---
_id: '10816'
abstract:
- lang: eng
text: Pattern separation is a fundamental brain computation that converts small
differences in input patterns into large differences in output patterns. Several
synaptic mechanisms of pattern separation have been proposed, including code expansion,
inhibition and plasticity; however, which of these mechanisms play a role in the
entorhinal cortex (EC)–dentate gyrus (DG)–CA3 circuit, a classical pattern separation
circuit, remains unclear. Here we show that a biologically realistic, full-scale
EC–DG–CA3 circuit model, including granule cells (GCs) and parvalbumin-positive
inhibitory interneurons (PV+-INs) in the DG, is an efficient pattern separator.
Both external gamma-modulated inhibition and internal lateral inhibition mediated
by PV+-INs substantially contributed to pattern separation. Both local connectivity
and fast signaling at GC–PV+-IN synapses were important for maximum effectiveness.
Similarly, mossy fiber synapses with conditional detonator properties contributed
to pattern separation. By contrast, perforant path synapses with Hebbian synaptic
plasticity and direct EC–CA3 connection shifted the network towards pattern completion.
Our results demonstrate that the specific properties of cells and synapses optimize
higher-order computations in biological networks and might be useful to improve
the deep learning capabilities of technical networks.
acknowledged_ssus:
- _id: SSU
acknowledgement: We thank A. Aertsen, N. Kopell, W. Maass, A. Roth, F. Stella and
T. Vogels for critically reading earlier versions of the manuscript. We are grateful
to F. Marr and C. Altmutter for excellent technical assistance, E. Kralli-Beller
for manuscript editing, and the Scientific Service Units of IST Austria for efficient
support. Finally, we thank T. Carnevale, L. Erdös, M. Hines, D. Nykamp and D. Schröder
for useful discussions, and R. Friedrich and S. Wiechert for sharing unpublished
data. This project received funding from the European Research Council (ERC) under
the European Union’s Horizon 2020 research and innovation programme (grant agreement
no. 692692, P.J.) and the Fond zur Förderung der Wissenschaftlichen Forschung (Z
312-B27, Wittgenstein award to P.J. and P 31815 to S.J.G.).
article_processing_charge: No
article_type: original
author:
- first_name: José
full_name: Guzmán, José
id: 30CC5506-F248-11E8-B48F-1D18A9856A87
last_name: Guzmán
orcid: 0000-0003-2209-5242
- first_name: Alois
full_name: Schlögl, Alois
id: 45BF87EE-F248-11E8-B48F-1D18A9856A87
last_name: Schlögl
orcid: 0000-0002-5621-8100
- first_name: 'Claudia '
full_name: 'Espinoza Martinez, Claudia '
id: 31FFEE2E-F248-11E8-B48F-1D18A9856A87
last_name: Espinoza Martinez
orcid: 0000-0003-4710-2082
- first_name: Xiaomin
full_name: Zhang, Xiaomin
id: 423EC9C2-F248-11E8-B48F-1D18A9856A87
last_name: Zhang
- first_name: Benjamin
full_name: Suter, Benjamin
id: 4952F31E-F248-11E8-B48F-1D18A9856A87
last_name: Suter
orcid: 0000-0002-9885-6936
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
citation:
ama: Guzmán J, Schlögl A, Espinoza Martinez C, Zhang X, Suter B, Jonas PM. How connectivity
rules and synaptic properties shape the efficacy of pattern separation in the
entorhinal cortex–dentate gyrus–CA3 network. Nature Computational Science.
2021;1(12):830-842. doi:10.1038/s43588-021-00157-1
apa: Guzmán, J., Schlögl, A., Espinoza Martinez, C., Zhang, X., