---
_id: '1423'
abstract:
- lang: eng
text: 'Direct reciprocity is a mechanism for the evolution of cooperation based
on repeated interactions. When individuals meet repeatedly, they can use conditional
strategies to enforce cooperative outcomes that would not be feasible in one-shot
social dilemmas. Direct reciprocity requires that individuals keep track of their
past interactions and find the right response. However, there are natural bounds
on strategic complexity: Humans find it difficult to remember past interactions
accurately, especially over long timespans. Given these limitations, it is natural
to ask how complex strategies need to be for cooperation to evolve. Here, we study
stochastic evolutionary game dynamics in finite populations to systematically
compare the evolutionary performance of reactive strategies, which only respond
to the co-player''s previous move, and memory-one strategies, which take into
account the own and the co-player''s previous move. In both cases, we compare
deterministic strategy and stochastic strategy spaces. For reactive strategies
and small costs, we find that stochasticity benefits cooperation, because it allows
for generous-tit-for-tat. For memory one strategies and small costs, we find that
stochasticity does not increase the propensity for cooperation, because the deterministic
rule of win-stay, lose-shift works best. For memory one strategies and large costs,
however, stochasticity can augment cooperation.'
acknowledgement: C.H. acknowledges generous funding from the Schrödinger scholarship
of the Austrian Science Fund (FWF), J3475.
article_number: '25676'
author:
- first_name: Seung
full_name: Baek, Seung
last_name: Baek
- first_name: Hyeongchai
full_name: Jeong, Hyeongchai
last_name: Jeong
- first_name: Christian
full_name: Hilbe, Christian
id: 2FDF8F3C-F248-11E8-B48F-1D18A9856A87
last_name: Hilbe
orcid: 0000-0001-5116-955X
- first_name: Martin
full_name: Nowak, Martin
last_name: Nowak
citation:
ama: Baek S, Jeong H, Hilbe C, Nowak M. Comparing reactive and memory-one strategies
of direct reciprocity. Scientific Reports. 2016;6. doi:10.1038/srep25676
apa: Baek, S., Jeong, H., Hilbe, C., & Nowak, M. (2016). Comparing reactive
and memory-one strategies of direct reciprocity. Scientific Reports. Nature
Publishing Group. https://doi.org/10.1038/srep25676
chicago: Baek, Seung, Hyeongchai Jeong, Christian Hilbe, and Martin Nowak. “Comparing
Reactive and Memory-One Strategies of Direct Reciprocity.” Scientific Reports.
Nature Publishing Group, 2016. https://doi.org/10.1038/srep25676.
ieee: S. Baek, H. Jeong, C. Hilbe, and M. Nowak, “Comparing reactive and memory-one
strategies of direct reciprocity,” Scientific Reports, vol. 6. Nature Publishing
Group, 2016.
ista: Baek S, Jeong H, Hilbe C, Nowak M. 2016. Comparing reactive and memory-one
strategies of direct reciprocity. Scientific Reports. 6, 25676.
mla: Baek, Seung, et al. “Comparing Reactive and Memory-One Strategies of Direct
Reciprocity.” Scientific Reports, vol. 6, 25676, Nature Publishing Group,
2016, doi:10.1038/srep25676.
short: S. Baek, H. Jeong, C. Hilbe, M. Nowak, Scientific Reports 6 (2016).
date_created: 2018-12-11T11:51:56Z
date_published: 2016-05-10T00:00:00Z
date_updated: 2021-01-12T06:50:38Z
day: '10'
ddc:
- '000'
department:
- _id: KrCh
doi: 10.1038/srep25676
file:
- access_level: open_access
checksum: ee17c482370d2e1b3add393710d3c696
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:18:08Z
date_updated: 2020-07-14T12:44:53Z
file_id: '5327'
file_name: IST-2016-590-v1+1_srep25676.pdf
file_size: 1349915
relation: main_file
file_date_updated: 2020-07-14T12:44:53Z
has_accepted_license: '1'
intvolume: ' 6'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
publication: Scientific Reports
publication_status: published
publisher: Nature Publishing Group
publist_id: '5784'
pubrep_id: '590'
quality_controlled: '1'
scopus_import: 1
status: public
title: Comparing reactive and memory-one strategies of direct reciprocity
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: 6
year: '2016'
...
---
_id: '1426'
abstract:
- lang: eng
text: 'Brood parasites exploit their host in order to increase their own fitness.
Typically, this results in an arms race between parasite trickery and host defence.
Thus, it is puzzling to observe hosts that accept parasitism without any resistance.
The ‘mafia’ hypothesis suggests that these hosts accept parasitism to avoid retaliation.
Retaliation has been shown to evolve when the hosts condition their response to
mafia parasites, who use depredation as a targeted response to rejection. However,
it is unclear if acceptance would also emerge when ‘farming’ parasites are present
in the population. Farming parasites use depredation to synchronize the timing
with the host, destroying mature clutches to force the host to re-nest. Herein,
we develop an evolutionary model to analyse the interaction between depredatory
parasites and their hosts. We show that coevolutionary cycles between farmers
and mafia can still induce host acceptance of brood parasites. However, this equilibrium
is unstable and in the long-run the dynamics of this host–parasite interaction
exhibits strong oscillations: when farmers are the majority, accepters conditional
to mafia (the host will reject first and only accept after retaliation by the
parasite) have a higher fitness than unconditional accepters (the host always
accepts parasitism). This leads to an increase in mafia parasites’ fitness and
in turn induce an optimal environment for accepter hosts.'
acknowledgement: C.H. gratefully acknowledges funding by the Schrödinger scholarship
of the Austrian Science Fund (FWF) J3475.
article_number: '160036'
author:
- first_name: Maria
full_name: Chakra, Maria
last_name: Chakra
- first_name: Christian
full_name: Hilbe, Christian
id: 2FDF8F3C-F248-11E8-B48F-1D18A9856A87
last_name: Hilbe
orcid: 0000-0001-5116-955X
- first_name: Arne
full_name: Traulsen, Arne
last_name: Traulsen
citation:
ama: Chakra M, Hilbe C, Traulsen A. Coevolutionary interactions between farmers
and mafia induce host acceptance of avian brood parasites. Royal Society Open
Science. 2016;3(5). doi:10.1098/rsos.160036
apa: Chakra, M., Hilbe, C., & Traulsen, A. (2016). Coevolutionary interactions
between farmers and mafia induce host acceptance of avian brood parasites. Royal
Society Open Science. Royal Society, The. https://doi.org/10.1098/rsos.160036
chicago: Chakra, Maria, Christian Hilbe, and Arne Traulsen. “Coevolutionary Interactions
between Farmers and Mafia Induce Host Acceptance of Avian Brood Parasites.” Royal
Society Open Science. Royal Society, The, 2016. https://doi.org/10.1098/rsos.160036.
ieee: M. Chakra, C. Hilbe, and A. Traulsen, “Coevolutionary interactions between
farmers and mafia induce host acceptance of avian brood parasites,” Royal Society
Open Science, vol. 3, no. 5. Royal Society, The, 2016.
ista: Chakra M, Hilbe C, Traulsen A. 2016. Coevolutionary interactions between farmers
and mafia induce host acceptance of avian brood parasites. Royal Society Open
Science. 3(5), 160036.
mla: Chakra, Maria, et al. “Coevolutionary Interactions between Farmers and Mafia
Induce Host Acceptance of Avian Brood Parasites.” Royal Society Open Science,
vol. 3, no. 5, 160036, Royal Society, The, 2016, doi:10.1098/rsos.160036.
short: M. Chakra, C. Hilbe, A. Traulsen, Royal Society Open Science 3 (2016).
date_created: 2018-12-11T11:51:57Z
date_published: 2016-05-01T00:00:00Z
date_updated: 2021-01-12T06:50:39Z
day: '01'
ddc:
- '000'
department:
- _id: KrCh
doi: 10.1098/rsos.160036
file:
- access_level: open_access
checksum: bf84211b31fe87451e738ba301d729c3
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:49Z
date_updated: 2020-07-14T12:44:53Z
file_id: '5104'
file_name: IST-2016-589-v1+1_160036.full.pdf
file_size: 937002
relation: main_file
file_date_updated: 2020-07-14T12:44:53Z
has_accepted_license: '1'
intvolume: ' 3'
issue: '5'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
publication: Royal Society Open Science
publication_status: published
publisher: Royal Society, The
publist_id: '5776'
pubrep_id: '589'
quality_controlled: '1'
scopus_import: 1
status: public
title: Coevolutionary interactions between farmers and mafia induce host acceptance
of avian brood parasites
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: 3
year: '2016'
...
---
_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: '1428'
abstract:
- lang: eng
text: We report on a mathematically rigorous analysis of the superfluid properties
of a Bose- Einstein condensate in the many-body ground state of a one-dimensional
model of interacting bosons in a random potential.
article_number: '012016'
author:
- first_name: Martin
full_name: Könenberg, Martin
last_name: Könenberg
- first_name: Thomas
full_name: Moser, Thomas
id: 2B5FC9A4-F248-11E8-B48F-1D18A9856A87
last_name: Moser
- first_name: Robert
full_name: Seiringer, Robert
id: 4AFD0470-F248-11E8-B48F-1D18A9856A87
last_name: Seiringer
orcid: 0000-0002-6781-0521
- first_name: Jakob
full_name: Yngvason, Jakob
last_name: Yngvason
citation:
ama: 'Könenberg M, Moser T, Seiringer R, Yngvason J. Superfluidity and BEC in a
Model of Interacting Bosons in a Random Potential. In: Journal of Physics:
Conference Series. Vol 691. IOP Publishing Ltd.; 2016. doi:10.1088/1742-6596/691/1/012016'
apa: 'Könenberg, M., Moser, T., Seiringer, R., & Yngvason, J. (2016). Superfluidity
and BEC in a Model of Interacting Bosons in a Random Potential. In Journal
of Physics: Conference Series (Vol. 691). Shanghai, China: IOP Publishing
Ltd. https://doi.org/10.1088/1742-6596/691/1/012016'
chicago: 'Könenberg, Martin, Thomas Moser, Robert Seiringer, and Jakob Yngvason.
“Superfluidity and BEC in a Model of Interacting Bosons in a Random Potential.”
In Journal of Physics: Conference Series, Vol. 691. IOP Publishing Ltd.,
2016. https://doi.org/10.1088/1742-6596/691/1/012016.'
ieee: 'M. Könenberg, T. Moser, R. Seiringer, and J. Yngvason, “Superfluidity and
BEC in a Model of Interacting Bosons in a Random Potential,” in Journal of
Physics: Conference Series, Shanghai, China, 2016, vol. 691, no. 1.'
ista: 'Könenberg M, Moser T, Seiringer R, Yngvason J. 2016. Superfluidity and BEC
in a Model of Interacting Bosons in a Random Potential. Journal of Physics: Conference
Series. 24th International Laser Physics Workshop (LPHYS’15) vol. 691, 012016.'
mla: 'Könenberg, Martin, et al. “Superfluidity and BEC in a Model of Interacting
Bosons in a Random Potential.” Journal of Physics: Conference Series, vol.
691, no. 1, 012016, IOP Publishing Ltd., 2016, doi:10.1088/1742-6596/691/1/012016.'
short: 'M. Könenberg, T. Moser, R. Seiringer, J. Yngvason, in:, Journal of Physics:
Conference Series, IOP Publishing Ltd., 2016.'
conference:
end_date: 2015-08-25
location: Shanghai, China
name: 24th International Laser Physics Workshop (LPHYS'15)
start_date: 2015-08-21
date_created: 2018-12-11T11:51:58Z
date_published: 2016-03-07T00:00:00Z
date_updated: 2021-01-12T06:50:40Z
day: '07'
ddc:
- '510'
- '530'
department:
- _id: RoSe
doi: 10.1088/1742-6596/691/1/012016
file:
- access_level: open_access
checksum: 109db801749072c3f6c8f1a1848700fa
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:10:55Z
date_updated: 2020-07-14T12:44:53Z
file_id: '4847'
file_name: IST-2016-585-v1+1_JPCS_691_1_012016.pdf
file_size: 1434688
relation: main_file
file_date_updated: 2020-07-14T12:44:53Z
has_accepted_license: '1'
intvolume: ' 691'
issue: '1'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
project:
- _id: 25C878CE-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P27533_N27
name: Structure of the Excitation Spectrum for Many-Body Quantum Systems
publication: 'Journal of Physics: Conference Series'
publication_status: published
publisher: IOP Publishing Ltd.
publist_id: '5770'
pubrep_id: '585'
quality_controlled: '1'
scopus_import: 1
status: public
title: Superfluidity and BEC in a Model of Interacting Bosons in a Random Potential
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: conference
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 691
year: '2016'
...
---
_id: '1429'
abstract:
- lang: eng
text: Solitons are localized waves formed by a balance of focusing and defocusing
effects. These nonlinear waves exist in diverse forms of matter yet exhibit similar
properties including stability, periodic recurrence and particle-like trajectories.
One important property is soliton fission, a process by which an energetic higher-order
soliton breaks apart due to dispersive or nonlinear perturbations. Here we demonstrate
through both experiment and theory that nonlinear photocarrier generation can
induce soliton fission. Using near-field measurements, we directly observe the
nonlinear spatial and temporal evolution of optical pulses in situ in a nanophotonic
semiconductor waveguide. We develop an analytic formalism describing the free-carrier
dispersion (FCD) perturbation and show the experiment exceeds the minimum threshold
by an order of magnitude. We confirm these observations with a numerical nonlinear
Schrödinger equation model. These results provide a fundamental explanation and
physical scaling of optical pulse evolution in free-carrier media and could enable
improved supercontinuum sources in gas based and integrated semiconductor waveguides.
acknowledgement: This research was supported by the Australian Research Council (ARC)
Center of Excellence CUDOS (CE110001018), ARC Laureate Fellowship (FL120100029),
ARC Discovery Early Career Researcher Award (DECRA DE120102069), the Netherlands
Foundation for Fundamental Research on Matter (FOM) and the Netherlands Organization
for Scientific Research (NWO). L.K. acknowledges funding from ERC Advanced Investigator
Grant (no. 240438-CONSTANS). A.D.R, S.C., and G.L. acknowledge financial support
from the ERC-Pharos programme lead by A. P. Mosk.
article_number: 11332 (2016)
author:
- first_name: Chad
full_name: Husko, Chad
last_name: Husko
- first_name: Matthias
full_name: Wulf, Matthias
id: 45598606-F248-11E8-B48F-1D18A9856A87
last_name: Wulf
orcid: 0000-0001-6613-1378
- first_name: Simon
full_name: Lefrançois, Simon
last_name: Lefrançois
- first_name: Sylvain
full_name: Combrié, Sylvain
last_name: Combrié
- first_name: Gaëlle
full_name: Lehoucq, Gaëlle
last_name: Lehoucq
- first_name: Alfredo
full_name: De Rossi, Alfredo
last_name: De Rossi
- first_name: Benjamin
full_name: Eggleton, Benjamin
last_name: Eggleton
- first_name: Laurens
full_name: Kuipers, Laurens
last_name: Kuipers
citation:
ama: Husko C, Wulf M, Lefrançois S, et al. Free-carrier-induced soliton fission
unveiled by in situ measurements in nanophotonic waveguides. Nature Communications.
2016;7. doi:10.1038/ncomms11332
apa: Husko, C., Wulf, M., Lefrançois, S., Combrié, S., Lehoucq, G., De Rossi, A.,
… Kuipers, L. (2016). Free-carrier-induced soliton fission unveiled by in situ
measurements in nanophotonic waveguides. Nature Communications. Nature
Publishing Group. https://doi.org/10.1038/ncomms11332
chicago: Husko, Chad, Matthias Wulf, Simon Lefrançois, Sylvain Combrié, Gaëlle Lehoucq,
Alfredo De Rossi, Benjamin Eggleton, and Laurens Kuipers. “Free-Carrier-Induced
Soliton Fission Unveiled by in Situ Measurements in Nanophotonic Waveguides.”
Nature Communications. Nature Publishing Group, 2016. https://doi.org/10.1038/ncomms11332.
ieee: C. Husko et al., “Free-carrier-induced soliton fission unveiled by
in situ measurements in nanophotonic waveguides,” Nature Communications,
vol. 7. Nature Publishing Group, 2016.
ista: Husko C, Wulf M, Lefrançois S, Combrié S, Lehoucq G, De Rossi A, Eggleton
B, Kuipers L. 2016. Free-carrier-induced soliton fission unveiled by in situ measurements
in nanophotonic waveguides. Nature Communications. 7, 11332 (2016).
mla: Husko, Chad, et al. “Free-Carrier-Induced Soliton Fission Unveiled by in Situ
Measurements in Nanophotonic Waveguides.” Nature Communications, vol. 7,
11332 (2016), Nature Publishing Group, 2016, doi:10.1038/ncomms11332.
short: C. Husko, M. Wulf, S. Lefrançois, S. Combrié, G. Lehoucq, A. De Rossi, B.
Eggleton, L. Kuipers, Nature Communications 7 (2016).
date_created: 2018-12-11T11:51:58Z
date_published: 2016-04-15T00:00:00Z
date_updated: 2021-01-12T06:50:40Z
day: '15'
ddc:
- '530'
department:
- _id: JoFi
doi: 10.1038/ncomms11332
file:
- access_level: open_access
checksum: 6484fa81a2e52e4fdd7935e1ae6091d4
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:15:53Z
date_updated: 2020-07-14T12:44:53Z
file_id: '5177'
file_name: IST-2016-583-v1+1_ncomms11332.pdf
file_size: 965176
relation: main_file
file_date_updated: 2020-07-14T12:44:53Z
has_accepted_license: '1'
intvolume: ' 7'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_status: published
publisher: Nature Publishing Group
publist_id: '5769'
pubrep_id: '583'
quality_controlled: '1'
scopus_import: 1
status: public
title: Free-carrier-induced soliton fission unveiled by in situ measurements in nanophotonic
waveguides
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: 7
year: '2016'
...
---
_id: '9456'
abstract:
- lang: eng
text: The discovery of introns four decades ago was one of the most unexpected findings
in molecular biology. Introns are sequences interrupting genes that must be removed
as part of messenger RNA production. Genome sequencing projects have shown that
most eukaryotic genes contain at least one intron, and frequently many. Comparison
of these genomes reveals a history of long evolutionary periods during which few
introns were gained, punctuated by episodes of rapid, extensive gain. However,
although several detailed mechanisms for such episodic intron generation have
been proposed, none has been empirically supported on a genomic scale. Here we
show how short, non-autonomous DNA transposons independently generated hundreds
to thousands of introns in the prasinophyte Micromonas pusilla and the pelagophyte
Aureococcus anophagefferens. Each transposon carries one splice site. The other
splice site is co-opted from the gene sequence that is duplicated upon transposon
insertion, allowing perfect splicing out of the RNA. The distributions of sequences
that can be co-opted are biased with respect to codons, and phasing of transposon-generated
introns is similarly biased. These transposons insert between pre-existing nucleosomes,
so that multiple nearby insertions generate nucleosome-sized intervening segments.
Thus, transposon insertion and sequence co-option may explain the intron phase
biases and prevalence of nucleosome-sized exons observed in eukaryotes. Overall,
the two independent examples of proliferating elements illustrate a general DNA
transposon mechanism that can plausibly account for episodes of rapid, extensive
intron gain during eukaryotic evolution.
article_processing_charge: No
article_type: letter_note
author:
- first_name: Jason T.
full_name: Huff, Jason T.
last_name: Huff
- first_name: Daniel
full_name: Zilberman, Daniel
id: 6973db13-dd5f-11ea-814e-b3e5455e9ed1
last_name: Zilberman
orcid: 0000-0002-0123-8649
- first_name: Scott W.
full_name: Roy, Scott W.
last_name: Roy
citation:
ama: Huff JT, Zilberman D, Roy SW. Mechanism for DNA transposons to generate introns
on genomic scales. Nature. 2016;538(7626):533-536. doi:10.1038/nature20110
apa: Huff, J. T., Zilberman, D., & Roy, S. W. (2016). Mechanism for DNA transposons
to generate introns on genomic scales. Nature. Springer Nature . https://doi.org/10.1038/nature20110
chicago: Huff, Jason T., Daniel Zilberman, and Scott W. Roy. “Mechanism for DNA
Transposons to Generate Introns on Genomic Scales.” Nature. Springer Nature
, 2016. https://doi.org/10.1038/nature20110.
ieee: J. T. Huff, D. Zilberman, and S. W. Roy, “Mechanism for DNA transposons to
generate introns on genomic scales,” Nature, vol. 538, no. 7626. Springer
Nature , pp. 533–536, 2016.
ista: Huff JT, Zilberman D, Roy SW. 2016. Mechanism for DNA transposons to generate
introns on genomic scales. Nature. 538(7626), 533–536.
mla: Huff, Jason T., et al. “Mechanism for DNA Transposons to Generate Introns on
Genomic Scales.” Nature, vol. 538, no. 7626, Springer Nature , 2016, pp.
533–36, doi:10.1038/nature20110.
short: J.T. Huff, D. Zilberman, S.W. Roy, Nature 538 (2016) 533–536.
date_created: 2021-06-04T11:34:55Z
date_published: 2016-10-27T00:00:00Z
date_updated: 2021-12-14T07:55:30Z
day: '27'
department:
- _id: DaZi
doi: 10.1038/nature20110
extern: '1'
external_id:
pmid:
- '27760113'
intvolume: ' 538'
issue: '7626'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5684705/
month: '10'
oa: 1
oa_version: Submitted Version
page: 533-536
pmid: 1
publication: Nature
publication_identifier:
eissn:
- 1476-4687
issn:
- 0028-0836
publication_status: published
publisher: 'Springer Nature '
quality_controlled: '1'
scopus_import: '1'
status: public
title: Mechanism for DNA transposons to generate introns on genomic scales
type: journal_article
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
volume: 538
year: '2016'
...
---
_id: '9473'
abstract:
- lang: eng
text: Cytosine DNA methylation regulates the expression of eukaryotic genes and
transposons. Methylation is copied by methyltransferases after DNA replication,
which results in faithful transmission of methylation patterns during cell division
and, at least in flowering plants, across generations. Transgenerational inheritance
is mediated by a small group of cells that includes gametes and their progenitors.
However, methylation is usually analyzed in somatic tissues that do not contribute
to the next generation, and the mechanisms of transgenerational inheritance are
inferred from such studies. To gain a better understanding of how DNA methylation
is inherited, we analyzed purified Arabidopsis thaliana sperm and vegetative cells-the
cell types that comprise pollen-with mutations in the DRM, CMT2, and CMT3 methyltransferases.
We find that DNA methylation dependency on these enzymes is similar in sperm,
vegetative cells, and somatic tissues, although DRM activity extends into heterochromatin
in vegetative cells, likely reflecting transcription of heterochromatic transposons
in this cell type. We also show that lack of histone H1, which elevates heterochromatic
DNA methylation in somatic tissues, does not have this effect in pollen. Instead,
levels of CG methylation in wild-type sperm and vegetative cells, as well as in
wild-type microspores from which both pollen cell types originate, are substantially
higher than in wild-type somatic tissues and similar to those of H1-depleted roots.
Our results demonstrate that the mechanisms of methylation maintenance are similar
between pollen and somatic cells, but the efficiency of CG methylation is higher
in pollen, allowing methylation patterns to be accurately inherited across generations.
article_processing_charge: No
article_type: original
author:
- first_name: Ping-Hung
full_name: Hsieh, Ping-Hung
last_name: Hsieh
- first_name: Shengbo
full_name: He, Shengbo
last_name: He
- first_name: Toby
full_name: Buttress, Toby
last_name: Buttress
- first_name: Hongbo
full_name: Gao, Hongbo
last_name: Gao
- first_name: Matthew
full_name: Couchman, Matthew
last_name: Couchman
- first_name: Robert L.
full_name: Fischer, Robert L.
last_name: Fischer
- first_name: Daniel
full_name: Zilberman, Daniel
id: 6973db13-dd5f-11ea-814e-b3e5455e9ed1
last_name: Zilberman
orcid: 0000-0002-0123-8649
- first_name: Xiaoqi
full_name: Feng, Xiaoqi
id: e0164712-22ee-11ed-b12a-d80fcdf35958
last_name: Feng
orcid: 0000-0002-4008-1234
citation:
ama: Hsieh P-H, He S, Buttress T, et al. Arabidopsis male sexual lineage exhibits
more robust maintenance of CG methylation than somatic tissues. Proceedings
of the National Academy of Sciences. 2016;113(52):15132-15137. doi:10.1073/pnas.1619074114
apa: Hsieh, P.-H., He, S., Buttress, T., Gao, H., Couchman, M., Fischer, R. L.,
… Feng, X. (2016). Arabidopsis male sexual lineage exhibits more robust maintenance
of CG methylation than somatic tissues. Proceedings of the National Academy
of Sciences. National Academy of Sciences. https://doi.org/10.1073/pnas.1619074114
chicago: Hsieh, Ping-Hung, Shengbo He, Toby Buttress, Hongbo Gao, Matthew Couchman,
Robert L. Fischer, Daniel Zilberman, and Xiaoqi Feng. “Arabidopsis Male Sexual
Lineage Exhibits More Robust Maintenance of CG Methylation than Somatic Tissues.”
Proceedings of the National Academy of Sciences. National Academy of Sciences,
2016. https://doi.org/10.1073/pnas.1619074114.
ieee: P.-H. Hsieh et al., “Arabidopsis male sexual lineage exhibits more
robust maintenance of CG methylation than somatic tissues,” Proceedings of
the National Academy of Sciences, vol. 113, no. 52. National Academy of Sciences,
pp. 15132–15137, 2016.
ista: Hsieh P-H, He S, Buttress T, Gao H, Couchman M, Fischer RL, Zilberman D, Feng
X. 2016. Arabidopsis male sexual lineage exhibits more robust maintenance of CG
methylation than somatic tissues. Proceedings of the National Academy of Sciences.
113(52), 15132–15137.
mla: Hsieh, Ping-Hung, et al. “Arabidopsis Male Sexual Lineage Exhibits More Robust
Maintenance of CG Methylation than Somatic Tissues.” Proceedings of the National
Academy of Sciences, vol. 113, no. 52, National Academy of Sciences, 2016,
pp. 15132–37, doi:10.1073/pnas.1619074114.
short: P.-H. Hsieh, S. He, T. Buttress, H. Gao, M. Couchman, R.L. Fischer, D. Zilberman,
X. Feng, Proceedings of the National Academy of Sciences 113 (2016) 15132–15137.
date_created: 2021-06-07T06:21:39Z
date_published: 2016-12-27T00:00:00Z
date_updated: 2023-05-08T11:00:40Z
day: '27'
department:
- _id: DaZi
- _id: XiFe
doi: 10.1073/pnas.1619074114
extern: '1'
external_id:
pmid:
- '27956643'
intvolume: ' 113'
issue: '52'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1073/pnas.1619074114
month: '12'
oa: 1
oa_version: Published Version
page: 15132-15137
pmid: 1
publication: Proceedings of the National Academy of Sciences
publication_identifier:
eissn:
- 1091-6490
issn:
- 0027-8424
publication_status: published
publisher: National Academy of Sciences
quality_controlled: '1'
scopus_import: '1'
status: public
title: Arabidopsis male sexual lineage exhibits more robust maintenance of CG methylation
than somatic tissues
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 113
year: '2016'
...
---
_id: '9477'
abstract:
- lang: eng
text: Cytosine methylation is a DNA modification with important regulatory functions
in eukaryotes. In flowering plants, sexual reproduction is accompanied by extensive
DNA demethylation, which is required for proper gene expression in the endosperm,
a nutritive extraembryonic seed tissue. Endosperm arises from a fusion of a sperm
cell carried in the pollen and a female central cell. Endosperm DNA demethylation
is observed specifically on the chromosomes inherited from the central cell in
Arabidopsis thaliana, rice, and maize, and requires the DEMETER DNA demethylase
in Arabidopsis. DEMETER is expressed in the central cell before fertilization,
suggesting that endosperm demethylation patterns are inherited from the central
cell. Down-regulation of the MET1 DNA methyltransferase has also been proposed
to contribute to central cell demethylation. However, with the exception of three
maize genes, central cell DNA methylation has not been directly measured, leaving
the origin and mechanism of endosperm demethylation uncertain. Here, we report
genome-wide analysis of DNA methylation in the central cells of Arabidopsis and
rice—species that diverged 150 million years ago—as well as in rice egg cells.
We find that DNA demethylation in both species is initiated in central cells,
which requires DEMETER in Arabidopsis. However, we do not observe a global reduction
of CG methylation that would be indicative of lowered MET1 activity; on the contrary,
CG methylation efficiency is elevated in female gametes compared with nonsexual
tissues. Our results demonstrate that locus-specific, active DNA demethylation
in the central cell is the origin of maternal chromosome hypomethylation in the
endosperm.
article_processing_charge: No
article_type: original
author:
- first_name: Kyunghyuk
full_name: Park, Kyunghyuk
last_name: Park
- first_name: M. Yvonne
full_name: Kim, M. Yvonne
last_name: Kim
- first_name: Martin
full_name: Vickers, Martin
last_name: Vickers
- first_name: Jin-Sup
full_name: Park, Jin-Sup
last_name: Park
- first_name: Youbong
full_name: Hyun, Youbong
last_name: Hyun
- first_name: Takashi
full_name: Okamoto, Takashi
last_name: Okamoto
- first_name: Daniel
full_name: Zilberman, Daniel
id: 6973db13-dd5f-11ea-814e-b3e5455e9ed1
last_name: Zilberman
orcid: 0000-0002-0123-8649
- first_name: Robert L.
full_name: Fischer, Robert L.
last_name: Fischer
- first_name: Xiaoqi
full_name: Feng, Xiaoqi
id: e0164712-22ee-11ed-b12a-d80fcdf35958
last_name: Feng
orcid: 0000-0002-4008-1234
- first_name: Yeonhee
full_name: Choi, Yeonhee
last_name: Choi
- first_name: Stefan
full_name: Scholten, Stefan
last_name: Scholten
citation:
ama: Park K, Kim MY, Vickers M, et al. DNA demethylation is initiated in the central
cells of Arabidopsis and rice. Proceedings of the National Academy of Sciences.
2016;113(52):15138-15143. doi:10.1073/pnas.1619047114
apa: Park, K., Kim, M. Y., Vickers, M., Park, J.-S., Hyun, Y., Okamoto, T., … Scholten,
S. (2016). DNA demethylation is initiated in the central cells of Arabidopsis
and rice. Proceedings of the National Academy of Sciences. National Academy
of Sciences. https://doi.org/10.1073/pnas.1619047114
chicago: Park, Kyunghyuk, M. Yvonne Kim, Martin Vickers, Jin-Sup Park, Youbong Hyun,
Takashi Okamoto, Daniel Zilberman, et al. “DNA Demethylation Is Initiated in the
Central Cells of Arabidopsis and Rice.” Proceedings of the National Academy
of Sciences. National Academy of Sciences, 2016. https://doi.org/10.1073/pnas.1619047114.
ieee: K. Park et al., “DNA demethylation is initiated in the central cells
of Arabidopsis and rice,” Proceedings of the National Academy of Sciences,
vol. 113, no. 52. National Academy of Sciences, pp. 15138–15143, 2016.
ista: Park K, Kim MY, Vickers M, Park J-S, Hyun Y, Okamoto T, Zilberman D, Fischer
RL, Feng X, Choi Y, Scholten S. 2016. DNA demethylation is initiated in the central
cells of Arabidopsis and rice. Proceedings of the National Academy of Sciences.
113(52), 15138–15143.
mla: Park, Kyunghyuk, et al. “DNA Demethylation Is Initiated in the Central Cells
of Arabidopsis and Rice.” Proceedings of the National Academy of Sciences,
vol. 113, no. 52, National Academy of Sciences, 2016, pp. 15138–43, doi:10.1073/pnas.1619047114.
short: K. Park, M.Y. Kim, M. Vickers, J.-S. Park, Y. Hyun, T. Okamoto, D. Zilberman,
R.L. Fischer, X. Feng, Y. Choi, S. Scholten, Proceedings of the National Academy
of Sciences 113 (2016) 15138–15143.
date_created: 2021-06-07T07:10:59Z
date_published: 2016-12-27T00:00:00Z
date_updated: 2023-05-08T11:00:07Z
day: '27'
department:
- _id: DaZi
- _id: XiFe
doi: 10.1073/pnas.1619047114
extern: '1'
external_id:
pmid:
- '27956642'
intvolume: ' 113'
issue: '52'
keyword:
- Multidisciplinary
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1073/pnas.1619047114
month: '12'
oa: 1
oa_version: Published Version
page: 15138-15143
pmid: 1
publication: Proceedings of the National Academy of Sciences
publication_identifier:
eissn:
- 1091-6490
issn:
- 0027-8424
publication_status: published
publisher: National Academy of Sciences
quality_controlled: '1'
scopus_import: '1'
status: public
title: DNA demethylation is initiated in the central cells of Arabidopsis and rice
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 113
year: '2016'
...
---
_id: '948'
abstract:
- lang: eng
text: Experience constantly shapes neural circuits through a variety of plasticity
mechanisms. While the functional roles of some plasticity mechanisms are well-understood,
it remains unclear how changes in neural excitability contribute to learning.
Here, we develop a normative interpretation of intrinsic plasticity (IP) as a
key component of unsupervised learning. We introduce a novel generative mixture
model that accounts for the class-specific statistics of stimulus intensities,
and we derive a neural circuit that learns the input classes and their intensities.
We will analytically show that inference and learning for our generative model
can be achieved by a neural circuit with intensity-sensitive neurons equipped
with a specific form of IP. Numerical experiments verify our analytical derivations
and show robust behavior for artificial and natural stimuli. Our results link
IP to non-trivial input statistics, in particular the statistics of stimulus intensities
for classes to which a neuron is sensitive. More generally, our work paves the
way toward new classification algorithms that are robust to intensity variations.
acknowledgement: DFG Cluster of Excellence EXC 1077/1 (Hearing4all) and LU 1196/5-1
(JL and TM), People Programme (Marie Curie Actions) FP7/2007-2013 grant agreement
no. 291734 (CS)
alternative_title:
- Advances in Neural Information Processing Systems
author:
- first_name: Travis
full_name: Monk, Travis
last_name: Monk
- first_name: Cristina
full_name: Savin, Cristina
id: 3933349E-F248-11E8-B48F-1D18A9856A87
last_name: Savin
- first_name: Jörg
full_name: Lücke, Jörg
last_name: Lücke
citation:
ama: 'Monk T, Savin C, Lücke J. Neurons equipped with intrinsic plasticity learn
stimulus intensity statistics. In: Vol 29. Neural Information Processing Systems;
2016:4285-4293.'
apa: 'Monk, T., Savin, C., & Lücke, J. (2016). Neurons equipped with intrinsic
plasticity learn stimulus intensity statistics (Vol. 29, pp. 4285–4293). Presented
at the NIPS: Neural Information Processing Systems, Barcelona, Spaine: Neural
Information Processing Systems.'
chicago: Monk, Travis, Cristina Savin, and Jörg Lücke. “Neurons Equipped with Intrinsic
Plasticity Learn Stimulus Intensity Statistics,” 29:4285–93. Neural Information
Processing Systems, 2016.
ieee: 'T. Monk, C. Savin, and J. Lücke, “Neurons equipped with intrinsic plasticity
learn stimulus intensity statistics,” presented at the NIPS: Neural Information
Processing Systems, Barcelona, Spaine, 2016, vol. 29, pp. 4285–4293.'
ista: 'Monk T, Savin C, Lücke J. 2016. Neurons equipped with intrinsic plasticity
learn stimulus intensity statistics. NIPS: Neural Information Processing Systems,
Advances in Neural Information Processing Systems, vol. 29, 4285–4293.'
mla: Monk, Travis, et al. Neurons Equipped with Intrinsic Plasticity Learn Stimulus
Intensity Statistics. Vol. 29, Neural Information Processing Systems, 2016,
pp. 4285–93.
short: T. Monk, C. Savin, J. Lücke, in:, Neural Information Processing Systems,
2016, pp. 4285–4293.
conference:
end_date: 2016-12-10
location: Barcelona, Spaine
name: 'NIPS: Neural Information Processing Systems'
start_date: 2016-12-05
date_created: 2018-12-11T11:49:21Z
date_published: 2016-01-01T00:00:00Z
date_updated: 2021-01-12T08:22:08Z
day: '01'
department:
- _id: GaTk
ec_funded: 1
intvolume: ' 29'
language:
- iso: eng
main_file_link:
- url: https://papers.nips.cc/paper/6582-neurons-equipped-with-intrinsic-plasticity-learn-stimulus-intensity-statistics
month: '01'
oa_version: None
page: 4285 - 4293
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
publication_status: published
publisher: Neural Information Processing Systems
publist_id: '6469'
quality_controlled: '1'
scopus_import: 1
status: public
title: Neurons equipped with intrinsic plasticity learn stimulus intensity statistics
type: conference
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 29
year: '2016'
...
---
_id: '1008'
abstract:
- lang: eng
text: Feedback loops in biological networks, among others, enable differentiation
and cell cycle progression, and increase robustness in signal transduction. In
natural networks, feedback loops are often complex and intertwined, making it
challenging to identify which loops are mainly responsible for an observed behavior.
However, minimal synthetic replicas could allow for such identification. Here,
we engineered a synthetic permease-inducer-repressor system in Saccharomyces cerevisiae
to analyze if a transport-mediated positive feedback loop could be a core mechanism
for the switch-like behavior in the regulation of metabolic gene networks such
as the S. cerevisiae GAL system or the Escherichia coli lac operon. We characterized
the synthetic circuit using deterministic and stochastic mathematical models.
Similar to its natural counterparts, our synthetic system shows bistable and hysteretic
behavior, and the inducer concentration range for bistability as well as the switching
rates between the two stable states depend on the repressor concentration. Our
results indicate that a generic permease–inducer–repressor circuit with a single
feedback loop is sufficient to explain the experimentally observed bistable behavior
of the natural systems. We anticipate that the approach of reimplementing natural
systems with orthogonal parts to identify crucial network components is applicable
to other natural systems such as signaling pathways.
acknowledgement: We thank Julio Polaina (Instituto de Agroqu ı ́ mica y Tecnolog ı
́ a de Alimentos, C.S.I.C., Paterna, Spain) for the gift of plasmid pMR4, Gregor
W. Schmidt for provision of and support with the micro fl uidic device, Markus Du
̈ rr for the cell tracking R script, and Lukas Widmer for the script for MEIGO using
“ parfor ” in MATLAB. We acknowledge the members of the Stelling group for discussions,
comments, and support.
author:
- first_name: Robert
full_name: Gnügge, Robert
last_name: Gnügge
- first_name: Lekshmi
full_name: Dharmarajan, Lekshmi
last_name: Dharmarajan
- first_name: Moritz
full_name: Lang, Moritz
id: 29E0800A-F248-11E8-B48F-1D18A9856A87
last_name: Lang
- first_name: Jörg
full_name: Stelling, Jörg
last_name: Stelling
citation:
ama: Gnügge R, Dharmarajan L, Lang M, Stelling J. An orthogonal permease–inducer–repressor
feedback loop shows bistability. ACS Synthetic Biology. 2016;5(10):1098-1107.
doi:10.1021/acssynbio.6b00013
apa: Gnügge, R., Dharmarajan, L., Lang, M., & Stelling, J. (2016). An orthogonal
permease–inducer–repressor feedback loop shows bistability. ACS Synthetic Biology.
American Chemical Society. https://doi.org/10.1021/acssynbio.6b00013
chicago: Gnügge, Robert, Lekshmi Dharmarajan, Moritz Lang, and Jörg Stelling. “An
Orthogonal Permease–Inducer–Repressor Feedback Loop Shows Bistability.” ACS
Synthetic Biology. American Chemical Society, 2016. https://doi.org/10.1021/acssynbio.6b00013.
ieee: R. Gnügge, L. Dharmarajan, M. Lang, and J. Stelling, “An orthogonal permease–inducer–repressor
feedback loop shows bistability,” ACS Synthetic Biology, vol. 5, no. 10.
American Chemical Society, pp. 1098–1107, 2016.
ista: Gnügge R, Dharmarajan L, Lang M, Stelling J. 2016. An orthogonal permease–inducer–repressor
feedback loop shows bistability. ACS Synthetic Biology. 5(10), 1098–1107.
mla: Gnügge, Robert, et al. “An Orthogonal Permease–Inducer–Repressor Feedback Loop
Shows Bistability.” ACS Synthetic Biology, vol. 5, no. 10, American Chemical
Society, 2016, pp. 1098–107, doi:10.1021/acssynbio.6b00013.
short: R. Gnügge, L. Dharmarajan, M. Lang, J. Stelling, ACS Synthetic Biology 5
(2016) 1098–1107.
date_created: 2018-12-11T11:49:40Z
date_published: 2016-05-05T00:00:00Z
date_updated: 2021-01-12T06:47:37Z
day: '05'
department:
- _id: CaGu
doi: 10.1021/acssynbio.6b00013
intvolume: ' 5'
issue: '10'
language:
- iso: eng
month: '05'
oa_version: None
page: 1098 - 1107
publication: ACS Synthetic Biology
publication_status: published
publisher: American Chemical Society
publist_id: '6390'
quality_controlled: '1'
status: public
title: An orthogonal permease–inducer–repressor feedback loop shows bistability
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 5
year: '2016'
...
---
_id: '1181'
abstract:
- lang: eng
text: 'This review accompanies a 2016 SFN mini-symposium presenting examples of
current studies that address a central question: How do neural stem cells (NSCs)
divide in different ways to produce heterogeneous daughter types at the right
time and in proper numbers to build a cerebral cortex with the appropriate size
and structure? We will focus on four aspects of corticogenesis: cytokinesis events
that follow apical mitoses of NSCs; coordinating abscission with delamination
from the apical membrane; timing of neurogenesis and its indirect regulation through
emergence of intermediate progenitors; and capacity of single NSCs to generate
the correct number and laminar fate of cortical neurons. Defects in these mechanisms
can cause microcephaly and other brain malformations, and understanding them is
critical to designing diagnostic tools and preventive and corrective therapies.'
acknowledgement: This work was supported by National Institutes of Health Grants R01NS089795
and R01NS098370 to H.T.G., R01NS076640 to N.D.D., and R01MH094589 and R01NS089777
to B.C., Academia Sinica AS-104-TPB09-2 to S.-J.C, European Union FP7-CIG618444
and Human Frontiers Science Program RGP0053 to S.H., and Fonds Léon Fredericq, from
the Fondation Médicale Reine Elisabeth, and from the Fonation Simone et Pierre Clerdent
to L.N. The authors apologize to colleagues whose work could not be cited due to
space limitations.
author:
- first_name: Noelle
full_name: Dwyer, Noelle
last_name: Dwyer
- first_name: Bin
full_name: Chen, Bin
last_name: Chen
- first_name: Shen
full_name: Chou, Shen
last_name: Chou
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Laurent
full_name: Nguyen, Laurent
last_name: Nguyen
- first_name: Troy
full_name: Ghashghaei, Troy
last_name: Ghashghaei
citation:
ama: 'Dwyer N, Chen B, Chou S, Hippenmeyer S, Nguyen L, Ghashghaei T. Neural stem
cells to cerebral cortex: Emerging mechanisms regulating progenitor behavior and
productivity. Journal of Neuroscience. 2016;36(45):11394-11401. doi:10.1523/JNEUROSCI.2359-16.2016'
apa: 'Dwyer, N., Chen, B., Chou, S., Hippenmeyer, S., Nguyen, L., & Ghashghaei,
T. (2016). Neural stem cells to cerebral cortex: Emerging mechanisms regulating
progenitor behavior and productivity. Journal of Neuroscience. Society
for Neuroscience. https://doi.org/10.1523/JNEUROSCI.2359-16.2016'
chicago: 'Dwyer, Noelle, Bin Chen, Shen Chou, Simon Hippenmeyer, Laurent Nguyen,
and Troy Ghashghaei. “Neural Stem Cells to Cerebral Cortex: Emerging Mechanisms
Regulating Progenitor Behavior and Productivity.” Journal of Neuroscience.
