract:
- lang: eng
text: Exposure of an isogenic bacterial population to a cidal antibiotic typically
fails to eliminate a small fraction of refractory cells. Historically, fractional
killing has been attributed to infrequently dividing or nondividing "persisters."
Using microfluidic cultures and time-lapse microscopy, we found that Mycobacterium
smegmatis persists by dividing in the presence of the drug isoniazid (INH). Although
persistence in these studies was characterized by stable numbers of cells, this
apparent stability was actually a dynamic state of balanced division and death.
Single cells expressed catalase-peroxidase (KatG), which activates INH, in stochastic
pulses that were negatively correlated with cell survival. These behaviors may
reflect epigenetic effects, because KatG pulsing and death were correlated between
sibling cells. Selection of lineages characterized by infrequent KatG pulsing
could allow nonresponsive adaptation during prolonged drug exposure.
author:
- first_name: Yurichi
full_name: Wakamoto, Yurichi
last_name: Wakamoto
- first_name: Neraaj
full_name: Dhar, Neraaj
last_name: Dhar
- first_name: Remy P
full_name: Chait, Remy P
id: 3464AE84-F248-11E8-B48F-1D18A9856A87
last_name: Chait
orcid: 0000-0003-0876-3187
- first_name: Katrin
full_name: Schneider, Katrin
last_name: Schneider
- first_name: François
full_name: Signorino Gelo, François
last_name: Signorino Gelo
- first_name: Stanislas
full_name: Leibler, Stanislas
last_name: Leibler
- first_name: John
full_name: Mckinney, John
last_name: Mckinney
citation:
ama: Wakamoto Y, Dhar N, Chait RP, et al. Dynamic persistence of antibiotic-stressed
mycobacteria. Science. 2013;339(6115):91-95. doi:10.1126/science.1229858
apa: Wakamoto, Y., Dhar, N., Chait, R. P., Schneider, K., Signorino Gelo, F., Leibler,
S., & Mckinney, J. (2013). Dynamic persistence of antibiotic-stressed mycobacteria.
Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.1229858
chicago: Wakamoto, Yurichi, Neraaj Dhar, Remy P Chait, Katrin Schneider, François
Signorino Gelo, Stanislas Leibler, and John Mckinney. “Dynamic Persistence of
Antibiotic-Stressed Mycobacteria.” Science. American Association for the
Advancement of Science, 2013. https://doi.org/10.1126/science.1229858.
ieee: Y. Wakamoto et al., “Dynamic persistence of antibiotic-stressed mycobacteria,”
Science, vol. 339, no. 6115. American Association for the Advancement of
Science, pp. 91–95, 2013.
ista: Wakamoto Y, Dhar N, Chait RP, Schneider K, Signorino Gelo F, Leibler S, Mckinney
J. 2013. Dynamic persistence of antibiotic-stressed mycobacteria. Science. 339(6115),
91–95.
mla: Wakamoto, Yurichi, et al. “Dynamic Persistence of Antibiotic-Stressed Mycobacteria.”
Science, vol. 339, no. 6115, American Association for the Advancement of
Science, 2013, pp. 91–95, doi:10.1126/science.1229858.
short: Y. Wakamoto, N. Dhar, R.P. Chait, K. Schneider, F. Signorino Gelo, S. Leibler,
J. Mckinney, Science 339 (2013) 91–95.
date_created: 2018-12-11T11:46:48Z
date_published: 2013-01-04T00:00:00Z
date_updated: 2021-01-12T08:01:06Z
day: '04'
department:
- _id: CaGu
- _id: GaTk
doi: 10.1126/science.1229858
intvolume: ' 339'
issue: '6115'
language:
- iso: eng
month: '01'
oa_version: None
page: 91 - 95
publication: Science
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '7321'
quality_controlled: '1'
scopus_import: 1
status: public
title: Dynamic persistence of antibiotic-stressed mycobacteria
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 339
year: '2013'
...
