---
_id: '9718'
article_processing_charge: No
author:
- first_name: Tamar
full_name: Friedlander, Tamar
id: 36A5845C-F248-11E8-B48F-1D18A9856A87
last_name: Friedlander
- first_name: Avraham E.
full_name: Mayo, Avraham E.
last_name: Mayo
- first_name: Tsvi
full_name: Tlusty, Tsvi
last_name: Tlusty
- first_name: Uri
full_name: Alon, Uri
last_name: Alon
citation:
ama: Friedlander T, Mayo AE, Tlusty T, Alon U. Supporting information text. 2015.
doi:10.1371/journal.pcbi.1004055.s001
apa: Friedlander, T., Mayo, A. E., Tlusty, T., & Alon, U. (2015). Supporting
information text. Public Library of Science. https://doi.org/10.1371/journal.pcbi.1004055.s001
chicago: Friedlander, Tamar, Avraham E. Mayo, Tsvi Tlusty, and Uri Alon. “Supporting
Information Text.” Public Library of Science, 2015. https://doi.org/10.1371/journal.pcbi.1004055.s001.
ieee: T. Friedlander, A. E. Mayo, T. Tlusty, and U. Alon, “Supporting information
text.” Public Library of Science, 2015.
ista: Friedlander T, Mayo AE, Tlusty T, Alon U. 2015. Supporting information text,
Public Library of Science, 10.1371/journal.pcbi.1004055.s001.
mla: Friedlander, Tamar, et al. Supporting Information Text. Public Library
of Science, 2015, doi:10.1371/journal.pcbi.1004055.s001.
short: T. Friedlander, A.E. Mayo, T. Tlusty, U. Alon, (2015).
date_created: 2021-07-26T08:35:23Z
date_published: 2015-03-23T00:00:00Z
date_updated: 2023-02-23T10:16:13Z
day: '23'
department:
- _id: GaTk
doi: 10.1371/journal.pcbi.1004055.s001
month: '03'
oa_version: Published Version
publisher: Public Library of Science
related_material:
record:
- id: '1827'
relation: used_in_publication
status: public
status: public
title: Supporting information text
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2015'
...
---
_id: '9719'
abstract:
- lang: eng
text: Parasitism creates selection for resistance mechanisms in host populations
and is hypothesized to promote increased host evolvability. However, the influence
of these traits on host evolution when parasites are no longer present is unclear.
We used experimental evolution and whole-genome sequencing of Escherichia coli
to determine the effects of past and present exposure to parasitic viruses (phages)
on the spread of mutator alleles, resistance, and bacterial competitive fitness.
We found that mutator alleles spread rapidly during adaptation to any of four
different phage species, and this pattern was even more pronounced with multiple
phages present simultaneously. However, hypermutability did not detectably accelerate
adaptation in the absence of phages and recovery of fitness costs associated with
resistance. Several lineages evolved phage resistance through elevated mucoidy,
and during subsequent evolution in phage-free conditions they rapidly reverted
to nonmucoid, phage-susceptible phenotypes. Genome sequencing revealed that this
phenotypic reversion was achieved by additional genetic changes rather than by
genotypic reversion of the initial resistance mutations. Insertion sequence (IS)
elements played a key role in both the acquisition of resistance and adaptation
in the absence of parasites; unlike single nucleotide polymorphisms, IS insertions
were not more frequent in mutator lineages. Our results provide a genetic explanation
for rapid reversion of mucoidy, a phenotype observed in other bacterial species
including human pathogens. Moreover, this demonstrates that the types of genetic
change underlying adaptation to fitness costs, and consequently the impact of
evolvability mechanisms such as increased point-mutation rates, depend critically
on the mechanism of resistance.
article_processing_charge: No
author:
- first_name: Sébastien
full_name: Wielgoss, Sébastien
last_name: Wielgoss
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Anna M.
full_name: Bischofberger, Anna M.
last_name: Bischofberger
- first_name: Alex R.
full_name: Hall, Alex R.
last_name: Hall
citation:
ama: 'Wielgoss S, Bergmiller T, Bischofberger AM, Hall AR. Data from: Adaptation
to parasites and costs of parasite resistance in mutator and non-mutator bacteria.
2015. doi:10.5061/dryad.cj910'
apa: 'Wielgoss, S., Bergmiller, T., Bischofberger, A. M., & Hall, A. R. (2015).
Data from: Adaptation to parasites and costs of parasite resistance in mutator
and non-mutator bacteria. Dryad. https://doi.org/10.5061/dryad.cj910'
chicago: 'Wielgoss, Sébastien, Tobias Bergmiller, Anna M. Bischofberger, and Alex
R. Hall. “Data from: Adaptation to Parasites and Costs of Parasite Resistance
in Mutator and Non-Mutator Bacteria.” Dryad, 2015. https://doi.org/10.5061/dryad.cj910.'
ieee: 'S. Wielgoss, T. Bergmiller, A. M. Bischofberger, and A. R. Hall, “Data from:
Adaptation to parasites and costs of parasite resistance in mutator and non-mutator
bacteria.” Dryad, 2015.'
ista: 'Wielgoss S, Bergmiller T, Bischofberger AM, Hall AR. 2015. Data from: Adaptation
to parasites and costs of parasite resistance in mutator and non-mutator bacteria,
Dryad, 10.5061/dryad.cj910.'
mla: 'Wielgoss, Sébastien, et al. Data from: Adaptation to Parasites and Costs
of Parasite Resistance in Mutator and Non-Mutator Bacteria. Dryad, 2015, doi:10.5061/dryad.cj910.'
short: S. Wielgoss, T. Bergmiller, A.M. Bischofberger, A.R. Hall, (2015).
date_created: 2021-07-26T08:44:04Z
date_published: 2015-12-21T00:00:00Z
date_updated: 2023-09-05T13:46:04Z
day: '21'
department:
- _id: CaGu
doi: 10.5061/dryad.cj910
main_file_link:
- open_access: '1'
url: https://doi.org/10.5061/dryad.cj910
month: '12'
oa: 1
oa_version: Published Version
publisher: Dryad
related_material:
record:
- id: '5749'
relation: used_in_publication
status: public
status: public
title: 'Data from: Adaptation to parasites and costs of parasite resistance in mutator
and non-mutator bacteria'
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2015'
...
---
_id: '9721'
abstract:
- lang: eng
text: To prevent epidemics, insect societies have evolved collective disease defences
that are highly effective at curing exposed individuals and limiting disease transmission
to healthy group members. Grooming is an important sanitary behaviour—either performed
towards oneself (self-grooming) or towards others (allogrooming)—to remove infectious
agents from the body surface of exposed individuals, but at the risk of disease
contraction by the groomer. We use garden ants (Lasius neglectus) and the fungal
pathogen Metarhizium as a model system to study how pathogen presence affects
self-grooming and allogrooming between exposed and healthy individuals. We develop
an epidemiological SIS model to explore how experimentally observed grooming patterns
affect disease spread within the colony, thereby providing a direct link between
the expression and direction of sanitary behaviours, and their effects on colony-level
epidemiology. We find that fungus-exposed ants increase self-grooming, while simultaneously
decreasing allogrooming. This behavioural modulation seems universally adaptive
and is predicted to contain disease spread in a great variety of host–pathogen
systems. In contrast, allogrooming directed towards pathogen-exposed individuals
might both increase and decrease disease risk. Our model reveals that the effect
of allogrooming depends on the balance between pathogen infectiousness and efficiency
of social host defences, which are likely to vary across host–pathogen systems.
article_processing_charge: No
author:
- first_name: Fabian
full_name: Theis, Fabian
last_name: Theis
- first_name: Line V
full_name: Ugelvig, Line V
id: 3DC97C8E-F248-11E8-B48F-1D18A9856A87
last_name: Ugelvig
orcid: 0000-0003-1832-8883
- first_name: Carsten
full_name: Marr, Carsten
last_name: Marr
- first_name: Sylvia
full_name: Cremer, Sylvia
id: 2F64EC8C-F248-11E8-B48F-1D18A9856A87
last_name: Cremer
orcid: 0000-0002-2193-3868
citation:
ama: 'Theis F, Ugelvig LV, Marr C, Cremer S. Data from: Opposing effects of allogrooming
on disease transmission in ant societies. 2015. doi:10.5061/dryad.dj2bf'
apa: 'Theis, F., Ugelvig, L. V., Marr, C., & Cremer, S. (2015). Data from: Opposing
effects of allogrooming on disease transmission in ant societies. Dryad. https://doi.org/10.5061/dryad.dj2bf'
chicago: 'Theis, Fabian, Line V Ugelvig, Carsten Marr, and Sylvia Cremer. “Data
from: Opposing Effects of Allogrooming on Disease Transmission in Ant Societies.”
Dryad, 2015. https://doi.org/10.5061/dryad.dj2bf.'
ieee: 'F. Theis, L. V. Ugelvig, C. Marr, and S. Cremer, “Data from: Opposing effects
of allogrooming on disease transmission in ant societies.” Dryad, 2015.'
ista: 'Theis F, Ugelvig LV, Marr C, Cremer S. 2015. Data from: Opposing effects
of allogrooming on disease transmission in ant societies, Dryad, 10.5061/dryad.dj2bf.'
mla: 'Theis, Fabian, et al. Data from: Opposing Effects of Allogrooming on Disease
Transmission in Ant Societies. Dryad, 2015, doi:10.5061/dryad.dj2bf.'
short: F. Theis, L.V. Ugelvig, C. Marr, S. Cremer, (2015).
date_created: 2021-07-26T09:38:36Z
date_published: 2015-12-29T00:00:00Z
date_updated: 2023-02-23T10:16:22Z
day: '29'
department:
- _id: SyCr
doi: 10.5061/dryad.dj2bf
main_file_link:
- open_access: '1'
url: https://doi.org/10.5061/dryad.dj2bf
month: '12'
oa: 1
oa_version: Published Version
publisher: Dryad
related_material:
record:
- id: '1830'
relation: used_in_publication
status: public
status: public
title: 'Data from: Opposing effects of allogrooming on disease transmission in ant
societies'
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2015'
...