Society for Neuroscience, 2016. https://doi.org/10.1523/JNEUROSCI.2359-16.2016.'
ieee: 'N. Dwyer, B. Chen, S. Chou, S. Hippenmeyer, L. Nguyen, and T. Ghashghaei,
“Neural stem cells to cerebral cortex: Emerging mechanisms regulating progenitor
behavior and productivity,” Journal of Neuroscience, vol. 36, no. 45. Society
for Neuroscience, pp. 11394–11401, 2016.'
ista: 'Dwyer N, Chen B, Chou S, Hippenmeyer S, Nguyen L, Ghashghaei T. 2016. Neural
stem cells to cerebral cortex: Emerging mechanisms regulating progenitor behavior
and productivity. Journal of Neuroscience. 36(45), 11394–11401.'
mla: 'Dwyer, Noelle, et al. “Neural Stem Cells to Cerebral Cortex: Emerging Mechanisms
Regulating Progenitor Behavior and Productivity.” Journal of Neuroscience,
vol. 36, no. 45, Society for Neuroscience, 2016, pp. 11394–401, doi:10.1523/JNEUROSCI.2359-16.2016.'
short: N. Dwyer, B. Chen, S. Chou, S. Hippenmeyer, L. Nguyen, T. Ghashghaei, Journal
of Neuroscience 36 (2016) 11394–11401.
date_created: 2018-12-11T11:50:35Z
date_published: 2016-11-09T00:00:00Z
date_updated: 2021-01-12T06:48:54Z
day: '09'
department:
- _id: SiHi
doi: 10.1523/JNEUROSCI.2359-16.2016
intvolume: ' 36'
issue: '45'
language:
- iso: eng
month: '11'
oa_version: None
page: 11394 - 11401
project:
- _id: 25D7962E-B435-11E9-9278-68D0E5697425
grant_number: RGP0053/2014
name: Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal
Level
publication: Journal of Neuroscience
publication_status: published
publisher: Society for Neuroscience
publist_id: '6172'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'Neural stem cells to cerebral cortex: Emerging mechanisms regulating progenitor
behavior and productivity'
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 36
year: '2016'
...
---
_id: '1182'
abstract:
- lang: eng
text: 'Balanced knockout tournaments are ubiquitous in sports competitions and are
also used in decisionmaking and elections. The traditional computational question,
that asks to compute a draw (optimal draw) that maximizes the winning probability
for a distinguished player, has received a lot of attention. Previous works consider
the problem where the pairwise winning probabilities are known precisely, while
we study how robust is the winning probability with respect to small errors in
the pairwise winning probabilities. First, we present several illuminating examples
to establish: (a) there exist deterministic tournaments (where the pairwise winning
probabilities are 0 or 1) where one optimal draw is much more robust than the
other; and (b) in general, there exist tournaments with slightly suboptimal draws
that are more robust than all the optimal draws. The above examples motivate the
study of the computational problem of robust draws that guarantee a specified
winning probability. Second, we present a polynomial-time algorithm for approximating
the robustness of a draw for sufficiently small errors in pairwise winning probabilities,
and obtain that the stated computational problem is NP-complete. We also show
that two natural cases of deterministic tournaments where the optimal draw could
be computed in polynomial time also admit polynomial-time algorithms to compute
robust optimal draws.'
author:
- first_name: Krishnendu
full_name: Chatterjee, Krishnendu
id: 2E5DCA20-F248-11E8-B48F-1D18A9856A87
last_name: Chatterjee
orcid: 0000-0002-4561-241X
- first_name: Rasmus
full_name: Ibsen-Jensen, Rasmus
id: 3B699956-F248-11E8-B48F-1D18A9856A87
last_name: Ibsen-Jensen
orcid: 0000-0003-4783-0389
- first_name: Josef
full_name: Tkadlec, Josef
id: 3F24CCC8-F248-11E8-B48F-1D18A9856A87
last_name: Tkadlec
orcid: 0000-0002-1097-9684
citation:
ama: 'Chatterjee K, Ibsen-Jensen R, Tkadlec J. Robust draws in balanced knockout
tournaments. In: Vol 2016-January. AAAI Press; 2016:172-179.'
apa: 'Chatterjee, K., Ibsen-Jensen, R., & Tkadlec, J. (2016). Robust draws in
balanced knockout tournaments (Vol. 2016–January, pp. 172–179). Presented at the
IJCAI: International Joint Conference on Artificial Intelligence, New York, NY,
USA: AAAI Press.'
chicago: Chatterjee, Krishnendu, Rasmus Ibsen-Jensen, and Josef Tkadlec. “Robust
Draws in Balanced Knockout Tournaments,” 2016–January:172–79. AAAI Press, 2016.
ieee: 'K. Chatterjee, R. Ibsen-Jensen, and J. Tkadlec, “Robust draws in balanced
knockout tournaments,” presented at the IJCAI: International Joint Conference
on Artificial Intelligence, New York, NY, USA, 2016, vol. 2016–January, pp. 172–179.'
ista: 'Chatterjee K, Ibsen-Jensen R, Tkadlec J. 2016. Robust draws in balanced knockout
tournaments. IJCAI: International Joint Conference on Artificial Intelligence
vol. 2016–January, 172–179.'
mla: Chatterjee, Krishnendu, et al. Robust Draws in Balanced Knockout Tournaments.
Vol. 2016–January, AAAI Press, 2016, pp. 172–79.
short: K. Chatterjee, R. Ibsen-Jensen, J. Tkadlec, in:, AAAI Press, 2016, pp. 172–179.
conference:
end_date: 2016-07-15
location: New York, NY, USA
name: 'IJCAI: International Joint Conference on Artificial Intelligence'
start_date: 2016-07-09
date_created: 2018-12-11T11:50:35Z
date_published: 2016-01-01T00:00:00Z
date_updated: 2023-02-21T10:04:26Z
day: '01'
department:
- _id: KrCh
ec_funded: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://arxiv.org/abs/1604.05090v1
month: '01'
oa: 1
oa_version: Preprint
page: 172 - 179
project:
- _id: 25832EC2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: S 11407_N23
name: Rigorous Systems Engineering
- _id: 25892FC0-B435-11E9-9278-68D0E5697425
grant_number: ICT15-003
name: Efficient Algorithms for Computer Aided Verification
- _id: 2581B60A-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '279307'
name: 'Quantitative Graph Games: Theory and Applications'
- _id: 25EE3708-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '267989'
name: Quantitative Reactive Modeling
publication_status: published
publisher: AAAI Press
publist_id: '6171'
quality_controlled: '1'
related_material:
link:
- relation: table_of_contents
url: https://www.ijcai.org/proceedings/2016
scopus_import: 1
status: public
title: Robust draws in balanced knockout tournaments
type: conference
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 2016-January
year: '2016'
...
---
_id: '1183'
abstract:
- lang: eng
text: Autism spectrum disorders (ASD) are a group of genetic disorders often overlapping
with other neurological conditions. We previously described abnormalities in the
branched-chain amino acid (BCAA) catabolic pathway as a cause of ASD. Here, we
show that the solute carrier transporter 7a5 (SLC7A5), a large neutral amino acid
transporter localized at the blood brain barrier (BBB), has an essential role
in maintaining normal levels of brain BCAAs. In mice, deletion of Slc7a5 from
the endothelial cells of the BBB leads to atypical brain amino acid profile, abnormal
mRNA translation, and severe neurological abnormalities. Furthermore, we identified
several patients with autistic traits and motor delay carrying deleterious homozygous
mutations in the SLC7A5 gene. Finally, we demonstrate that BCAA intracerebroventricular
administration ameliorates abnormal behaviors in adult mutant mice. Our data elucidate
a neurological syndrome defined by SLC7A5 mutations and support an essential role
for the BCAA in human brain function.
acknowledgement: "This work was supported by NICHD (P01HD070494) and SFARI (grant
275275) to J.G.G., and FWF (SFB35_3523) to G.N.\r\nWe thank A.C. Manzano, Mike Liu,
and F. Marr for technical assistance, and R. Shigemoto and the IST Austria Electron
Microscopy (EM) Facility for assistance. We acknowledge support from CIDR for genome-wide
SNP analysis (X01HG008823) and Broad Institute Center for Mendelian Disorders (UM1HG008900
to D. MacArthur), the Yale Center for Mendelian Disorders (U54HG006504 to M.G.),
the Gregory M. Kiez and Mehmet Kutman Foundation (M.G.), Italian Ministry of Instruction
University and Research (PON01_00937 to C.I.), and NIH (R01-GM108911 to A.S.). This
work was supported by NICHD (P01HD070494) and SFARI (grant 275275) to J.G.G., and
FWF (SFB35_3523) to G.N.\r\n\r\n#EMFacility"
article_processing_charge: No
article_type: original
author:
- first_name: Dora-Clara
full_name: Tarlungeanu, Dora-Clara
id: 2ABCE612-F248-11E8-B48F-1D18A9856A87
last_name: Tarlungeanu
- first_name: Elena
full_name: Deliu, Elena
id: 37A40D7E-F248-11E8-B48F-1D18A9856A87
last_name: Deliu
orcid: 0000-0002-7370-5293
- first_name: Christoph
full_name: Dotter, Christoph
id: 4C66542E-F248-11E8-B48F-1D18A9856A87
last_name: Dotter
orcid: 0000-0002-9033-9096
- first_name: Majdi
full_name: Kara, Majdi
last_name: Kara
- first_name: Philipp
full_name: Janiesch, Philipp
last_name: Janiesch
- first_name: Mariafrancesca
full_name: Scalise, Mariafrancesca
last_name: Scalise
- first_name: Michele
full_name: Galluccio, Michele
last_name: Galluccio
- first_name: Mateja
full_name: Tesulov, Mateja
last_name: Tesulov
- first_name: Emanuela
full_name: Morelli, Emanuela
id: 3F4D1282-F248-11E8-B48F-1D18A9856A87
last_name: Morelli
- first_name: Fatma
full_name: Sönmez, Fatma
last_name: Sönmez
- first_name: Kaya
full_name: Bilgüvar, Kaya
last_name: Bilgüvar
- first_name: Ryuichi
full_name: Ohgaki, Ryuichi
last_name: Ohgaki
- first_name: Yoshikatsu
full_name: Kanai, Yoshikatsu
last_name: Kanai
- first_name: Anide
full_name: Johansen, Anide
last_name: Johansen
- first_name: Seham
full_name: Esharif, Seham
last_name: Esharif
- first_name: Tawfeg
full_name: Ben Omran, Tawfeg
last_name: Ben Omran
- first_name: Meral
full_name: Topcu, Meral
last_name: Topcu
- first_name: Avner
full_name: Schlessinger, Avner
last_name: Schlessinger
- first_name: Cesare
full_name: Indiveri, Cesare
last_name: Indiveri
- first_name: Kent
full_name: Duncan, Kent
last_name: Duncan
- first_name: Ahmet
full_name: Caglayan, Ahmet
last_name: Caglayan
- first_name: Murat
full_name: Günel, Murat
last_name: Günel
- first_name: Joseph
full_name: Gleeson, Joseph
last_name: Gleeson
- first_name: Gaia
full_name: Novarino, Gaia
id: 3E57A680-F248-11E8-B48F-1D18A9856A87
last_name: Novarino
orcid: 0000-0002-7673-7178
citation:
ama: Tarlungeanu D-C, Deliu E, Dotter C, et al. Impaired amino acid transport at
the blood brain barrier is a cause of autism spectrum disorder. Cell. 2016;167(6):1481-1494.
doi:10.1016/j.cell.2016.11.013
apa: Tarlungeanu, D.-C., Deliu, E., Dotter, C., Kara, M., Janiesch, P., Scalise,
M., … Novarino, G. (2016). Impaired amino acid transport at the blood brain barrier
is a cause of autism spectrum disorder. Cell. Cell Press. https://doi.org/10.1016/j.cell.2016.11.013
chicago: Tarlungeanu, Dora-Clara, Elena Deliu, Christoph Dotter, Majdi Kara, Philipp
Janiesch, Mariafrancesca Scalise, Michele Galluccio, et al. “Impaired Amino Acid
Transport at the Blood Brain Barrier Is a Cause of Autism Spectrum Disorder.”
Cell. Cell Press, 2016. https://doi.org/10.1016/j.cell.2016.11.013.
ieee: D.-C. Tarlungeanu et al., “Impaired amino acid transport at the blood
brain barrier is a cause of autism spectrum disorder,” Cell, vol. 167,
no. 6. Cell Press, pp. 1481–1494, 2016.
ista: Tarlungeanu D-C, Deliu E, Dotter C, Kara M, Janiesch P, Scalise M, Galluccio
M, Tesulov M, Morelli E, Sönmez F, Bilgüvar K, Ohgaki R, Kanai Y, Johansen A,
Esharif S, Ben Omran T, Topcu M, Schlessinger A, Indiveri C, Duncan K, Caglayan
A, Günel M, Gleeson J, Novarino G. 2016. Impaired amino acid transport at the
blood brain barrier is a cause of autism spectrum disorder. Cell. 167(6), 1481–1494.
mla: Tarlungeanu, Dora-Clara, et al. “Impaired Amino Acid Transport at the Blood
Brain Barrier Is a Cause of Autism Spectrum Disorder.” Cell, vol. 167,
no. 6, Cell Press, 2016, pp. 1481–94, doi:10.1016/j.cell.2016.11.013.
short: D.-C. Tarlungeanu, E. Deliu, C. Dotter, M. Kara, P. Janiesch, M. Scalise,
M. Galluccio, M. Tesulov, E. Morelli, F. Sönmez, K. Bilgüvar, R. Ohgaki, Y. Kanai,
A. Johansen, S. Esharif, T. Ben Omran, M. Topcu, A. Schlessinger, C. Indiveri,
K. Duncan, A. Caglayan, M. Günel, J. Gleeson, G. Novarino, Cell 167 (2016) 1481–1494.
date_created: 2018-12-11T11:50:35Z
date_published: 2016-12-01T00:00:00Z
date_updated: 2024-03-25T23:30:07Z
day: '01'
ddc:
- '576'
- '616'
department:
- _id: GaNo
doi: 10.1016/j.cell.2016.11.013
file:
- access_level: open_access
checksum: 7fe01ab12a6610d3db421e0136db2f77
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:13:44Z
date_updated: 2020-07-14T12:44:37Z
file_id: '5030'
file_name: IST-2017-771-v1+1_Tarlungeanu_et_al._Final_edited.pdf
file_size: 73907957
relation: main_file
file_date_updated: 2020-07-14T12:44:37Z
has_accepted_license: '1'
intvolume: ' 167'
issue: '6'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Submitted Version
page: 1481 - 1494
project:
- _id: 25473368-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: F03523
name: Transmembrane Transporters in Health and Disease
publication: Cell
publication_status: published
publisher: Cell Press
publist_id: '6170'
pubrep_id: '771'
quality_controlled: '1'
related_material:
record:
- id: '395'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Impaired amino acid transport at the blood brain barrier is a cause of autism
spectrum disorder
type: journal_article
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
volume: 167
year: '2016'
...
---
_id: '1184'
abstract:
- lang: eng
text: Across multicellular organisms, the costs of reproduction and self-maintenance
result in a life history trade-off between fecundity and longevity. Queens of
perennial social Hymenoptera are both highly fertile and long-lived, and thus,
this fundamental trade-off is lacking. Whether social insect males similarly evade
the fecundity/longevity trade-off remains largely unstudied. Wingless males of
the ant genus Cardiocondyla stay in their natal colonies throughout their relatively
long lives and mate with multiple female sexuals. Here, we show that Cardiocondyla
obscurior males that were allowed to mate with large numbers of female sexuals
had a shortened life span compared to males that mated at a low frequency or virgin
males. Although frequent mating negatively affects longevity, males clearly benefit
from a “live fast, die young strategy” by inseminating as many female sexuals
as possible at a cost to their own survival.
acknowledgement: 'German Science Foundation. Grant Number: SCHR 1135/2-1. We thank
M. Adam for handling part of the setups and J. Zoellner for behavioral observations.'
author:
- first_name: Sina
full_name: Metzler, Sina
id: 48204546-F248-11E8-B48F-1D18A9856A87
last_name: Metzler
- first_name: Jürgen
full_name: Heinze, Jürgen
last_name: Heinze
- first_name: Alexandra
full_name: Schrempf, Alexandra
last_name: Schrempf
citation:
ama: Metzler S, Heinze J, Schrempf A. Mating and longevity in ant males. Ecology
and Evolution. 2016;6(24):8903-8906. doi:10.1002/ece3.2474
apa: Metzler, S., Heinze, J., & Schrempf, A. (2016). Mating and longevity in
ant males. Ecology and Evolution. Wiley-Blackwell. https://doi.org/10.1002/ece3.2474
chicago: Metzler, Sina, Jürgen Heinze, and Alexandra Schrempf. “Mating and Longevity
in Ant Males.” Ecology and Evolution. Wiley-Blackwell, 2016. https://doi.org/10.1002/ece3.2474.
ieee: S. Metzler, J. Heinze, and A. Schrempf, “Mating and longevity in ant males,”
Ecology and Evolution, vol. 6, no. 24. Wiley-Blackwell, pp. 8903–8906,
2016.
ista: Metzler S, Heinze J, Schrempf A. 2016. Mating and longevity in ant males.
Ecology and Evolution. 6(24), 8903–8906.
mla: Metzler, Sina, et al. “Mating and Longevity in Ant Males.” Ecology and Evolution,
vol. 6, no. 24, Wiley-Blackwell, 2016, pp. 8903–06, doi:10.1002/ece3.2474.
short: S. Metzler, J. Heinze, A. Schrempf, Ecology and Evolution 6 (2016) 8903–8906.
date_created: 2018-12-11T11:50:36Z
date_published: 2016-12-01T00:00:00Z
date_updated: 2021-01-12T06:48:55Z
day: '01'
ddc:
- '576'
- '592'
department:
- _id: SyCr
doi: 10.1002/ece3.2474
file:
- access_level: open_access
checksum: 789026eb9e1be2a0da08376f29f569cf
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:12Z
date_updated: 2020-07-14T12:44:37Z
file_id: '5062'
file_name: IST-2017-736-v1+1_Metzler_et_al-2016-Ecology_and_Evolution.pdf
file_size: 328414
relation: main_file
file_date_updated: 2020-07-14T12:44:37Z
has_accepted_license: '1'
intvolume: ' 6'
issue: '24'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
page: 8903 - 8906
publication: Ecology and Evolution
publication_status: published
publisher: Wiley-Blackwell
publist_id: '6169'
pubrep_id: '736'
quality_controlled: '1'
scopus_import: 1
status: public
title: Mating and longevity in ant males
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: 6
year: '2016'
...
---
_id: '1185'
abstract:
- lang: eng
text: The developmental programme of the pistil is under the control of both auxin
and cytokinin. Crosstalk between these factors converges on regulation of the
auxin carrier PIN-FORMED 1 (PIN1). Here, we show that in the triple transcription
factor mutant cytokinin response factor 2 (crf2) crf3 crf6 both pistil length
and ovule number were reduced. PIN1 expression was also lower in the triple mutant
and the phenotypes could not be rescued by exogenous cytokinin application. pin1
complementation studies using genomic PIN1 constructs showed that the pistil phenotypes
were only rescued when the PCRE1 domain, to which CRFs bind, was present. Without
this domain, pin mutants resemble the crf2 crf3 crf6 triple mutant, indicating
the pivotal role of CRFs in auxin-cytokinin crosstalk.
acknowledgement: M.C. was funded by a PhD fellowship from the Università degli Studi
di Milano-Bicocca and from Ministero dell'Istruzione, dell'Università e della Ricerca
(MIUR) [MIUR-PRIN 2012]. L.C. is also supported by MIUR [MIUR-PRIN 2012]. We would
like to thank Andrew MacCabe and Edward Kiegle for editing the paper.
author:
- first_name: Mara
full_name: Cucinotta, Mara
last_name: Cucinotta
- first_name: Silvia
full_name: Manrique, Silvia
last_name: Manrique
- first_name: Andrea
full_name: Guazzotti, Andrea
last_name: Guazzotti
- first_name: Nadia
full_name: Quadrelli, Nadia
last_name: Quadrelli
- first_name: Marta
full_name: Mendes, Marta
last_name: Mendes
- first_name: Eva
full_name: Benková, Eva
id: 38F4F166-F248-11E8-B48F-1D18A9856A87
last_name: Benková
orcid: 0000-0002-8510-9739
- first_name: Lucia
full_name: Colombo, Lucia
last_name: Colombo
citation:
ama: Cucinotta M, Manrique S, Guazzotti A, et al. Cytokinin response factors integrate
auxin and cytokinin pathways for female reproductive organ development. Development.
2016;143(23):4419-4424. doi:10.1242/dev.143545
apa: Cucinotta, M., Manrique, S., Guazzotti, A., Quadrelli, N., Mendes, M., Benková,
E., & Colombo, L. (2016). Cytokinin response factors integrate auxin and cytokinin
pathways for female reproductive organ development. Development. Company
of Biologists. https://doi.org/10.1242/dev.143545
chicago: Cucinotta, Mara, Silvia Manrique, Andrea Guazzotti, Nadia Quadrelli, Marta
Mendes, Eva Benková, and Lucia Colombo. “Cytokinin Response Factors Integrate
Auxin and Cytokinin Pathways for Female Reproductive Organ Development.” Development.
Company of Biologists, 2016. https://doi.org/10.1242/dev.143545.
ieee: M. Cucinotta et al., “Cytokinin response factors integrate auxin and
cytokinin pathways for female reproductive organ development,” Development,
vol. 143, no. 23. Company of Biologists, pp. 4419–4424, 2016.
ista: Cucinotta M, Manrique S, Guazzotti A, Quadrelli N, Mendes M, Benková E, Colombo
L. 2016. Cytokinin response factors integrate auxin and cytokinin pathways for
female reproductive organ development. Development. 143(23), 4419–4424.
mla: Cucinotta, Mara, et al. “Cytokinin Response Factors Integrate Auxin and Cytokinin
Pathways for Female Reproductive Organ Development.” Development, vol.
143, no. 23, Company of Biologists, 2016, pp. 4419–24, doi:10.1242/dev.143545.
short: M. Cucinotta, S. Manrique, A. Guazzotti, N. Quadrelli, M. Mendes, E. Benková,
L. Colombo, Development 143 (2016) 4419–4424.
date_created: 2018-12-11T11:50:36Z
date_published: 2016-12-01T00:00:00Z
date_updated: 2021-01-12T06:48:56Z
day: '01'
department:
- _id: EvBe
doi: 10.1242/dev.143545
intvolume: ' 143'
issue: '23'
language:
- iso: eng
month: '12'
oa_version: None
page: 4419 - 4424
publication: Development
publication_status: published
publisher: Company of Biologists
publist_id: '6168'
quality_controlled: '1'
scopus_import: 1
status: public
title: Cytokinin response factors integrate auxin and cytokinin pathways for female
reproductive organ development
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 143
year: '2016'
...