---
_id: '9751'
abstract:
- lang: eng
text: High relatedness among interacting individuals has generally been considered
a precondition for the evolution of altruism. However, kin-selection theory also
predicts the evolution of altruism when relatedness is low, as long as the cost
of the altruistic act is minor compared to its benefit. Here, we demonstrate evidence
for a low-cost altruistic act in bacteria. We investigated Escherichia coli responding
to the attack of an obligately lytic phage by committing suicide in order to prevent
parasite transmission to nearby relatives. We found that bacterial suicide provides
large benefits to survivors at marginal costs to committers. The cost of suicide
was low because infected cells are moribund, rapidly dying upon phage infection,
such that no more opportunity for reproduction remains. As a consequence of its
marginal cost, host suicide was selectively favoured even when relatedness between
committers and survivors approached zero. Altogether, our findings demonstrate
that low-cost suicide can evolve with ease, represents an effective host-defence
strategy, and seems to be widespread among microbes. Moreover, low-cost suicide
might also occur in higher organisms as exemplified by infected social insect
workers leaving the colony to die in isolation.
article_processing_charge: No
author:
- first_name: Dominik
full_name: Refardt, Dominik
last_name: Refardt
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Rolf
full_name: Kümmerli, Rolf
last_name: Kümmerli
citation:
ama: 'Refardt D, Bergmiller T, Kümmerli R. Data from: Altruism can evolve when relatedness
is low: evidence from bacteria committing suicide upon phage infection. 2013.
doi:10.5061/dryad.b1q2n'
apa: 'Refardt, D., Bergmiller, T., & Kümmerli, R. (2013). Data from: Altruism
can evolve when relatedness is low: evidence from bacteria committing suicide
upon phage infection. Dryad. https://doi.org/10.5061/dryad.b1q2n'
chicago: 'Refardt, Dominik, Tobias Bergmiller, and Rolf Kümmerli. “Data from: Altruism
Can Evolve When Relatedness Is Low: Evidence from Bacteria Committing Suicide
upon Phage Infection.” Dryad, 2013. https://doi.org/10.5061/dryad.b1q2n.'
ieee: 'D. Refardt, T. Bergmiller, and R. Kümmerli, “Data from: Altruism can evolve
when relatedness is low: evidence from bacteria committing suicide upon phage
infection.” Dryad, 2013.'
ista: 'Refardt D, Bergmiller T, Kümmerli R. 2013. Data from: Altruism can evolve
when relatedness is low: evidence from bacteria committing suicide upon phage
infection, Dryad, 10.5061/dryad.b1q2n.'
mla: 'Refardt, Dominik, et al. Data from: Altruism Can Evolve When Relatedness
Is Low: Evidence from Bacteria Committing Suicide upon Phage Infection. Dryad,
2013, doi:10.5061/dryad.b1q2n.'
short: D. Refardt, T. Bergmiller, R. Kümmerli, (2013).
date_created: 2021-07-30T08:08:09Z
date_published: 2013-03-21T00:00:00Z
date_updated: 2023-10-18T06:43:22Z
day: '21'
department:
- _id: CaGu
doi: 10.5061/dryad.b1q2n
main_file_link:
- open_access: '1'
url: https://doi.org/10.5061/dryad.b1q2n
month: '03'
oa: 1
oa_version: Published Version
publisher: Dryad
related_material:
record:
- id: '2853'
relation: used_in_publication
status: public
status: public
title: 'Data from: Altruism can evolve when relatedness is low: evidence from bacteria
committing suicide upon phage infection'
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2013'
...
---
_id: '2943'
abstract:
- lang: eng
text: We examine whether the Escherichia coli chromosome is folded into a self-adherent
nucleoprotein complex, or alternately is a confined but otherwise unconstrained
self-avoiding polymer. We address this through in vivo visualization, using an
inducible GFP fusion to the nucleoid-associated protein Fis to non-specifically
decorate the entire chromosome. For a range of different growth conditions, the
chromosome is a compact structure that does not fill the volume of the cell, and
which moves from the new pole to the cell centre. During rapid growth, chromosome
segregation occurs well before cell division, with daughter chromosomes coupled
by a thin inter-daughter filament before complete segregation, whereas during
slow growth chromosomes stay adjacent until cell division occurs. Image correlation
analysis indicates that sub-nucleoid structure is stable on a 1min timescale,
comparable to the timescale for redistribution time measured for GFP-Fis after
photobleaching. Optical deconvolution and writhe calculation analysis indicate
that the nucleoid has a large-scale coiled organization rather than being an amorphous
mass. Our observations are consistent with the chromosome having a self-adherent
filament organization.