---
_id: '9737'
article_processing_charge: No
author:
- first_name: Olga
full_name: Symonova, Olga
id: 3C0C7BC6-F248-11E8-B48F-1D18A9856A87
last_name: Symonova
- first_name: Christopher
full_name: Topp, Christopher
last_name: Topp
- first_name: Herbert
full_name: Edelsbrunner, Herbert
id: 3FB178DA-F248-11E8-B48F-1D18A9856A87
last_name: Edelsbrunner
orcid: 0000-0002-9823-6833
citation:
ama: Symonova O, Topp C, Edelsbrunner H. Root traits computed by DynamicRoots for
the maize root shown in fig 2. 2015. doi:10.1371/journal.pone.0127657.s001
apa: Symonova, O., Topp, C., & Edelsbrunner, H. (2015). Root traits computed
by DynamicRoots for the maize root shown in fig 2. Public Library of Science.
https://doi.org/10.1371/journal.pone.0127657.s001
chicago: Symonova, Olga, Christopher Topp, and Herbert Edelsbrunner. “Root Traits
Computed by DynamicRoots for the Maize Root Shown in Fig 2.” Public Library of
Science, 2015. https://doi.org/10.1371/journal.pone.0127657.s001.
ieee: O. Symonova, C. Topp, and H. Edelsbrunner, “Root traits computed by DynamicRoots
for the maize root shown in fig 2.” Public Library of Science, 2015.
ista: Symonova O, Topp C, Edelsbrunner H. 2015. Root traits computed by DynamicRoots
for the maize root shown in fig 2, Public Library of Science, 10.1371/journal.pone.0127657.s001.
mla: Symonova, Olga, et al. Root Traits Computed by DynamicRoots for the Maize
Root Shown in Fig 2. Public Library of Science, 2015, doi:10.1371/journal.pone.0127657.s001.
short: O. Symonova, C. Topp, H. Edelsbrunner, (2015).
date_created: 2021-07-28T06:20:13Z
date_published: 2015-06-01T00:00:00Z
date_updated: 2023-02-23T10:14:42Z
day: '01'
department:
- _id: MaJö
- _id: HeEd
doi: 10.1371/journal.pone.0127657.s001
month: '06'
oa_version: Published Version
publisher: Public Library of Science
related_material:
record:
- id: '1793'
relation: used_in_publication
status: public
status: public
title: Root traits computed by DynamicRoots for the maize root shown in fig 2
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2015'
...
---
_id: '9742'
abstract:
- lang: eng
text: 'Repeated pathogen exposure is a common threat in colonies of social insects,
posing selection pressures on colony members to respond with improved disease-defense
performance. We here tested whether experience gained by repeated tending of low-level
fungus-exposed (Metarhizium robertsii) larvae may alter the performance of sanitary
brood care in the clonal ant, Platythyrea punctata. We trained ants individually
over nine consecutive trials to either sham-treated or fungus-exposed larvae.
We then compared the larval grooming behavior of naive and trained ants and measured
how effectively they removed infectious fungal conidiospores from the fungus-exposed
larvae. We found that the ants changed the duration of larval grooming in response
to both, larval treatment and their level of experience: (1) sham-treated larvae
received longer grooming than the fungus-exposed larvae and (2) trained ants performed
less self-grooming but longer larval grooming than naive ants, which was true
for both, ants trained to fungus-exposed and also to sham-treated larvae. Ants
that groomed the fungus-exposed larvae for longer periods removed a higher number
of fungal conidiospores from the surface of the fungus-exposed larvae. As experienced
ants performed longer larval grooming, they were more effective in fungal removal,
thus making them better caretakers under pathogen attack of the colony. By studying
this clonal ant, we can thus conclude that even in the absence of genetic variation
between colony members, differences in experience levels of brood care may affect
performance of sanitary brood care in social insects.'
article_processing_charge: No
author:
- first_name: Claudia
full_name: Westhus, Claudia
last_name: Westhus
- first_name: Line V
full_name: Ugelvig, Line V
id: 3DC97C8E-F248-11E8-B48F-1D18A9856A87
last_name: Ugelvig
orcid: 0000-0003-1832-8883
- first_name: Edouard
full_name: Tourdot, Edouard
last_name: Tourdot
- first_name: Jürgen
full_name: Heinze, Jürgen
last_name: Heinze
- first_name: Claudie
full_name: Doums, Claudie
last_name: Doums
- first_name: Sylvia
full_name: Cremer, Sylvia
id: 2F64EC8C-F248-11E8-B48F-1D18A9856A87
last_name: Cremer
orcid: 0000-0002-2193-3868
citation:
ama: 'Westhus C, Ugelvig LV, Tourdot E, Heinze J, Doums C, Cremer S. Data from:
Increased grooming after repeated brood care provides sanitary benefits in a clonal
ant. 2015. doi:10.5061/dryad.7kc79'
apa: 'Westhus, C., Ugelvig, L. V., Tourdot, E., Heinze, J., Doums, C., & Cremer,
S. (2015). Data from: Increased grooming after repeated brood care provides sanitary
benefits in a clonal ant. Dryad. https://doi.org/10.5061/dryad.7kc79'
chicago: 'Westhus, Claudia, Line V Ugelvig, Edouard Tourdot, Jürgen Heinze, Claudie
Doums, and Sylvia Cremer. “Data from: Increased Grooming after Repeated Brood
Care Provides Sanitary Benefits in a Clonal Ant.” Dryad, 2015. https://doi.org/10.5061/dryad.7kc79.'
ieee: 'C. Westhus, L. V. Ugelvig, E. Tourdot, J. Heinze, C. Doums, and S. Cremer,
“Data from: Increased grooming after repeated brood care provides sanitary benefits
in a clonal ant.” Dryad, 2015.'
ista: 'Westhus C, Ugelvig LV, Tourdot E, Heinze J, Doums C, Cremer S. 2015. Data
from: Increased grooming after repeated brood care provides sanitary benefits
in a clonal ant, Dryad, 10.5061/dryad.7kc79.'
mla: 'Westhus, Claudia, et al. Data from: Increased Grooming after Repeated Brood
Care Provides Sanitary Benefits in a Clonal Ant. Dryad, 2015, doi:10.5061/dryad.7kc79.'
short: C. Westhus, L.V. Ugelvig, E. Tourdot, J. Heinze, C. Doums, S. Cremer, (2015).
date_created: 2021-07-28T08:52:53Z
date_published: 2015-07-09T00:00:00Z
date_updated: 2023-02-23T10:30:52Z
day: '09'
department:
- _id: SyCr
doi: 10.5061/dryad.7kc79
main_file_link:
- open_access: '1'
url: https://doi.org/10.5061/dryad.7kc79
month: '07'
oa: 1
oa_version: Published Version
publisher: Dryad
related_material:
record:
- id: '2161'
relation: used_in_publication
status: public
status: public
title: 'Data from: Increased grooming after repeated brood care provides sanitary
benefits in a clonal ant'
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2015'
...
---
_id: '9765'
article_processing_charge: No
author:
- first_name: Guillaume
full_name: Chevereau, Guillaume
id: 424D78A0-F248-11E8-B48F-1D18A9856A87
last_name: Chevereau
- first_name: Marta
full_name: Lukacisinova, Marta
id: 4342E402-F248-11E8-B48F-1D18A9856A87
last_name: Lukacisinova
orcid: 0000-0002-2519-8004
- first_name: Tugce
full_name: Batur, Tugce
last_name: Batur
- first_name: Aysegul
full_name: Guvenek, Aysegul
last_name: Guvenek
- first_name: Dilay Hazal
full_name: Ayhan, Dilay Hazal
last_name: Ayhan
- first_name: Erdal
full_name: Toprak, Erdal
last_name: Toprak
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
citation:
ama: Chevereau G, Lukacisinova M, Batur T, et al. Gene ontology enrichment analysis
for the most sensitive gene deletion strains for all drugs. 2015. doi:10.1371/journal.pbio.1002299.s008
apa: Chevereau, G., Lukacisinova, M., Batur, T., Guvenek, A., Ayhan, D. H., Toprak,
E., & Bollenbach, M. T. (2015). Gene ontology enrichment analysis for the
most sensitive gene deletion strains for all drugs. Public Library of Science.
https://doi.org/10.1371/journal.pbio.1002299.s008
chicago: Chevereau, Guillaume, Marta Lukacisinova, Tugce Batur, Aysegul Guvenek,
Dilay Hazal Ayhan, Erdal Toprak, and Mark Tobias Bollenbach. “Gene Ontology Enrichment
Analysis for the Most Sensitive Gene Deletion Strains for All Drugs.” Public Library
of Science, 2015. https://doi.org/10.1371/journal.pbio.1002299.s008.
ieee: G. Chevereau et al., “Gene ontology enrichment analysis for the most
sensitive gene deletion strains for all drugs.” Public Library of Science, 2015.
ista: Chevereau G, Lukacisinova M, Batur T, Guvenek A, Ayhan DH, Toprak E, Bollenbach
MT. 2015. Gene ontology enrichment analysis for the most sensitive gene deletion
strains for all drugs, Public Library of Science, 10.1371/journal.pbio.1002299.s008.
mla: Chevereau, Guillaume, et al. Gene Ontology Enrichment Analysis for the Most
Sensitive Gene Deletion Strains for All Drugs. Public Library of Science,
2015, doi:10.1371/journal.pbio.1002299.s008.
short: G. Chevereau, M. Lukacisinova, T. Batur, A. Guvenek, D.H. Ayhan, E. Toprak,
M.T. Bollenbach, (2015).
date_created: 2021-08-03T07:05:16Z
date_published: 2015-11-18T00:00:00Z
date_updated: 2023-02-23T10:07:02Z
day: '18'
department:
- _id: ToBo
doi: 10.1371/journal.pbio.1002299.s008
month: '11'
oa_version: Published Version
publisher: Public Library of Science
related_material:
record:
- id: '1619'
relation: used_in_publication
status: public
status: public
title: Gene ontology enrichment analysis for the most sensitive gene deletion strains
for all drugs
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2015'
...