---
_id: '1186'
abstract:
- lang: eng
text: The human pathogen Streptococcus pneumoniae is decorated with a special class
of surface-proteins known as choline-binding proteins (CBPs) attached to phosphorylcholine
(PCho) moieties from cell-wall teichoic acids. By a combination of X-ray crystallography,
NMR, molecular dynamics techniques and in vivo virulence and phagocytosis studies,
we provide structural information of choline-binding protein L (CbpL) and demonstrate
its impact on pneumococcal pathogenesis and immune evasion. CbpL is a very elongated
three-module protein composed of (i) an Excalibur Ca 2+ -binding domain -reported
in this work for the very first time-, (ii) an unprecedented anchorage module
showing alternate disposition of canonical and non-canonical choline-binding sites
that allows vine-like binding of fully-PCho-substituted teichoic acids (with two
choline moieties per unit), and (iii) a Ltp-Lipoprotein domain. Our structural
and infection assays indicate an important role of the whole multimodular protein
allowing both to locate CbpL at specific places on the cell wall and to interact
with host components in order to facilitate pneumococcal lung infection and transmigration
from nasopharynx to the lungs and blood. CbpL implication in both resistance against
killing by phagocytes and pneumococcal pathogenesis further postulate this surface-protein
as relevant among the pathogenic arsenal of the pneumococcus.
acknowledgement: We gratefully acknowledge Karsta Barnekow and Kristine Sievert-Giermann,
for technical assistance and Lothar Petruschka for in silico analysis (all Dept.
of Genetics, University of Greifswald). We are further grateful to the staff from
SLS synchrotron beamline for help in data collection. This work was supported by
grants from the Deutsche Forschungsgemeinschaft DFG GRK 1870 (to SH) and the Spanish
Ministry of Economy and Competitiveness (BFU2014-59389-P to JAH, CTQ2014-52633-P
to MB and SAF2012-39760-C02-02 to FG) and S2010/BMD-2457 (Community of Madrid to
JAH and FG).
article_number: '38094'
author:
- first_name: Javier
full_name: Gutierrez-Fernandez, Javier
id: 3D9511BA-F248-11E8-B48F-1D18A9856A87
last_name: Gutierrez-Fernandez
- first_name: Malek
full_name: Saleh, Malek
last_name: Saleh
- first_name: Martín
full_name: Alcorlo, Martín
last_name: Alcorlo
- first_name: Alejandro
full_name: Gómez Mejóa, Alejandro
last_name: Gómez Mejóa
- first_name: David
full_name: Pantoja Uceda, David
last_name: Pantoja Uceda
- first_name: Miguel
full_name: Treviño, Miguel
last_name: Treviño
- first_name: Franziska
full_name: Vob, Franziska
last_name: Vob
- first_name: Mohammed
full_name: Abdullah, Mohammed
last_name: Abdullah
- first_name: Sergio
full_name: Galán Bartual, Sergio
last_name: Galán Bartual
- first_name: Jolien
full_name: Seinen, Jolien
last_name: Seinen
- first_name: Pedro
full_name: Sánchez Murcia, Pedro
last_name: Sánchez Murcia
- first_name: Federico
full_name: Gago, Federico
last_name: Gago
- first_name: Marta
full_name: Bruix, Marta
last_name: Bruix
- first_name: Sven
full_name: Hammerschmidt, Sven
last_name: Hammerschmidt
- first_name: Juan
full_name: Hermoso, Juan
last_name: Hermoso
citation:
ama: Gutierrez-Fernandez J, Saleh M, Alcorlo M, et al. Modular architecture and
unique teichoic acid recognition features of choline-binding protein L CbpL contributing
to pneumococcal pathogenesis. Scientific Reports. 2016;6. doi:10.1038/srep38094
apa: Gutierrez-Fernandez, J., Saleh, M., Alcorlo, M., Gómez Mejóa, A., Pantoja Uceda,
D., Treviño, M., … Hermoso, J. (2016). Modular architecture and unique teichoic
acid recognition features of choline-binding protein L CbpL contributing to pneumococcal
pathogenesis. Scientific Reports. Nature Publishing Group. https://doi.org/10.1038/srep38094
chicago: Gutierrez-Fernandez, Javier, Malek Saleh, Martín Alcorlo, Alejandro Gómez
Mejóa, David Pantoja Uceda, Miguel Treviño, Franziska Vob, et al. “Modular Architecture
and Unique Teichoic Acid Recognition Features of Choline-Binding Protein L CbpL
Contributing to Pneumococcal Pathogenesis.” Scientific Reports. Nature
Publishing Group, 2016. https://doi.org/10.1038/srep38094.
ieee: J. Gutierrez-Fernandez et al., “Modular architecture and unique teichoic
acid recognition features of choline-binding protein L CbpL contributing to pneumococcal
pathogenesis,” Scientific Reports, vol. 6. Nature Publishing Group, 2016.
ista: Gutierrez-Fernandez J, Saleh M, Alcorlo M, Gómez Mejóa A, Pantoja Uceda D,
Treviño M, Vob F, Abdullah M, Galán Bartual S, Seinen J, Sánchez Murcia P, Gago
F, Bruix M, Hammerschmidt S, Hermoso J. 2016. Modular architecture and unique
teichoic acid recognition features of choline-binding protein L CbpL contributing
to pneumococcal pathogenesis. Scientific Reports. 6, 38094.
mla: Gutierrez-Fernandez, Javier, et al. “Modular Architecture and Unique Teichoic
Acid Recognition Features of Choline-Binding Protein L CbpL Contributing to Pneumococcal
Pathogenesis.” Scientific Reports, vol. 6, 38094, Nature Publishing Group,
2016, doi:10.1038/srep38094.
short: J. Gutierrez-Fernandez, M. Saleh, M. Alcorlo, A. Gómez Mejóa, D. Pantoja
Uceda, M. Treviño, F. Vob, M. Abdullah, S. Galán Bartual, J. Seinen, P. Sánchez
Murcia, F. Gago, M. Bruix, S. Hammerschmidt, J. Hermoso, Scientific Reports 6
(2016).
date_created: 2018-12-11T11:50:36Z
date_published: 2016-12-05T00:00:00Z
date_updated: 2021-01-12T06:48:56Z
day: '05'
ddc:
- '576'
- '610'
department:
- _id: LeSa
doi: 10.1038/srep38094
file:
- access_level: open_access
checksum: e007d78b483bc59bf5ab98e9d42a6ec1
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:10:18Z
date_updated: 2020-07-14T12:44:37Z
file_id: '4804'
file_name: IST-2017-735-v1+1_srep38094.pdf
file_size: 2716045
relation: main_file
file_date_updated: 2020-07-14T12:44:37Z
has_accepted_license: '1'
intvolume: ' 6'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
publication: Scientific Reports
publication_status: published
publisher: Nature Publishing Group
publist_id: '6167'
pubrep_id: '735'
quality_controlled: '1'
scopus_import: 1
status: public
title: Modular architecture and unique teichoic acid recognition features of choline-binding
protein L CbpL contributing to pneumococcal pathogenesis
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: 6
year: '2016'
...
---
_id: '1188'
abstract:
- lang: eng
text: "We consider a population dynamics model coupling cell growth to a diffusion
in the space of metabolic phenotypes as it can be obtained from realistic constraints-based
modelling. \r\nIn the asymptotic regime of slow\r\ndiffusion, that coincides with
the relevant experimental range, the resulting\r\nnon-linear Fokker–Planck equation
is solved for the steady state in the WKB\r\napproximation that maps it into the
ground state of a quantum particle in an\r\nAiry potential plus a centrifugal
term. We retrieve scaling laws for growth rate\r\nfluctuations and time response
with respect to the distance from the maximum\r\ngrowth rate suggesting that suboptimal
populations can have a faster response\r\nto perturbations."
acknowledgement: D De Martino is supported by the People Programme (Marie Curie Actions)
of the European Union's Seventh Framework Programme (FP7/2007–2013) under REA grant
agreement no. [291734]. D Masoero is supported by the FCT scholarship, number SFRH/BPD/75908/2011.
D De Martino thanks the Grupo de Física Matemática of the Universidade de Lisboa
for the kind hospitality. We also wish to thank Matteo Osella, Vincenzo Vitagliano
and Vera Luz Masoero for useful discussions, also late at night.
article_number: '123502'
author:
- first_name: Daniele
full_name: De Martino, Daniele
id: 3FF5848A-F248-11E8-B48F-1D18A9856A87
last_name: De Martino
orcid: 0000-0002-5214-4706
- first_name: Davide
full_name: Masoero, Davide
last_name: Masoero
citation:
ama: 'De Martino D, Masoero D. Asymptotic analysis of noisy fitness maximization,
applied to metabolism & growth. Journal of Statistical Mechanics:
Theory and Experiment. 2016;2016(12). doi:10.1088/1742-5468/aa4e8f'
apa: 'De Martino, D., & Masoero, D. (2016). Asymptotic analysis of noisy fitness
maximization, applied to metabolism & growth. Journal of Statistical
Mechanics: Theory and Experiment. IOPscience. https://doi.org/10.1088/1742-5468/aa4e8f'
chicago: 'De Martino, Daniele, and Davide Masoero. “Asymptotic Analysis of Noisy
Fitness Maximization, Applied to Metabolism & Growth.” Journal of
Statistical Mechanics: Theory and Experiment. IOPscience, 2016. https://doi.org/10.1088/1742-5468/aa4e8f.'
ieee: 'D. De Martino and D. Masoero, “Asymptotic analysis of noisy fitness maximization,
applied to metabolism & growth,” Journal of Statistical Mechanics:
Theory and Experiment, vol. 2016, no. 12. IOPscience, 2016.'
ista: 'De Martino D, Masoero D. 2016. Asymptotic analysis of noisy fitness maximization,
applied to metabolism & growth. Journal of Statistical Mechanics: Theory
and Experiment. 2016(12), 123502.'
mla: 'De Martino, Daniele, and Davide Masoero. “Asymptotic Analysis of Noisy Fitness
Maximization, Applied to Metabolism & Growth.” Journal of Statistical
Mechanics: Theory and Experiment, vol. 2016, no. 12, 123502, IOPscience, 2016,
doi:10.1088/1742-5468/aa4e8f.'
short: 'D. De Martino, D. Masoero, Journal of Statistical Mechanics: Theory and
Experiment 2016 (2016).'
date_created: 2018-12-11T11:50:37Z
date_published: 2016-12-30T00:00:00Z
date_updated: 2021-01-12T06:48:57Z
day: '30'
department:
- _id: GaTk
doi: 10.1088/1742-5468/aa4e8f
ec_funded: 1
intvolume: ' 2016'
issue: '12'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://arxiv.org/abs/1606.09048
month: '12'
oa: 1
oa_version: Preprint
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
publication: ' Journal of Statistical Mechanics: Theory and Experiment'
publication_status: published
publisher: IOPscience
publist_id: '6165'
quality_controlled: '1'
scopus_import: 1
status: public
title: Asymptotic analysis of noisy fitness maximization, applied to metabolism &
growth
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 2016
year: '2016'
...
---
_id: '1193'
abstract:
- lang: eng
text: We consider the recent formulation of the Algorithmic Lovász Local Lemma [1],
[2] for finding objects that avoid "bad features", or "flaws".
It extends the Moser-Tardos resampling algorithm [3] to more general discrete
spaces. At each step the method picks a flaw present in the current state and
"resamples" it using a "resampling oracle" provided by the
user. However, it is less flexible than the Moser-Tardos method since [1], [2]
require a specific flaw selection rule, whereas [3] allows an arbitrary rule (and
thus can potentially be implemented more efficiently). We formulate a new "commutativity"
condition, and prove that it is sufficient for an arbitrary rule to work. It also
enables an efficient parallelization under an additional assumption. We then show
that existing resampling oracles for perfect matchings and permutations do satisfy
this condition. Finally, we generalize the precondition in [2] (in the case of
symmetric potential causality graphs). This unifies special cases that previously
were treated separately.
acknowledgement: European Unions Seventh Framework Programme (FP7/2007-2013)/ERC grant
agreement no 616160
article_number: '7782993'
article_processing_charge: No
arxiv: 1
author:
- first_name: Vladimir
full_name: Kolmogorov, Vladimir
id: 3D50B0BA-F248-11E8-B48F-1D18A9856A87
last_name: Kolmogorov
citation:
ama: 'Kolmogorov V. Commutativity in the algorithmic Lovasz local lemma. In: Proceedings
- Annual IEEE Symposium on Foundations of Computer Science. Vol 2016-December.