acknowledgement: We thank Professor Philippe Cluzel and Mr Lance Min for providing
advice and materials. Jeannette Chau provided technical support. Work at NU was
supported by NSF Grants DMR-0715099, MCB-1022117, DMR-1206868, DMR-0520513 and DMR-1121262
(NU-MRSEC), by NIH-NCI Grant U54CA143869-01 (NU-PS-OC) and by the Chicago Biomedical
Consortium with support from the Searle Funds at the Chicago Community Trust. Work
at UCLA was supported by NIH Grant GM038509.
author:
- first_name: Nastaran
full_name: Hadizadeh Yazdi, Nastaran
last_name: Hadizadeh Yazdi
- 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: Reid
full_name: Johnson, Reid
last_name: Johnson
- first_name: John
full_name: Marko, John
last_name: Marko
citation:
ama: Hadizadeh Yazdi N, Guet CC, Johnson R, Marko J. Variation of the folding and
dynamics of the Escherichia coli chromosome with growth conditions. Molecular
Microbiology. 2012;86(6):1318-1333. doi:10.1111/mmi.12071
apa: Hadizadeh Yazdi, N., Guet, C. C., Johnson, R., & Marko, J. (2012). Variation
of the folding and dynamics of the Escherichia coli chromosome with growth conditions.
Molecular Microbiology. Wiley-Blackwell. https://doi.org/10.1111/mmi.12071
chicago: Hadizadeh Yazdi, Nastaran, Calin C Guet, Reid Johnson, and John Marko.
“Variation of the Folding and Dynamics of the Escherichia Coli Chromosome with
Growth Conditions.” Molecular Microbiology. Wiley-Blackwell, 2012. https://doi.org/10.1111/mmi.12071.
ieee: N. Hadizadeh Yazdi, C. C. Guet, R. Johnson, and J. Marko, “Variation of the
folding and dynamics of the Escherichia coli chromosome with growth conditions,”
Molecular Microbiology, vol. 86, no. 6. Wiley-Blackwell, pp. 1318–1333,
2012.
ista: Hadizadeh Yazdi N, Guet CC, Johnson R, Marko J. 2012. Variation of the folding
and dynamics of the Escherichia coli chromosome with growth conditions. Molecular
Microbiology. 86(6), 1318–1333.
mla: Hadizadeh Yazdi, Nastaran, et al. “Variation of the Folding and Dynamics of
the Escherichia Coli Chromosome with Growth Conditions.” Molecular Microbiology,
vol. 86, no. 6, Wiley-Blackwell, 2012, pp. 1318–33, doi:10.1111/mmi.12071.
short: N. Hadizadeh Yazdi, C.C. Guet, R. Johnson, J. Marko, Molecular Microbiology
86 (2012) 1318–1333.
date_created: 2018-12-11T12:00:28Z
date_published: 2012-11-09T00:00:00Z
date_updated: 2021-01-12T07:39:56Z
day: '09'
department:
- _id: CaGu
doi: 10.1111/mmi.12071
intvolume: ' 86'
issue: '6'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://europepmc.org/articles/pmc3524407
month: '11'
oa: 1
oa_version: Submitted Version
page: 1318 - 1333
publication: Molecular Microbiology
publication_status: published
publisher: Wiley-Blackwell
publist_id: '3790'
quality_controlled: '1'
scopus_import: 1
status: public
title: Variation of the folding and dynamics of the Escherichia coli chromosome with
growth conditions
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 86
year: '2012'
...