---
_id: '9772'
article_processing_charge: No
author:
- first_name: Barbora
full_name: Trubenova, Barbora
id: 42302D54-F248-11E8-B48F-1D18A9856A87
last_name: Trubenova
orcid: 0000-0002-6873-2967
- first_name: Sebastian
full_name: Novak, Sebastian
id: 461468AE-F248-11E8-B48F-1D18A9856A87
last_name: Novak
- first_name: Reinmar
full_name: Hager, Reinmar
last_name: Hager
citation:
ama: Trubenova B, Novak S, Hager R. Description of the agent based simulations.
2015. doi:10.1371/journal.pone.0126907.s003
apa: Trubenova, B., Novak, S., & Hager, R. (2015). Description of the agent
based simulations. Public Library of Science. https://doi.org/10.1371/journal.pone.0126907.s003
chicago: Trubenova, Barbora, Sebastian Novak, and Reinmar Hager. “Description of
the Agent Based Simulations.” Public Library of Science, 2015. https://doi.org/10.1371/journal.pone.0126907.s003.
ieee: B. Trubenova, S. Novak, and R. Hager, “Description of the agent based simulations.”
Public Library of Science, 2015.
ista: Trubenova B, Novak S, Hager R. 2015. Description of the agent based simulations,
Public Library of Science, 10.1371/journal.pone.0126907.s003.
mla: Trubenova, Barbora, et al. Description of the Agent Based Simulations.
Public Library of Science, 2015, doi:10.1371/journal.pone.0126907.s003.
short: B. Trubenova, S. Novak, R. Hager, (2015).
date_created: 2021-08-05T12:55:20Z
date_published: 2015-05-18T00:00:00Z
date_updated: 2023-02-23T10:15:25Z
day: '18'
department:
- _id: NiBa
doi: 10.1371/journal.pone.0126907.s003
month: '05'
oa_version: Published Version
publisher: Public Library of Science
related_material:
record:
- id: '1809'
relation: used_in_publication
status: public
status: public
title: Description of the agent based simulations
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2015'
...
---
_id: '9773'
article_processing_charge: No
author:
- first_name: Tamar
full_name: Friedlander, Tamar
id: 36A5845C-F248-11E8-B48F-1D18A9856A87
last_name: Friedlander
- first_name: Avraham E.
full_name: Mayo, Avraham E.
last_name: Mayo
- first_name: Tsvi
full_name: Tlusty, Tsvi
last_name: Tlusty
- first_name: Uri
full_name: Alon, Uri
last_name: Alon
citation:
ama: Friedlander T, Mayo AE, Tlusty T, Alon U. Evolutionary simulation code. 2015.
doi:10.1371/journal.pcbi.1004055.s002
apa: Friedlander, T., Mayo, A. E., Tlusty, T., & Alon, U. (2015). Evolutionary
simulation code. Public Library of Science. https://doi.org/10.1371/journal.pcbi.1004055.s002
chicago: Friedlander, Tamar, Avraham E. Mayo, Tsvi Tlusty, and Uri Alon. “Evolutionary
Simulation Code.” Public Library of Science, 2015. https://doi.org/10.1371/journal.pcbi.1004055.s002.
ieee: T. Friedlander, A. E. Mayo, T. Tlusty, and U. Alon, “Evolutionary simulation
code.” Public Library of Science, 2015.
ista: Friedlander T, Mayo AE, Tlusty T, Alon U. 2015. Evolutionary simulation code,
Public Library of Science, 10.1371/journal.pcbi.1004055.s002.
mla: Friedlander, Tamar, et al. Evolutionary Simulation Code. Public Library
of Science, 2015, doi:10.1371/journal.pcbi.1004055.s002.
short: T. Friedlander, A.E. Mayo, T. Tlusty, U. Alon, (2015).
date_created: 2021-08-05T12:58:07Z
date_published: 2015-03-23T00:00:00Z
date_updated: 2023-02-23T10:16:13Z
day: '23'
department:
- _id: GaTk
doi: 10.1371/journal.pcbi.1004055.s002
month: '03'
oa_version: Published Version
publisher: Public Library of Science
related_material:
record:
- id: '1827'
relation: used_in_publication
status: public
status: public
title: Evolutionary simulation code
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2015'
...
---
_id: '981'
abstract:
- lang: eng
text: The tunability of topological surface states and controllable opening of the
Dirac gap are of fundamental and practical interest in the field of topological
materials. In the newly discovered topological crystalline insulators (TCIs),
theory predicts that the Dirac node is protected by a crystalline symmetry and
that the surface state electrons can acquire a mass if this symmetry is broken.
Recent studies have detected signatures of a spontaneously generated Dirac gap
in TCIs; however, the mechanism of mass formation remains elusive. In this work,
we present scanning tunnelling microscopy (STM) measurements of the TCI Pb 1â'x
Sn x Se for a wide range of alloy compositions spanning the topological and non-topological
regimes. The STM topographies reveal a symmetry-breaking distortion on the surface,
which imparts mass to the otherwise massless Dirac electrons-a mechanism analogous
to the long sought-after Higgs mechanism in particle physics. Interestingly, the
measured Dirac gap decreases on approaching the trivial phase, whereas the magnitude
of the distortion remains nearly constant. Our data and calculations reveal that
the penetration depth of Dirac surface states controls the magnitude of the Dirac
mass. At the limit of the critical composition, the penetration depth is predicted
to go to infinity, resulting in zero mass, consistent with our measurements. Finally,
we discover the existence of surface states in the non-topological regime, which
have the characteristics of gapped, double-branched Dirac fermions and could be
exploited in realizing superconductivity in these materials.
acknowledgement: We thank R. Buczko, C. Chamon, J. C. Seamus Davis, M. El-Batanouny,
A. Mesaros, Y. Ran and A. Soumyanarayanan for useful conversations and G. McMahon
for help with EDS measurements. V.M. gratefully acknowledges funding from the US
Department of Energy, Scanned Probe Division under Award Number DE-FG02-12ER46880
for the support of I.Z., Y.O., W.Z. and D.W. for this project. Work at Massachusetts
Institute of Technology is supported by US Department of Energy, Office of Basic
Energy Sciences, Division of Materials Sciences and Engineering under Award DE-SC0010526
(L.F.), and NSF-DMR-1104498 (M.S.). H.L. acknowledges the Singapore National Research
Foundation for support under NRF Award No. NRF-NRFF2013-03. Y.O. was partly supported
by JSPS KAKENHI Grant Numbers 26707016 and 00707656. The work at Northeastern University
is supported by the US Department of Energy grant number DE-FG02-07ER46352, and
benefited from Northeastern University’s Advanced Scientific Computation Center
(ASCC), theory support at the Advanced Light Source, Berkeley and the allocation
of supercomputer time at the NERSC through DOE grant number DE-AC02-05CH11231. Work
at Princeton University is supported by the US National Science Foundation Grant,
NSF-DMR-1006492. F.C. acknowledges the support provided by MOST-Taiwan under project
number NSC-102-2119-M-002-004.
author:
- first_name: Ilija
full_name: Zeljkovic, Ilija
last_name: Zeljkovic
- first_name: Yoshinori
full_name: Okada, Yoshinori
last_name: Okada
- first_name: Maksym
full_name: Maksym Serbyn
id: 47809E7E-F248-11E8-B48F-1D18A9856A87
last_name: Serbyn
orcid: 0000-0002-2399-5827
- first_name: Raman
full_name: Sankar, Raman
last_name: Sankar
- first_name: Daniel
full_name: Walkup, Daniel
last_name: Walkup
- first_name: Wenwen
full_name: Zhou, Wenwen
last_name: Zhou
- first_name: Junwei
full_name: Liu, Junwei
last_name: Liu
- first_name: Guoqing
full_name: Chang, Guoqing
last_name: Chang
- first_name: Yungjui
full_name: Wang, Yungjui
last_name: Wang
- first_name: Md
full_name: Hasan, Md Z
last_name: Hasan
- first_name: Fangcheng
full_name: Chou, Fangcheng
last_name: Chou
- first_name: Hsin
full_name: Lin, Hsin
last_name: Lin
- first_name: Arun
full_name: Bansil, Arun
last_name: Bansil
- first_name: Liang
full_name: Fu, Liang
last_name: Fu
- first_name: Vidya
full_name: Madhavan, Vidya
last_name: Madhavan
citation:
ama: Zeljkovic I, Okada Y, Serbyn M, et al. Dirac mass generation from crystal symmetry
breaking on the surfaces of topological crystalline insulators. Nature Materials.
2015;14(3):318-324. doi:10.1038/nmat4215
apa: Zeljkovic, I., Okada, Y., Serbyn, M., Sankar, R., Walkup, D., Zhou, W., … Madhavan,
V. (2015). Dirac mass generation from crystal symmetry breaking on the surfaces
of topological crystalline insulators. Nature Materials. Nature Publishing
Group. https://doi.org/10.1038/nmat4215
chicago: Zeljkovic, Ilija, Yoshinori Okada, Maksym Serbyn, Raman Sankar, Daniel
Walkup, Wenwen Zhou, Junwei Liu, et al. “Dirac Mass Generation from Crystal Symmetry
Breaking on the Surfaces of Topological Crystalline Insulators.” Nature Materials.
Nature Publishing Group, 2015. https://doi.org/10.1038/nmat4215.
ieee: I. Zeljkovic et al., “Dirac mass generation from crystal symmetry breaking
on the surfaces of topological crystalline insulators,” Nature Materials,
vol. 14, no. 3. Nature Publishing Group, pp. 318–324, 2015.
ista: Zeljkovic I, Okada Y, Serbyn M, Sankar R, Walkup D, Zhou W, Liu J, Chang G,
Wang Y, Hasan M, Chou F, Lin H, Bansil A, Fu L, Madhavan V. 2015. Dirac mass generation
from crystal symmetry breaking on the surfaces of topological crystalline insulators.