IEEE; 2016. doi:10.1109/FOCS.2016.88'
apa: 'Kolmogorov, V. (2016). Commutativity in the algorithmic Lovasz local lemma.
In Proceedings - Annual IEEE Symposium on Foundations of Computer Science
(Vol. 2016–December). New Brunswick, NJ, USA : IEEE. https://doi.org/10.1109/FOCS.2016.88'
chicago: Kolmogorov, Vladimir. “Commutativity in the Algorithmic Lovasz Local Lemma.”
In Proceedings - Annual IEEE Symposium on Foundations of Computer Science,
Vol. 2016–December. IEEE, 2016. https://doi.org/10.1109/FOCS.2016.88.
ieee: V. Kolmogorov, “Commutativity in the algorithmic Lovasz local lemma,” in Proceedings
- Annual IEEE Symposium on Foundations of Computer Science, New Brunswick,
NJ, USA , 2016, vol. 2016–December.
ista: 'Kolmogorov V. 2016. Commutativity in the algorithmic Lovasz local lemma.
Proceedings - Annual IEEE Symposium on Foundations of Computer Science. FOCS:
Foundations of Computer Science vol. 2016–December, 7782993.'
mla: Kolmogorov, Vladimir. “Commutativity in the Algorithmic Lovasz Local Lemma.”
Proceedings - Annual IEEE Symposium on Foundations of Computer Science,
vol. 2016–December, 7782993, IEEE, 2016, doi:10.1109/FOCS.2016.88.
short: V. Kolmogorov, in:, Proceedings - Annual IEEE Symposium on Foundations of
Computer Science, IEEE, 2016.
conference:
end_date: 2016-09-11
location: 'New Brunswick, NJ, USA '
name: 'FOCS: Foundations of Computer Science'
start_date: 2016-09-09
date_created: 2018-12-11T11:50:38Z
date_published: 2016-12-15T00:00:00Z
date_updated: 2023-09-19T14:24:57Z
day: '15'
department:
- _id: VlKo
doi: 10.1109/FOCS.2016.88
ec_funded: 1
external_id:
arxiv:
- '1506.08547'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://arxiv.org/abs/1506.08547v7
month: '12'
oa: 1
oa_version: Preprint
project:
- _id: 25FBA906-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '616160'
name: 'Discrete Optimization in Computer Vision: Theory and Practice'
publication: Proceedings - Annual IEEE Symposium on Foundations of Computer Science
publication_status: published
publisher: IEEE
publist_id: '6158'
quality_controlled: '1'
related_material:
record:
- id: '5975'
relation: later_version
status: public
scopus_import: 1
status: public
title: Commutativity in the algorithmic Lovasz local lemma
type: conference
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 2016-December
year: '2016'
...
---
_id: '1195'
abstract:
- lang: eng
text: 'The genetic analysis of experimentally evolving populations typically relies
on short reads from pooled individuals (Pool-Seq). While this method provides
reliable allele frequency estimates, the underlying haplotype structure remains
poorly characterized. With small population sizes and adaptive variants that start
from low frequencies, the interpretation of selection signatures in most Evolve
and Resequencing studies remains challenging. To facilitate the characterization
of selection targets, we propose a new approach that reconstructs selected haplotypes
from replicated time series, using Pool-Seq data. We identify selected haplotypes
through the correlated frequencies of alleles carried by them. Computer simulations
indicate that selected haplotype-blocks of several Mb can be reconstructed with
high confidence and low error rates, even when allele frequencies change only
by 20% across three replicates. Applying this method to real data from D. melanogaster
populations adapting to a hot environment, we identify a selected haplotype-block
of 6.93 Mb. We confirm the presence of this haplotype-block in evolved populations
by experimental haplotyping, demonstrating the power and accuracy of our haplotype
reconstruction from Pool-Seq data. We propose that the combination of allele frequency
estimates with haplotype information will provide the key to understanding the
dynamics of adaptive alleles. '
acknowledgement: "The authors thank all members of the Institute of Population\r\nGenetics
for discussion and support on the project and par-\r\nticularly N. Barghi for helpful
comments on earlier versions of\r\nthe manuscript. This work was supported
\ by the European\r\nResearch Council (ERC) grants “ArchAdapt” and “250152”."
author:
- first_name: Susan
full_name: Franssen, Susan
last_name: Franssen
- 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: Christian
full_name: Schlötterer, Christian
last_name: Schlötterer
citation:
ama: Franssen S, Barton NH, Schlötterer C. Reconstruction of haplotype-blocks selected
during experimental evolution. Molecular Biology and Evolution. 2016;34(1):174-184.
doi:10.1093/molbev/msw210
apa: Franssen, S., Barton, N. H., & Schlötterer, C. (2016). Reconstruction of
haplotype-blocks selected during experimental evolution. Molecular Biology
and Evolution. Oxford University Press. https://doi.org/10.1093/molbev/msw210
chicago: Franssen, Susan, Nicholas H Barton, and Christian Schlötterer. “Reconstruction
of Haplotype-Blocks Selected during Experimental Evolution.” Molecular Biology
and Evolution. Oxford University Press, 2016. https://doi.org/10.1093/molbev/msw210.
ieee: S. Franssen, N. H. Barton, and C. Schlötterer, “Reconstruction of haplotype-blocks
selected during experimental evolution.,” Molecular Biology and Evolution,
vol. 34, no. 1. Oxford University Press, pp. 174–184, 2016.
ista: Franssen S, Barton NH, Schlötterer C. 2016. Reconstruction of haplotype-blocks
selected during experimental evolution. Molecular Biology and Evolution. 34(1),
174–184.
mla: Franssen, Susan, et al. “Reconstruction of Haplotype-Blocks Selected during
Experimental Evolution.” Molecular Biology and Evolution, vol. 34, no.
1, Oxford University Press, 2016, pp. 174–84, doi:10.1093/molbev/msw210.
short: S. Franssen, N.H. Barton, C. Schlötterer, Molecular Biology and Evolution
34 (2016) 174–184.
date_created: 2018-12-11T11:50:39Z
date_published: 2016-10-03T00:00:00Z
date_updated: 2021-01-12T06:49:00Z
day: '03'
ddc:
- '576'
department:
- _id: NiBa
doi: 10.1093/molbev/msw210
ec_funded: 1
file:
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creator: system
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creator: system
date_created: 2018-12-12T10:16:38Z
date_updated: 2020-07-14T12:44:38Z
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date_created: 2018-12-12T10:16:39Z
date_updated: 2020-07-14T12:44:38Z
file_id: '5228'
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file_size: 50705
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file_date_updated: 2020-07-14T12:44:38Z
has_accepted_license: '1'
intvolume: ' 34'
issue: '1'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Submitted Version
page: 174 - 184
project:
- _id: 25B07788-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '250152'
name: Limits to selection in biology and in evolutionary computation
publication: Molecular Biology and Evolution
publication_status: published
publisher: Oxford University Press
publist_id: '6155'
pubrep_id: '770'
quality_controlled: '1'
scopus_import: 1
status: public
title: Reconstruction of haplotype-blocks selected during experimental evolution.
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 34
year: '2016'
...
---
_id: '1197'
abstract:
- lang: eng
text: Across the nervous system, certain population spiking patterns are observed
far more frequently than others. A hypothesis about this structure is that these
collective activity patterns function as population codewords–collective modes–carrying
information distinct from that of any single cell. We investigate this phenomenon
in recordings of ∼150 retinal ganglion cells, the retina’s output. We develop
a novel statistical model that decomposes the population response into modes;
it predicts the distribution of spiking activity in the ganglion cell population
with high accuracy. We found that the modes represent localized features of the
visual stimulus that are distinct from the features represented by single neurons.
Modes form clusters of activity states that are readily discriminated from one
another. When we repeated the same visual stimulus, we found that the same mode
was robustly elicited. These results suggest that retinal ganglion cells’ collective
signaling is endowed with a form of error-correcting code–a principle that may
hold in brain areas beyond retina.
acknowledgement: JSP was supported by a C.V. Starr Fellowship from the Starr Foundation
(http://www.starrfoundation.org/). GT was supported by Austrian Research Foundation
(https://www.fwf.ac.at/en/) grant FWF P25651. MJB received support from National
Eye Institute (https://nei.nih.gov/) grant EY 14196 and from the National Science
Foundation grant 1504977. The authors thank Cristina Savin and Vicent Botella-Soler
for helpful comments on the manuscript.
article_number: e1005855
author:
- first_name: Jason
full_name: Prentice, Jason
last_name: Prentice
- first_name: Olivier
full_name: Marre, Olivier
last_name: Marre
- first_name: Mark
full_name: Ioffe, Mark
last_name: Ioffe
- first_name: Adrianna
full_name: Loback, Adrianna
last_name: Loback
- first_name: Gasper
full_name: Tkacik, Gasper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkacik
orcid: 0000-0002-6699-1455
- first_name: Michael
full_name: Berry, Michael
last_name: Berry
citation:
ama: Prentice J, Marre O, Ioffe M, Loback A, Tkačik G, Berry M. Error-robust modes
of the retinal population code. PLoS Computational Biology. 2016;12(11).
doi:10.1371/journal.pcbi.1005148
apa: Prentice, J., Marre, O., Ioffe, M., Loback, A., Tkačik, G., & Berry, M.
(2016). Error-robust modes of the retinal population code. PLoS Computational
Biology. Public Library of Science. https://doi.org/10.1371/journal.pcbi.1005148
chicago: Prentice, Jason, Olivier Marre, Mark Ioffe, Adrianna Loback, Gašper Tkačik,
and Michael Berry. “Error-Robust Modes of the Retinal Population Code.” PLoS
Computational Biology. Public Library of Science, 2016. https://doi.org/10.1371/journal.pcbi.1005148.
ieee: J. Prentice, O. Marre, M. Ioffe, A. Loback, G. Tkačik, and M. Berry, “Error-robust
modes of the retinal population code,” PLoS Computational Biology, vol.
12, no. 11. Public Library of Science, 2016.
ista: Prentice J, Marre O, Ioffe M, Loback A, Tkačik G, Berry M. 2016. Error-robust
modes of the retinal population code. PLoS Computational Biology. 12(11), e1005855.
mla: Prentice, Jason, et al. “Error-Robust Modes of the Retinal Population Code.”
PLoS Computational Biology, vol. 12, no. 11, e1005855, Public Library of
Science, 2016, doi:10.1371/journal.pcbi.1005148.
short: J. Prentice, O. Marre, M. Ioffe, A. Loback, G. Tkačik, M. Berry, PLoS Computational
Biology 12 (2016).
date_created: 2018-12-11T11:50:40Z
date_published: 2016-11-17T00:00:00Z
date_updated: 2023-02-23T14:05:40Z
day: '17'
ddc:
- '570'
department:
- _id: GaTk
doi: 10.1371/journal.pcbi.1005148
file:
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title: Error-robust modes of the retinal population code
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