---
_id: '3130'
abstract:
- lang: eng
text: 'Essential genes code for fundamental cellular functions required for the
viability of an organism. For this reason, essential genes are often highly conserved
across organisms. However, this is not always the case: orthologues of genes that
are essential in one organism are sometimes not essential in other organisms or
are absent from their genomes. This suggests that, in the course of evolution,
essential genes can be rendered nonessential. How can a gene become non-essential?
Here we used genetic manipulation to deplete the products of 26 different essential
genes in Escherichia coli. This depletion results in a lethal phenotype, which
could often be rescued by the overexpression of a non-homologous, non-essential
gene, most likely through replacement of the essential function. We also show
that, in a smaller number of cases, the essential genes can be fully deleted from
the genome, suggesting that complete functional replacement is possible. Finally,
we show that essential genes whose function can be replaced in the laboratory
are more likely to be non-essential or not present in other taxa. These results
are consistent with the notion that patterns of evolutionary conservation of essential
genes are influenced by their compensability-that is, by how easily they can be
functionally replaced, for example through increased expression of other genes.'
acknowledgement: We thank Alex Boehm for discussions and comments.
article_number: e1002803
author:
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Martin
full_name: Ackermann, Martin
last_name: Ackermann
- first_name: Olin
full_name: Silander, Olin
last_name: Silander
citation:
ama: Bergmiller T, Ackermann M, Silander O. Patterns of evolutionary conservation
of essential genes correlate with their compensability. PLoS Genetics.
2012;8(6). doi:10.1371/journal.pgen.1002803
apa: Bergmiller, T., Ackermann, M., & Silander, O. (2012). Patterns of evolutionary
conservation of essential genes correlate with their compensability. PLoS Genetics.
Public Library of Science. https://doi.org/10.1371/journal.pgen.1002803
chicago: Bergmiller, Tobias, Martin Ackermann, and Olin Silander. “Patterns of Evolutionary
Conservation of Essential Genes Correlate with Their Compensability.” PLoS
Genetics. Public Library of Science, 2012. https://doi.org/10.1371/journal.pgen.1002803.
ieee: T. Bergmiller, M. Ackermann, and O. Silander, “Patterns of evolutionary conservation
of essential genes correlate with their compensability,” PLoS Genetics,
vol. 8, no. 6. Public Library of Science, 2012.
ista: Bergmiller T, Ackermann M, Silander O. 2012. Patterns of evolutionary conservation
of essential genes correlate with their compensability. PLoS Genetics. 8(6), e1002803.
mla: Bergmiller, Tobias, et al. “Patterns of Evolutionary Conservation of Essential
Genes Correlate with Their Compensability.” PLoS Genetics, vol. 8, no.
6, e1002803, Public Library of Science, 2012, doi:10.1371/journal.pgen.1002803.
short: T. Bergmiller, M. Ackermann, O. Silander, PLoS Genetics 8 (2012).
date_created: 2018-12-11T12:01:34Z
date_published: 2012-06-28T00:00:00Z
date_updated: 2021-01-12T07:41:16Z
day: '28'
ddc:
- '576'
department:
- _id: CaGu
doi: 10.1371/journal.pgen.1002803
file:
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checksum: f8506fb579eda6fc5613ba9bf421b86a
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date_created: 2018-12-12T10:12:52Z
date_updated: 2020-07-14T12:46:01Z
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file_name: IST-2015-386-v1+1_journal.pgen.1002803.pdf
file_size: 2674138
relation: main_file
file_date_updated: 2020-07-14T12:46:01Z
has_accepted_license: '1'
intvolume: ' 8'
issue: '6'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
publication: PLoS Genetics
publication_status: published
publisher: Public Library of Science
publist_id: '3567'
pubrep_id: '386'
quality_controlled: '1'
scopus_import: 1
status: public
title: Patterns of evolutionary conservation of essential genes correlate with their
compensability
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: 8
year: '2012'
...