Nature Materials. 14(3), 318–324.
mla: Zeljkovic, Ilija, et al. “Dirac Mass Generation from Crystal Symmetry Breaking
on the Surfaces of Topological Crystalline Insulators.” Nature Materials,
vol. 14, no. 3, Nature Publishing Group, 2015, pp. 318–24, doi:10.1038/nmat4215.
short: I. Zeljkovic, Y. Okada, M. Serbyn, R. Sankar, D. Walkup, W. Zhou, J. Liu,
G. Chang, Y. Wang, M. Hasan, F. Chou, H. Lin, A. Bansil, L. Fu, V. Madhavan, Nature
Materials 14 (2015) 318–324.
date_created: 2018-12-11T11:49:31Z
date_published: 2015-03-01T00:00:00Z
date_updated: 2021-01-12T08:22:24Z
day: '01'
doi: 10.1038/nmat4215
extern: 1
intvolume: ' 14'
issue: '3'
main_file_link:
- open_access: '1'
url: https://arxiv.org/abs/1403.4906
month: '03'
oa: 1
page: 318 - 324
publication: Nature Materials
publication_status: published
publisher: Nature Publishing Group
publist_id: '6419'
quality_controlled: 0
status: public
title: Dirac mass generation from crystal symmetry breaking on the surfaces of topological
crystalline insulators
type: journal_article
volume: 14
year: '2015'
...
---
_id: '982'
abstract:
- lang: eng
text: We propose a new approach to probing ergodicity and its breakdown in one-dimensional
quantum manybody systems based on their response to a local perturbation. We study
the distribution of matrix elements of a local operator between the system's eigenstates,
finding a qualitatively different behavior in the manybody localized (MBL) and
ergodic phases. To characterize how strongly a local perturbation modifies the
eigenstates, we introduce the parameter g(L) = (In (Vnm/δ)) which represents the
disorder-averaged ratio of a typical matrix element of a local operator V to energy
level spacing δ this parameter is reminiscent of the Thouless conductance in the
single-particle localization. We show that the parameter g(L) decreases with system
size L in the MBL phase and grows in the ergodic phase. We surmise that the delocalization
transition occurs when g(L) is independent of system size, g(L)=gc ~ 1. We illustrate
our approach by studying the many-body localization transition and resolving the
many-body mobility edge in a disordered one-dimensional XXZ spin-1=2 chain using
exact diagonalization and time-evolving block-decimation methods. Our criterion
for the MBL transition gives insights into microscopic details of transition.
Its direct physical consequences, in particular, logarithmically slow transport
at the transition and extensive entanglement entropy of the eigenstates, are consistent
with recent renormalization-group predictions.
acknowledgement: We acknowledge helpful discussions with Sid Parameswaran, Andrew
Potter, Antonello Scardicchio, Romain Vasseur, and especially with Ehud Altman and
David Huse. We would like to thank Miles Stoudenmire for the assistance with ITensor
library. Research at Perimeter Institute is supported by the Government of Canada
through Industry Canada and by the Province of Ontario through the Ministry of Economic
Development & Innovation. This research was supported by Gordon and Betty Moore
Foundation EPiQS Initiative through Grant No. GBMF4307 (M. S.), Sloan Foundation,
NSERC, and Early Researcher Award of Ontario (D. A.). This work made use of the
facilities of N8 HPC Centre of Excellence, provided and funded by the N8 consortium
and EPSRC (Grant No. EP/K000225/1). The Centre is coordinated by the Universities
of Leeds and Manchester.
author:
- first_name: Maksym
full_name: Maksym Serbyn
id: 47809E7E-F248-11E8-B48F-1D18A9856A87
last_name: Serbyn
orcid: 0000-0002-2399-5827
- first_name: Zlatko
full_name: Papić, Zlatko
last_name: Papić
- first_name: Dmitry
full_name: Abanin, Dmitry A
last_name: Abanin
citation:
ama: Serbyn M, Papić Z, Abanin D. Criterion for many-body localization-delocalization
phase transition. Physical Review X. 2015;5(4). doi:10.1103/PhysRevX.5.041047
apa: Serbyn, M., Papić, Z., & Abanin, D. (2015). Criterion for many-body localization-delocalization
phase transition. Physical Review X. American Physical Society. https://doi.org/10.1103/PhysRevX.5.041047
chicago: Serbyn, Maksym, Zlatko Papić, and Dmitry Abanin. “Criterion for Many-Body
Localization-Delocalization Phase Transition.” Physical Review X. American
Physical Society, 2015. https://doi.org/10.1103/PhysRevX.5.041047.
ieee: M. Serbyn, Z. Papić, and D. Abanin, “Criterion for many-body localization-delocalization
phase transition,” Physical Review X, vol. 5, no. 4. American Physical
Society, 2015.
ista: Serbyn M, Papić Z, Abanin D. 2015. Criterion for many-body localization-delocalization
phase transition. Physical Review X. 5(4).
mla: Serbyn, Maksym, et al. “Criterion for Many-Body Localization-Delocalization
Phase Transition.” Physical Review X, vol. 5, no. 4, American Physical
Society, 2015, doi:10.1103/PhysRevX.5.041047.
short: M. Serbyn, Z. Papić, D. Abanin, Physical Review X 5 (2015).
date_created: 2018-12-11T11:49:32Z
date_published: 2015-01-01T00:00:00Z
date_updated: 2021-01-12T08:22:25Z
day: '01'
doi: 10.1103/PhysRevX.5.041047
extern: 1
intvolume: ' 5'
issue: '4'
main_file_link:
- open_access: '1'
url: https://arxiv.org/abs/1507.01635
month: '01'
oa: 1
publication: Physical Review X
publication_status: published
publisher: American Physical Society
publist_id: '6418'
quality_controlled: 0
status: public
title: Criterion for many-body localization-delocalization phase transition
type: journal_article
volume: 5
year: '2015'
...
---
_id: '99'
abstract:
- lang: eng
text: Quasiparticle excitations can compromise the performance of superconducting
devices, causing high-frequency dissipation, decoherence in Josephson qubits,
and braiding errors in proposed Majorana-based topological quantum computers.
Quasiparticle dynamics have been studied in detail in metallic superconductors
but remain relatively unexplored in semiconductor-superconductor structures, which
are now being intensely pursued in the context of topological superconductivity.
To this end, we use a system comprising a gate-confined semiconductor nanowire
with an epitaxially grown superconductor layer, yielding an isolated, proximitized
nanowire segment. We identify bound states in the semiconductor by means of bias
spectroscopy, determine the characteristic temperatures and magnetic fields for
quasiparticle excitations, and extract a parity lifetime (poisoning time) of the
bound state in the semiconductor exceeding 10 ms.
acknowledgement: Research support by Microsoft Project Q, the Danish National Research
Foundation, the Lundbeck Foundation, the Carlsberg Foundation, and the European
Commission. A.P.H. acknowledges support from the US Department of Energy, C.M.M.
acknowledges support from the Villum Foundation.
arxiv: 1
author:
- first_name: Andrew P
full_name: Higginbotham, Andrew P
id: 4AD6785A-F248-11E8-B48F-1D18A9856A87
last_name: Higginbotham
orcid: 0000-0003-2607-2363
- first_name: S M
full_name: Albrecht, S M
last_name: Albrecht
- first_name: Gediminas
full_name: Kiršanskas, Gediminas
last_name: Kiršanskas
- first_name: W
full_name: Chang, W
last_name: Chang
- first_name: Ferdinand
full_name: Kuemmeth, Ferdinand
last_name: Kuemmeth
- first_name: Peter
full_name: Krogstrup, Peter
last_name: Krogstrup
- first_name: Thomas
full_name: Jespersen, Thomas
last_name: Jespersen
- first_name: Jesper
full_name: Nygård, Jesper
last_name: Nygård
- first_name: Karsten
full_name: Flensberg, Karsten
last_name: Flensberg
- first_name: Charles
full_name: Marcus, Charles
last_name: Marcus
citation:
ama: Higginbotham AP, Albrecht SM, Kiršanskas G, et al. Parity lifetime of bound
states in a proximitized semiconductor nanowire. Nature Physics. 2015;11(12):1017-1021.
doi:10.1038/nphys3461
apa: Higginbotham, A. P., Albrecht, S. M., Kiršanskas, G., Chang, W., Kuemmeth,
F., Krogstrup, P., … Marcus, C. (2015). Parity lifetime of bound states in a proximitized
semiconductor nanowire. Nature Physics. Nature Publishing Group. https://doi.org/10.1038/nphys3461
chicago: Higginbotham, Andrew P, S M Albrecht, Gediminas Kiršanskas, W Chang, Ferdinand
Kuemmeth, Peter Krogstrup, Thomas Jespersen, Jesper Nygård, Karsten Flensberg,
and Charles Marcus. “Parity Lifetime of Bound States in a Proximitized Semiconductor
Nanowire.” Nature Physics. Nature Publishing Group, 2015. https://doi.org/10.1038/nphys3461.
ieee: A. P. Higginbotham et al., “Parity lifetime of bound states in a proximitized
semiconductor nanowire,” Nature Physics, vol. 11, no. 12. Nature Publishing
Group, pp. 1017–1021, 2015.
ista: Higginbotham AP, Albrecht SM, Kiršanskas G, Chang W, Kuemmeth F, Krogstrup
P, Jespersen T, Nygård J, Flensberg K, Marcus C. 2015. Parity lifetime of bound
states in a proximitized semiconductor nanowire. Nature Physics. 11(12), 1017–1021.
mla: Higginbotham, Andrew P., et al. “Parity Lifetime of Bound States in a Proximitized
Semiconductor Nanowire.” Nature Physics, vol. 11, no. 12, Nature Publishing
Group, 2015, pp. 1017–21, doi:10.1038/nphys3461.
short: A.P. Higginbotham, S.M. Albrecht, G. Kiršanskas, W. Chang, F. Kuemmeth, P.
Krogstrup, T. Jespersen, J. Nygård, K. Flensberg, C. Marcus, Nature Physics 11
(2015) 1017–1021.
date_created: 2018-12-11T11:44:37Z
date_published: 2015-09-14T00:00:00Z
date_updated: 2021-01-12T08:22:28Z
day: '14'
doi: 10.1038/nphys3461
extern: '1'
external_id:
arxiv:
- '1501.05155'
intvolume: ' 11'
issue: '12'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://arxiv.org/abs/1501.05155
month: '09'
oa: 1
oa_version: Preprint
page: 1017 - 1021
publication: Nature Physics
publication_status: published
publisher: Nature Publishing Group
publist_id: '7955'
quality_controlled: '1'
status: public
title: Parity lifetime of bound states in a proximitized semiconductor nanowire
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 11
year: '2015'
...
---
_id: '1106'
abstract:
- lang: eng
text: Circumferential skin creases Kunze type (CSC-KT) is a specific congenital
entity with an unknown genetic cause. The disease phenotype comprises characteristic
circumferential skin creases accompanied by intellectual disability, a cleft palate,
short stature, and dysmorphic features. Here, we report that mutations in either
MAPRE2 or TUBB underlie the genetic origin of this syndrome. MAPRE2 encodes a
member of the microtubule end-binding family of proteins that bind to the guanosine
triphosphate cap at growing microtubule plus ends, and TUBB encodes a β-tubulin
isotype that is expressed abundantly in the developing brain. Functional analyses
of the TUBB mutants show multiple defects in the chaperone-dependent tubulin heterodimer
folding and assembly pathway that leads to a compromised yield of native heterodimers.
The TUBB mutations also have an impact on microtubule dynamics. For MAPRE2, we
show that the mutations result in enhanced MAPRE2 binding to microtubules, implying
an increased dwell time at microtubule plus ends. Further, in vivo analysis of
MAPRE2 mutations in a zebrafish model of craniofacial development shows that the
variants most likely perturb the patterning of branchial arches, either through
excessive activity (under a recessive paradigm) or through haploinsufficiency
(dominant de novo paradigm). Taken together, our data add CSC-KT to the growing
list of tubulinopathies and highlight how multiple inheritance paradigms can affect
dosage-sensitive biological systems so as to result in the same clinical defect.
author:
- first_name: Mala
full_name: Isrie, Mala
last_name: Isrie
- first_name: Martin
full_name: Breuss, Martin
last_name: Breuss
- first_name: Guoling
full_name: Tian, Guoling
last_name: Tian
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
- first_name: Francesca
full_name: Cristofoli, Francesca
last_name: Cristofoli
- first_name: Jasmin
full_name: Morandell, Jasmin
id: 4739D480-F248-11E8-B48F-1D18A9856A87
last_name: Morandell
- first_name: Zachari A
full_name: Kupchinsky, Zachari A
last_name: Kupchinsky
- first_name: Alejandro
full_name: Sifrim, Alejandro
last_name: Sifrim
- first_name: Celia
full_name: Rodriguez Rodriguez, Celia
last_name: Rodriguez Rodriguez
- first_name: Elena P
full_name: Dapena, Elena P
last_name: Dapena
- first_name: Kurston
full_name: Doonanco, Kurston
last_name: Doonanco
- first_name: Norma
full_name: Leonard, Norma
last_name: Leonard
- first_name: Faten
full_name: Tinsa, Faten
last_name: Tinsa
- first_name: Stéphanie
full_name: Moortgat, Stéphanie
last_name: Moortgat
- first_name: Hakan
full_name: Ulucan, Hakan
last_name: Ulucan
- first_name: Erkan
full_name: Koparir, Erkan
last_name: Koparir
- first_name: Ender
full_name: Karaca, Ender
last_name: Karaca
- first_name: Nicholas
full_name: Katsanis, Nicholas
last_name: Katsanis
- first_name: Valeria
full_name: Marton, Valeria
last_name: Marton
- first_name: Joris R
full_name: Vermeesch, Joris R
last_name: Vermeesch
- first_name: Erica E
full_name: Davis, Erica E
last_name: Davis
- first_name: Nicholas J
full_name: Cowan, Nicholas J
last_name: Cowan
- first_name: David
full_name: Keays, David
last_name: Keays
- first_name: Hilde
full_name: Van Esch, Hilde
last_name: Van Esch
citation:
ama: Isrie M, Breuss M, Tian G, et al. Mutations in either TUBB or MAPRE2 cause
circumferential skin creases Kunze type. The American Journal of Human Genetics.
2015;97(6):790-800. doi:10.1016/j.ajhg.2015.10.014
apa: Isrie, M., Breuss, M., Tian, G., Hansen, A. H., Cristofoli, F., Morandell,
J., … Van Esch, H. (2015). Mutations in either TUBB or MAPRE2 cause circumferential
skin creases Kunze type. The American Journal of Human Genetics. Cell Press.
https://doi.org/10.1016/j.ajhg.2015.10.014
chicago: Isrie, Mala, Martin Breuss, Guoling Tian, Andi H Hansen, Francesca Cristofoli,
Jasmin Morandell, Zachari A Kupchinsky, et al. “Mutations in Either TUBB or MAPRE2
Cause Circumferential Skin Creases Kunze Type.” The American Journal of Human
Genetics. Cell Press, 2015. https://doi.org/10.1016/j.ajhg.2015.10.014.
ieee: M. Isrie et al., “Mutations in either TUBB or MAPRE2 cause circumferential
skin creases Kunze type,” The American Journal of Human Genetics, vol.
97, no. 6. Cell Press, pp. 790–800, 2015.
ista: Isrie M, Breuss M, Tian G, Hansen AH, Cristofoli F, Morandell J, Kupchinsky
ZA, Sifrim A, Rodriguez Rodriguez C, Dapena EP, Doonanco K, Leonard N, Tinsa F,
Moortgat S, Ulucan H, Koparir E, Karaca E, Katsanis N, Marton V, Vermeesch JR,
Davis EE, Cowan NJ, Keays D, Van Esch H. 2015. Mutations in either TUBB or MAPRE2
cause circumferential skin creases Kunze type. The American Journal of Human Genetics.
97(6), 790–800.
mla: Isrie, Mala, et al. “Mutations in Either TUBB or MAPRE2 Cause Circumferential
Skin Creases Kunze Type.” The American Journal of Human Genetics, vol.
97, no. 6, Cell Press, 2015, pp. 790–800, doi:10.1016/j.ajhg.2015.10.014.
short: M. Isrie, M. Breuss, G. Tian, A.H. Hansen, F. Cristofoli, J. Morandell, Z.A.
Kupchinsky, A. Sifrim, C. Rodriguez Rodriguez, E.P. Dapena, K. Doonanco, N. Leonard,
F. Tinsa, S. Moortgat, H. Ulucan, E. Koparir, E. Karaca, N. Katsanis, V. Marton,
J.R. Vermeesch, E.E. Davis, N.J. Cowan, D. Keays, H. Van Esch, The American Journal
of Human Genetics 97 (2015) 790–800.
date_created: 2018-12-11T11:50:11Z
date_published: 2015-12-03T00:00:00Z
date_updated: 2021-01-12T06:48:19Z
day: '03'
doi: 10.1016/j.ajhg.2015.10.014
extern: '1'
intvolume: ' 97'
issue: '6'
language:
- iso: eng
month: '12'
oa_version: None
page: 790 - 800
publication: The American Journal of Human Genetics
publication_status: published
publisher: Cell Press
publist_id: '6264'
quality_controlled: '1'
status: public
title: Mutations in either TUBB or MAPRE2 cause circumferential skin creases Kunze
type
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 97
year: '2015'
...
---
_id: '11073'
abstract:
- lang: eng
text: Human cancer cells bear complex chromosome rearrangements that can be potential
drivers of cancer development. However, the molecular mechanisms underlying these
rearrangements have been unclear. Zhang et al. use a new technique combining live-cell
imaging and single-cell sequencing to demonstrate that chromosomes mis-segregated
to micronuclei frequently undergo chromothripsis-like rearrangements in the subsequent
cell cycle.
article_processing_charge: No
article_type: original
author:
- first_name: Emily M.
full_name: Hatch, Emily M.
last_name: Hatch
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
citation:
ama: Hatch EM, Hetzer M. Linking micronuclei to chromosome fragmentation. Cell.
2015;161(7):1502-1504. doi:10.1016/j.cell.2015.06.005
apa: Hatch, E. M., & Hetzer, M. (2015). Linking micronuclei to chromosome fragmentation.
Cell. Elsevier. https://doi.org/10.1016/j.cell.2015.06.005
chicago: Hatch, Emily M., and Martin Hetzer. “Linking Micronuclei to Chromosome
Fragmentation.” Cell. Elsevier, 2015. https://doi.org/10.1016/j.cell.2015.06.005.
ieee: E. M. Hatch and M. Hetzer, “Linking micronuclei to chromosome fragmentation,”
Cell, vol. 161, no. 7. Elsevier, pp. 1502–1504, 2015.
ista: Hatch EM, Hetzer M. 2015. Linking micronuclei to chromosome fragmentation.
Cell. 161(7), 1502–1504.
mla: Hatch, Emily M., and Martin Hetzer. “Linking Micronuclei to Chromosome Fragmentation.”
Cell, vol. 161, no. 7, Elsevier, 2015, pp. 1502–04, doi:10.1016/j.cell.2015.06.005.
short: E.M. Hatch, M. Hetzer, Cell 161 (2015) 1502–1504.
date_created: 2022-04-07T07:48:49Z
date_published: 2015-06-18T00:00:00Z
date_updated: 2022-07-18T08:34:33Z
day: '18'
doi: 10.1016/j.cell.2015.06.005
extern: '1'
external_id:
pmid:
- '26091034'
intvolume: ' 161'
issue: '7'
keyword:
- General Biochemistry
- Genetics and Molecular Biology
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.cell.2015.06.005
month: '06'
oa: 1
oa_version: Published Version
page: 1502-1504
pmid: 1
publication: Cell
publication_identifier:
issn:
- 0092-8674
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Linking micronuclei to chromosome fragmentation
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 161
year: '2015'
...
---
_id: '11074'
article_processing_charge: No
article_type: original
author:
- first_name: Emily M.
full_name: Hatch, Emily M.
last_name: Hatch
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
citation:
ama: Hatch EM, Hetzer M. Chromothripsis. Current Biology. 2015;25(10):PR397-R399.
doi:10.1016/j.cub.2015.02.033
apa: Hatch, E. M., & Hetzer, M. (2015). Chromothripsis. Current Biology.
Elsevier. https://doi.org/10.1016/j.cub.2015.02.033
chicago: Hatch, Emily M., and Martin Hetzer. “Chromothripsis.” Current Biology.
Elsevier, 2015. https://doi.org/10.1016/j.cub.2015.02.033.
ieee: E. M. Hatch and M. Hetzer, “Chromothripsis,” Current Biology, vol.