---
_id: '3136'
abstract:
- lang: eng
text: 'Continuous-time Markov chains (CTMC) with their rich theory and efficient
simulation algorithms have been successfully used in modeling stochastic processes
in diverse areas such as computer science, physics, and biology. However, systems
that comprise non-instantaneous events cannot be accurately and efficiently modeled
with CTMCs. In this paper we define delayed CTMCs, an extension of CTMCs that
allows for the specification of a lower bound on the time interval between an
event''s initiation and its completion, and we propose an algorithm for the computation
of their behavior. Our algorithm effectively decomposes the computation into two
stages: a pure CTMC governs event initiations while a deterministic process guarantees
lower bounds on event completion times. Furthermore, from the nature of delayed
CTMCs, we obtain a parallelized version of our algorithm. We use our formalism
to model genetic regulatory circuits (biological systems where delayed events
are common) and report on the results of our numerical algorithm as run on a cluster.
We compare performance and accuracy of our results with results obtained by using
pure CTMCs. © 2012 Springer-Verlag.'
acknowledgement: This work was supported by the ERC Advanced Investigator grant on
Quantitative Reactive Modeling (QUAREM) and by the Swiss National Science Foundation.
alternative_title:
- LNCS
author:
- 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: Maria
full_name: Mateescu, Maria
id: 3B43276C-F248-11E8-B48F-1D18A9856A87
last_name: Mateescu
- first_name: Ali
full_name: Sezgin, Ali
id: 4C7638DA-F248-11E8-B48F-1D18A9856A87
last_name: Sezgin
citation:
ama: 'Guet CC, Gupta A, Henzinger TA, Mateescu M, Sezgin A. Delayed continuous time
Markov chains for genetic regulatory circuits. In: Vol 7358. Springer; 2012:294-309.
doi:10.1007/978-3-642-31424-7_24'
apa: 'Guet, C. C., Gupta, A., Henzinger, T. A., Mateescu, M., & Sezgin, A. (2012).
Delayed continuous time Markov chains for genetic regulatory circuits (Vol. 7358,
pp. 294–309). Presented at the CAV: Computer Aided Verification, Berkeley, CA,
USA: Springer. https://doi.org/10.1007/978-3-642-31424-7_24'
chicago: Guet, Calin C, Ashutosh Gupta, Thomas A Henzinger, Maria Mateescu, and
Ali Sezgin. “Delayed Continuous Time Markov Chains for Genetic Regulatory Circuits,”
7358:294–309. Springer, 2012. https://doi.org/10.1007/978-3-642-31424-7_24.
ieee: 'C. C. Guet, A. Gupta, T. A. Henzinger, M. Mateescu, and A. Sezgin, “Delayed
continuous time Markov chains for genetic regulatory circuits,” presented at the
CAV: Computer Aided Verification, Berkeley, CA, USA, 2012, vol. 7358, pp. 294–309.'
ista: 'Guet CC, Gupta A, Henzinger TA, Mateescu M, Sezgin A. 2012. Delayed continuous
time Markov chains for genetic regulatory circuits. CAV: Computer Aided Verification,
LNCS, vol. 7358, 294–309.'
mla: Guet, Calin C., et al. Delayed Continuous Time Markov Chains for Genetic
Regulatory Circuits. Vol. 7358, Springer, 2012, pp. 294–309, doi:10.1007/978-3-642-31424-7_24.
short: C.C. Guet, A. Gupta, T.A. Henzinger, M. Mateescu, A. Sezgin, in:, Springer,
2012, pp. 294–309.
conference:
end_date: 2012-07-13
location: Berkeley, CA, USA
name: 'CAV: Computer Aided Verification'
start_date: 2012-07-07
date_created: 2018-12-11T12:01:36Z
date_published: 2012-07-01T00:00:00Z
date_updated: 2021-01-12T07:41:18Z
day: '01'
department:
- _id: CaGu
- _id: ToHe
doi: 10.1007/978-3-642-31424-7_24
ec_funded: 1
language:
- iso: eng
month: '07'
oa_version: None
page: 294 - 309
project:
- _id: 25EE3708-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '267989'
name: Quantitative Reactive Modeling
publication_status: published
publisher: Springer
publist_id: '3561'
quality_controlled: '1'
scopus_import: 1
status: public
title: Delayed continuous time Markov chains for genetic regulatory circuits
type: conference
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: '7358 '
year: '2012'
...