25, no. 10. Elsevier, pp. PR397-R399, 2015.
ista: Hatch EM, Hetzer M. 2015. Chromothripsis. Current Biology. 25(10), PR397-R399.
mla: Hatch, Emily M., and Martin Hetzer. “Chromothripsis.” Current Biology,
vol. 25, no. 10, Elsevier, 2015, pp. PR397-R399, doi:10.1016/j.cub.2015.02.033.
short: E.M. Hatch, M. Hetzer, Current Biology 25 (2015) PR397-R399.
date_created: 2022-04-07T07:49:00Z
date_published: 2015-05-18T00:00:00Z
date_updated: 2022-07-18T08:34:34Z
day: '18'
doi: 10.1016/j.cub.2015.02.033
extern: '1'
external_id:
pmid:
- '25989073'
intvolume: ' 25'
issue: '10'
keyword:
- General Agricultural and Biological Sciences
- General Biochemistry
- Genetics and Molecular Biology
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.cub.2015.02.033
month: '05'
oa: 1
oa_version: Published Version
page: PR397-R399
pmid: 1
publication: Current Biology
publication_identifier:
issn:
- 0960-9822
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Chromothripsis
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 25
year: '2015'
...
---
_id: '11075'
abstract:
- lang: eng
text: Previously, we identified the nucleoporin gp210/Nup210 as a critical regulator
of muscle and neuronal differentiation, but how this nucleoporin exerts its function
and whether it modulates nuclear pore complex (NPC) activity remain unknown. Here,
we show that gp210/Nup210 mediates muscle cell differentiation in vitro via its
conserved N-terminal domain that extends into the perinuclear space. Removal of
the C-terminal domain, which partially mislocalizes gp210/Nup210 away from NPCs,
efficiently rescues the differentiation defect caused by the knockdown of endogenous
gp210/Nup210. Unexpectedly, a gp210/Nup210 mutant lacking the NPC-targeting transmembrane
and C-terminal domains is sufficient for C2C12 myoblast differentiation. We demonstrate
that the endoplasmic reticulum (ER) stress-specific caspase cascade is exacerbated
during Nup210 depletion and that blocking ER stress-mediated apoptosis rescues
differentiation of Nup210-deficient cells. Our results suggest that the role of
gp210/Nup210 in cell differentiation is mediated by its large luminal domain,
which can act independently of NPC association and appears to play a pivotal role
in the maintenance of nuclear envelope/ER homeostasis.
article_processing_charge: No
article_type: original
author:
- first_name: J. Sebastian
full_name: Gomez-Cavazos, J. Sebastian
last_name: Gomez-Cavazos
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
citation:
ama: Gomez-Cavazos JS, Hetzer M. The nucleoporin gp210/Nup210 controls muscle differentiation
by regulating nuclear envelope/ER homeostasis. Journal of Cell Biology.
2015;208(6):671-681. doi:10.1083/jcb.201410047
apa: Gomez-Cavazos, J. S., & Hetzer, M. (2015). The nucleoporin gp210/Nup210
controls muscle differentiation by regulating nuclear envelope/ER homeostasis.
Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.201410047
chicago: Gomez-Cavazos, J. Sebastian, and Martin Hetzer. “The Nucleoporin Gp210/Nup210
Controls Muscle Differentiation by Regulating Nuclear Envelope/ER Homeostasis.”
Journal of Cell Biology. Rockefeller University Press, 2015. https://doi.org/10.1083/jcb.201410047.
ieee: J. S. Gomez-Cavazos and M. Hetzer, “The nucleoporin gp210/Nup210 controls
muscle differentiation by regulating nuclear envelope/ER homeostasis,” Journal
of Cell Biology, vol. 208, no. 6. Rockefeller University Press, pp. 671–681,
2015.
ista: Gomez-Cavazos JS, Hetzer M. 2015. The nucleoporin gp210/Nup210 controls muscle
differentiation by regulating nuclear envelope/ER homeostasis. Journal of Cell
Biology. 208(6), 671–681.
mla: Gomez-Cavazos, J. Sebastian, and Martin Hetzer. “The Nucleoporin Gp210/Nup210
Controls Muscle Differentiation by Regulating Nuclear Envelope/ER Homeostasis.”
Journal of Cell Biology, vol. 208, no. 6, Rockefeller University Press,
2015, pp. 671–81, doi:10.1083/jcb.201410047.
short: J.S. Gomez-Cavazos, M. Hetzer, Journal of Cell Biology 208 (2015) 671–681.
date_created: 2022-04-07T07:49:10Z
date_published: 2015-03-16T00:00:00Z
date_updated: 2022-07-18T08:43:00Z
day: '16'
doi: 10.1083/jcb.201410047
extern: '1'
external_id:
pmid:
- '25778917'
intvolume: ' 208'
issue: '6'
keyword:
- Cell Biology
language:
- iso: eng
month: '03'
oa_version: Published Version
page: 671-681
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: The nucleoporin gp210/Nup210 controls muscle differentiation by regulating
nuclear envelope/ER homeostasis
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 208
year: '2015'
...
---
_id: '11076'
abstract:
- lang: eng
text: Nuclear pore complexes (NPCs) are composed of several copies of ∼30 different
proteins called nucleoporins (Nups). NPCs penetrate the nuclear envelope (NE)
and regulate the nucleocytoplasmic trafficking of macromolecules. Beyond this
vital role, NPC components influence genome functions in a transport-independent
manner. Nups play an evolutionarily conserved role in gene expression regulation
that, in metazoans, extends into the nuclear interior. Additionally, in proliferative
cells, Nups play a crucial role in genome integrity maintenance and mitotic progression.
Here we discuss genome-related functions of Nups and their impact on essential
DNA metabolism processes such as transcription, chromosome duplication, and segregation.
article_processing_charge: No
article_type: original
author:
- first_name: Arkaitz
full_name: Ibarra, Arkaitz
last_name: Ibarra
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
citation:
ama: Ibarra A, Hetzer M. Nuclear pore proteins and the control of genome functions.
Genes & Development. 2015;29(4):337-349. doi:10.1101/gad.256495.114
apa: Ibarra, A., & Hetzer, M. (2015). Nuclear pore proteins and the control
of genome functions. Genes & Development. Cold Spring Harbor Laboratory.
https://doi.org/10.1101/gad.256495.114
chicago: Ibarra, Arkaitz, and Martin Hetzer. “Nuclear Pore Proteins and the Control
of Genome Functions.” Genes & Development. Cold Spring Harbor Laboratory,
2015. https://doi.org/10.1101/gad.256495.114.
ieee: A. Ibarra and M. Hetzer, “Nuclear pore proteins and the control of genome
functions,” Genes & Development, vol. 29, no. 4. Cold Spring Harbor
Laboratory, pp. 337–349, 2015.
ista: Ibarra A, Hetzer M. 2015. Nuclear pore proteins and the control of genome
functions. Genes & Development. 29(4), 337–349.
mla: Ibarra, Arkaitz, and Martin Hetzer. “Nuclear Pore Proteins and the Control
of Genome Functions.” Genes & Development, vol. 29, no. 4, Cold Spring
Harbor Laboratory, 2015, pp. 337–49, doi:10.1101/gad.256495.114.
short: A. Ibarra, M. Hetzer, Genes & Development 29 (2015) 337–349.
date_created: 2022-04-07T07:49:21Z
date_published: 2015-02-01T00:00:00Z
date_updated: 2022-07-18T08:43:20Z
day: '01'
doi: 10.1101/gad.256495.114
extern: '1'
external_id:
pmid:
- '25691464'
intvolume: ' 29'
issue: '4'
keyword:
- Developmental Biology
- Genetics
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/gad.256495.114
month: '02'
oa: 1
oa_version: Published Version
page: 337-349
pmid: 1
publication: Genes & Development
publication_identifier:
eissn:
- 1549-5477
issn:
- 0890-9369
publication_status: published
publisher: Cold Spring Harbor Laboratory
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nuclear pore proteins and the control of genome functions
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 29
year: '2015'
...
---
_id: '11077'
abstract:
- lang: eng
text: Nucleoporins (Nups) are a family of proteins best known as the constituent
building blocks of nuclear pore complexes (NPCs), membrane-embedded channels that
mediate nuclear transport across the nuclear envelope. Recent evidence suggests
that several Nups have additional roles in controlling the activation and silencing
of developmental genes; however, the mechanistic details of these functions remain
poorly understood. Here, we show that depletion of Nup153 in mouse embryonic stem
cells (mESCs) causes the derepression of developmental genes and induction of
early differentiation. This loss of stem cell identity is not associated with
defects in the nuclear import of key pluripotency factors. Rather, Nup153 binds
around the transcriptional start site (TSS) of developmental genes and mediates
the recruitment of the polycomb-repressive complex 1 (PRC1) to a subset of its
target loci. Our results demonstrate a chromatin-associated role of Nup153 in
maintaining stem cell pluripotency by functioning in mammalian epigenetic gene
silencing.
article_processing_charge: No
article_type: original
author:
- first_name: Filipe V.
full_name: Jacinto, Filipe V.
last_name: Jacinto
- first_name: Chris
full_name: Benner, Chris
last_name: Benner
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
citation:
ama: Jacinto FV, Benner C, Hetzer M. The nucleoporin Nup153 regulates embryonic
stem cell pluripotency through gene silencing. Genes & Development.
2015;29(12):1224-1238. doi:10.1101/gad.260919.115
apa: Jacinto, F. V., Benner, C., & Hetzer, M. (2015). The nucleoporin Nup153
regulates embryonic stem cell pluripotency through gene silencing. Genes &
Development. Cold Spring Harbor Laboratory. https://doi.org/10.1101/gad.260919.115
chicago: Jacinto, Filipe V., Chris Benner, and Martin Hetzer. “The Nucleoporin Nup153
Regulates Embryonic Stem Cell Pluripotency through Gene Silencing.” Genes &
Development. Cold Spring Harbor Laboratory, 2015. https://doi.org/10.1101/gad.260919.115.
ieee: F. V. Jacinto, C. Benner, and M. Hetzer, “The nucleoporin Nup153 regulates
embryonic stem cell pluripotency through gene silencing,” Genes & Development,
vol. 29, no. 12. Cold Spring Harbor Laboratory, pp. 1224–1238, 2015.
ista: Jacinto FV, Benner C, Hetzer M. 2015. The nucleoporin Nup153 regulates embryonic
stem cell pluripotency through gene silencing. Genes & Development. 29(12),
1224–1238.
mla: Jacinto, Filipe V., et al. “The Nucleoporin Nup153 Regulates Embryonic Stem
Cell Pluripotency through Gene Silencing.” Genes & Development, vol.
29, no. 12, Cold Spring Harbor Laboratory, 2015, pp. 1224–38, doi:10.1101/gad.260919.115.
short: F.V. Jacinto, C. Benner, M. Hetzer, Genes & Development 29 (2015) 1224–1238.
date_created: 2022-04-07T07:49:31Z
date_published: 2015-06-16T00:00:00Z
date_updated: 2022-07-18T08:43:51Z
day: '16'
doi: 10.1101/gad.260919.115
extern: '1'
external_id:
pmid:
- '26080816'
intvolume: ' 29'
issue: '12'
keyword:
- Developmental Biology
- Genetics
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/gad.260919.115
month: '06'
oa: 1
oa_version: Published Version
page: 1224-1238
pmid: 1
publication: Genes & Development
publication_identifier:
eissn:
- 1549-5477
issn:
- 0890-9369
publication_status: published
publisher: Cold Spring Harbor Laboratory
quality_controlled: '1'
scopus_import: '1'
status: public
title: The nucleoporin Nup153 regulates embryonic stem cell pluripotency through gene
silencing
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 29
year: '2015'
...
---
_id: '11078'
abstract:
- lang: eng
text: Aging is associated with the decline of protein, cell, and organ function.
Here, we use an integrated approach to characterize gene expression, bulk translation,
and cell biology in the brains and livers of young and old rats. We identify 468
differences in protein abundance between young and old animals. The majority are
a consequence of altered translation output, that is, the combined effect of changes
in transcript abundance and translation efficiency. In addition, we identify 130
proteins whose overall abundance remains unchanged but whose sub-cellular localization,
phosphorylation state, or splice-form varies. While some protein-level differences
appear to be a generic property of the rats’ chronological age, the majority are
specific to one organ. These may be a consequence of the organ’s physiology or
the chronological age of the cells within the tissue. Taken together, our study
provides an initial view of the proteome at the molecular, sub-cellular, and organ
level in young and old rats.
article_processing_charge: No
article_type: original
author:
- first_name: Alessandro
full_name: Ori, Alessandro
last_name: Ori
- first_name: Brandon H.
full_name: Toyama, Brandon H.
last_name: Toyama
- first_name: Michael S.
full_name: Harris, Michael S.
last_name: Harris
- first_name: Thomas
full_name: Bock, Thomas
last_name: Bock
- first_name: Murat
full_name: Iskar, Murat
last_name: Iskar
- first_name: Peer
full_name: Bork, Peer
last_name: Bork
- first_name: Nicholas T.
full_name: Ingolia, Nicholas T.
last_name: Ingolia
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
- first_name: Martin
full_name: Beck, Martin
last_name: Beck
citation:
ama: Ori A, Toyama BH, Harris MS, et al. Integrated transcriptome and proteome analyses
reveal organ-specific proteome deterioration in old rats. Cell Systems.
2015;1(3):P224-237. doi:10.1016/j.cels.2015.08.012
apa: Ori, A., Toyama, B. H., Harris, M. S., Bock, T., Iskar, M., Bork, P., … Beck,
M. (2015). Integrated transcriptome and proteome analyses reveal organ-specific
proteome deterioration in old rats. Cell Systems. Elsevier. https://doi.org/10.1016/j.cels.2015.08.012
chicago: Ori, Alessandro, Brandon H. Toyama, Michael S. Harris, Thomas Bock, Murat
Iskar, Peer Bork, Nicholas T. Ingolia, Martin Hetzer, and Martin Beck. “Integrated
Transcriptome and Proteome Analyses Reveal Organ-Specific Proteome Deterioration
in Old Rats.” Cell Systems. Elsevier, 2015. https://doi.org/10.1016/j.cels.2015.08.012.
ieee: A. Ori et al., “Integrated transcriptome and proteome analyses reveal
organ-specific proteome deterioration in old rats,” Cell Systems, vol.
1, no. 3. Elsevier, pp. P224-237, 2015.
ista: Ori A, Toyama BH, Harris MS, Bock T, Iskar M, Bork P, Ingolia NT, Hetzer M,
Beck M. 2015. Integrated transcriptome and proteome analyses reveal organ-specific
proteome deterioration in old rats. Cell Systems. 1(3), P224-237.
mla: Ori, Alessandro, et al. “Integrated Transcriptome and Proteome Analyses Reveal
Organ-Specific Proteome Deterioration in Old Rats.” Cell Systems, vol.
1, no. 3, Elsevier, 2015, pp. P224-237, doi:10.1016/j.cels.2015.08.012.
short: A. Ori, B.H. Toyama, M.S. Harris, T. Bock, M. Iskar, P. Bork, N.T. Ingolia,
M. Hetzer, M. Beck, Cell Systems 1 (2015) P224-237.
date_created: 2022-04-07T07:49:39Z
date_published: 2015-09-23T00:00:00Z
date_updated: 2022-07-18T08:44:07Z
day: '23'
doi: 10.1016/j.cels.2015.08.012
extern: '1'
external_id:
pmid:
- '27135913'
intvolume: ' 1'
issue: '3'
keyword:
- Cell Biology
- Histology
- Pathology and Forensic Medicine
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.cels.2015.08.012
month: '09'
oa: 1
oa_version: Published Version
page: P224-237
pmid: 1
publication: Cell Systems
publication_identifier:
issn:
- 2405-4712
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Integrated transcriptome and proteome analyses reveal organ-specific proteome
deterioration in old rats
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 1
year: '2015'
...
---
_id: '11079'
abstract:
- lang: eng
text: Aging is a major risk factor for many human diseases, and in vitro generation
of human neurons is an attractive approach for modeling aging-related brain disorders.
However, modeling aging in differentiated human neurons has proved challenging.
We generated neurons from human donors across a broad range of ages, either by
iPSC-based reprogramming and differentiation or by direct conversion into induced
neurons (iNs). While iPSCs and derived neurons did not retain aging-associated
gene signatures, iNs displayed age-specific transcriptional profiles and revealed
age-associated decreases in the nuclear transport receptor RanBP17. We detected
an age-dependent loss of nucleocytoplasmic compartmentalization (NCC) in donor
fibroblasts and corresponding iNs and found that reduced RanBP17 impaired NCC
in young cells, while iPSC rejuvenation restored NCC in aged cells. These results
show that iNs retain important aging-related signatures, thus allowing modeling
of the aging process in vitro, and they identify impaired NCC as an important
factor in human aging.
article_processing_charge: No
article_type: original
author:
- first_name: Jerome
full_name: Mertens, Jerome
last_name: Mertens
- first_name: Apuã C.M.
full_name: Paquola, Apuã C.M.
last_name: Paquola
- first_name: Manching
full_name: Ku, Manching
last_name: Ku
- first_name: Emily
full_name: Hatch, Emily
last_name: Hatch
- first_name: Lena
full_name: Böhnke, Lena
last_name: Böhnke
- first_name: Shauheen
full_name: Ladjevardi, Shauheen
last_name: Ladjevardi
- first_name: Sean
full_name: McGrath, Sean
last_name: McGrath
- first_name: Benjamin
full_name: Campbell, Benjamin
last_name: Campbell
- first_name: Hyungjun
full_name: Lee, Hyungjun
last_name: Lee
- first_name: Joseph R.
full_name: Herdy, Joseph R.
last_name: Herdy
- first_name: J. Tiago
full_name: Gonçalves, J. Tiago
last_name: Gonçalves
- first_name: Tomohisa
full_name: Toda, Tomohisa
last_name: Toda
- first_name: Yongsung
full_name: Kim, Yongsung
last_name: Kim
- first_name: Jürgen
full_name: Winkler, Jürgen
last_name: Winkler
- first_name: Jun
full_name: Yao, Jun
last_name: Yao
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
- first_name: Fred H.
full_name: Gage, Fred H.
last_name: Gage
citation:
ama: Mertens J, Paquola ACM, Ku M, et al. Directly reprogrammed human neurons retain
aging-associated transcriptomic signatures and reveal age-related nucleocytoplasmic
defects. Cell Stem Cell. 2015;17(6):705-718. doi:10.1016/j.stem.2015.09.001
apa: Mertens, J., Paquola, A. C. M., Ku, M., Hatch, E., Böhnke, L., Ladjevardi,
S., … Gage, F. H. (2015). Directly reprogrammed human neurons retain aging-associated
transcriptomic signatures and reveal age-related nucleocytoplasmic defects. Cell
Stem Cell. Elsevier. https://doi.org/10.1016/j.stem.2015.09.001
chicago: Mertens, Jerome, Apuã C.M. Paquola, Manching Ku, Emily Hatch, Lena Böhnke,
Shauheen Ladjevardi, Sean McGrath, et al. “Directly Reprogrammed Human Neurons
Retain Aging-Associated Transcriptomic Signatures and Reveal Age-Related Nucleocytoplasmic
Defects.” Cell Stem Cell. Elsevier, 2015. https://doi.org/10.1016/j.stem.2015.09.001.
ieee: J. Mertens et al., “Directly reprogrammed human neurons retain aging-associated
transcriptomic signatures and reveal age-related nucleocytoplasmic defects,” Cell
Stem Cell, vol. 17, no. 6. Elsevier, pp. 705–718, 2015.
ista: Mertens J, Paquola ACM, Ku M, Hatch E, Böhnke L, Ladjevardi S, McGrath S,
Campbell B, Lee H, Herdy JR, Gonçalves JT, Toda T, Kim Y, Winkler J, Yao J, Hetzer
M, Gage FH. 2015. Directly reprogrammed human neurons retain aging-associated
transcriptomic signatures and reveal age-related nucleocytoplasmic defects. Cell
Stem Cell. 17(6), 705–718.
mla: Mertens, Jerome, et al. “Directly Reprogrammed Human Neurons Retain Aging-Associated
Transcriptomic Signatures and Reveal Age-Related Nucleocytoplasmic Defects.” Cell
Stem Cell, vol. 17, no. 6, Elsevier, 2015, pp. 705–18, doi:10.1016/j.stem.2015.09.001.
short: J. Mertens, A.C.M. Paquola, M. Ku, E. Hatch, L. Böhnke, S. Ladjevardi, S.
McGrath, B. Campbell, H. Lee, J.R. Herdy, J.T. Gonçalves, T. Toda, Y. Kim, J.
Winkler, J. Yao, M. Hetzer, F.H. Gage, Cell Stem Cell 17 (2015) 705–718.
date_created: 2022-04-07T07:49:51Z
date_published: 2015-12-03T00:00:00Z
date_updated: 2022-07-18T08:44:21Z
day: '03'
doi: 10.1016/j.stem.2015.09.001
extern: '1'
external_id:
pmid:
- '26456686'
intvolume: ' 17'
issue: '6'
keyword:
- Cell Biology
- Genetics
- Molecular Medicine
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.stem.2015.09.001
month: '12'
oa: 1
oa_version: Published Version
page: 705-718
pmid: 1
publication: Cell Stem Cell
publication_identifier:
issn:
- 1934-5909
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Directly reprogrammed human neurons retain aging-associated transcriptomic
signatures and reveal age-related nucleocytoplasmic defects
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 17
year: '2015'
...
---
_id: '11519'
abstract:
- lang: eng
text: 'Faint Lyα emitters become increasingly rarer toward the reionization epoch
(z ∼ 6–7). However, observations from a very large (∼5 deg2) Lyα narrow-band survey
at z = 6.6 show that this is not the case for the most luminous emitters, capable
of ionizing their own local bubbles. Here we present follow-up observations of
the two most luminous Lyα candidates in the COSMOS field: “MASOSA” and “CR7.”
We used X-SHOOTER, SINFONI, and FORS2 on the Very Large Telescope, and DEIMOS
on Keck, to confirm both candidates beyond any doubt. We find redshifts of z =
6.541 and z = 6.604 for “MASOSA” and “CR7,” respectively. MASOSA has a strong
detection in Lyα with a line width of 386 ± 30 km s−1 (FWHM) and with very high
EW0 (>200 Å), but undetected in the continuum, implying very low stellar mass
and a likely young, metal-poor stellar population. “CR7,” with an observed Lyα
luminosity of 1043.92±0.05 erg s−1 is the most luminous Lyα emitter ever found
at z > 6 and is spatially extended (∼16 kpc). “CR7” reveals a narrow Lyα line
with 266 ± 15 km s−1 FWHM, being detected in the near-infrared (NIR) (rest-frame
UV; β = −2.3 ± 0.1) and in IRAC/Spitzer. We detect a narrow He II 1640 Å emission
line (6σ, FWHM = 130 ± 30 km s−1 ) in CR7 which can explain the clear excess seen
in the J-band photometry (EW0 ∼ 80 Å). We find no other emission lines from the
UV to the NIR in our X-SHOOTER spectra (He II/O III] 1663 Å > 3 and He II/C III]
1908 Å > 2.5). We conclude that CR7 is best explained by a combination of a PopIII-like
population, which dominates the rest-frame UV and the nebular emission, and a
more normal stellar population, which presumably dominates the mass. Hubble Space
Telescope/WFC3 observations show that the light is indeed spatially separated
between a very blue component, coincident with Lyα and He II emission, and two
red components (∼5 kpc away), which dominate the mass. Our findings are consistent
with theoretical predictions of a PopIII wave, with PopIII star formation migrating
away from the original sites of star formation.'
acknowledgement: We thank the anonymous reviewer for useful and constructive comments
and suggestions which greatly improved the quality and clarity of our work. D.S.
acknowledges financial support from the Netherlands Organisation for Scientific
research (NWO) through a Veni fellowship, from FCT through a FCT Investigator Starting
Grant and Start-up Grant (IF/01154/2012/CP0189/CT0010), from FCT grant UID/FIS/04434/2013,
and from LSF and LKBF. J.M. acknowledges the award of a Huygens PhD fellowship.
H.R. acknowledges support from the ERC Advanced Investigator program NewClusters
321271. The authors thank Mark Dijkstra, Bhaskar Agarwal, Jarrett Johnson, Andrea
Ferrara, Jarle Brinchmann, Rebecca Bowler, George Becker, Emma Curtis-Lake, Milos
Milosavljevic, Raffaella Schneider, Paul Shapiro, and Erik Zackrisson for interesting,
stimulating and helpful discussions. The authors are extremely grateful to ESO for
the award of ESO DDT time (294.A-5018 and 294.A-5039) which allowed the spectroscopic
confirmation of both sources and the detailed investigation of their nature. Observations
are also based on data from W.M. Keck Observatory. The W.M. Keck Observatory is
operated as a scientific partnership of Caltech, the University of California and
the National Aeronautics and Space Administration. Based on observations obtained
with MegaPrime/Megacam, a joint project of CFHT and CEA/IRFU, at the Canada–France–Hawaii
Telescope (CFHT) which is operated by the National Research Council (NRC) of Canada,
the Institut National des Science de lUnivers of the Centre National de la Recherche
Scientifique (CNRS) of France, and the University of Hawaii. This work is based
in part on data products produced at Terapix available at the Canadian Astronomy
Data Centre as part of the Canada–France–Hawaii Telescope Legacy Survey, a collaborative
project of NRC and CNRS. Based on data products from observations made with ESO
Telescopes at the La Silla Paranal Observatory under ESO programme IDs 294.A-5018,
294.A-5039, and 179.A-2005, and on data products produced by TERAPIX and the Cambridge
Astronomy Survey Unit on behalf of the UltraVISTA consortium. The authors acknowledge
the award of service time (SW2014b20) on the William Herschel Telescope (WHT). WHT
and its service programme are operated on the island of La Palma by the Isaac Newton
Group in the Spanish Observatorio del Roque de los Muchachos of the Instituto de
Astrofisica de Canarias.
article_processing_charge: No
article_type: original
arxiv: 1
author:
- first_name: David
full_name: Sobral, David
last_name: Sobral
- first_name: Jorryt J
full_name: Matthee, Jorryt J
id: 7439a258-f3c0-11ec-9501-9df22fe06720
last_name: Matthee
orcid: 0000-0003-2871-127X
- first_name: Behnam
full_name: Darvish, Behnam
last_name: Darvish
- first_name: Daniel
full_name: Schaerer, Daniel
last_name: Schaerer
- first_name: Bahram
full_name: Mobasher, Bahram
last_name: Mobasher
- first_name: Huub
full_name: Röttgering, Huub
last_name: Röttgering
- first_name: Sérgio
full_name: Santos, Sérgio
last_name: Santos
- first_name: Shoubaneh
full_name: Hemmati, Shoubaneh
last_name: Hemmati
citation:
ama: 'Sobral D, Matthee JJ, Darvish B, et al. Evidence for PopIII-like stellar populations
in the most luminous Lyα emitters at the epoch of reionisation: Spectroscopic
confirmation. The Astrophysical Journal. 2015;808(2):139. doi:10.1088/0004-637X/808/2/139'
apa: 'Sobral, D., Matthee, J. J., Darvish, B., Schaerer, D., Mobasher, B., Röttgering,
H., … Hemmati, S. (2015). Evidence for PopIII-like stellar populations in the
most luminous Lyα emitters at the epoch of reionisation: Spectroscopic confirmation.
The Astrophysical Journal. IOP Publishing. https://doi.org/10.1088/0004-637X/808/2/139'
chicago: 'Sobral, David, Jorryt J Matthee, Behnam Darvish, Daniel Schaerer, Bahram
Mobasher, Huub Röttgering, Sérgio Santos, and Shoubaneh Hemmati. “Evidence for
PopIII-like Stellar Populations in the Most Luminous Lyα Emitters at the Epoch
of Reionisation: Spectroscopic Confirmation.” The Astrophysical Journal.
IOP Publishing, 2015. https://doi.org/10.1088/0004-637X/808/2/139.'
ieee: 'D. Sobral et al., “Evidence for PopIII-like stellar populations in
the most luminous Lyα emitters at the epoch of reionisation: Spectroscopic confirmation,”
The Astrophysical Journal, vol. 808, no. 2. IOP Publishing, p. 139, 2015.'
ista: 'Sobral D, Matthee JJ, Darvish B, Schaerer D, Mobasher B, Röttgering H, Santos
S, Hemmati S. 2015. Evidence for PopIII-like stellar populations in the most luminous
Lyα emitters at the epoch of reionisation: Spectroscopic confirmation. The Astrophysical
Journal. 808(2), 139.'
mla: 'Sobral, David, et al. “Evidence for PopIII-like Stellar Populations in the
Most Luminous Lyα Emitters at the Epoch of Reionisation: Spectroscopic Confirmation.”
The Astrophysical Journal, vol. 808, no. 2, IOP Publishing, 2015, p. 139,
doi:10.1088/0004-637X/808/2/139.'
short: D. Sobral, J.J. Matthee, B. Darvish, D. Schaerer, B. Mobasher, H. Röttgering,
S. Santos, S. Hemmati, The Astrophysical Journal 808 (2015) 139.
date_created: 2022-07-07T09:00:58Z
date_published: 2015-07-28T00:00:00Z
date_updated: 2022-08-18T10:30:13Z
day: '28'
doi: 10.1088/0004-637X/808/2/139
extern: '1'
external_id:
arxiv:
- '1504.01734'
intvolume: ' 808'
issue: '2'
keyword:
- Space and Planetary Science
- Astronomy and Astrophysics
- dark ages
- reionization
- 'first stars – early universe – galaxies: evolution'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://arxiv.org/abs/1504.01734
month: '07'
oa: 1
oa_version: Preprint
page: '139'
publication: The Astrophysical Journal
publication_identifier:
eissn:
- 1538-4357
issn:
- 0004-637X
publication_status: published
publisher: IOP Publishing
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Evidence for PopIII-like stellar populations in the most luminous Lyα emitters
at the epoch of reionisation: Spectroscopic confirmation'
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 808
year: '2015'
...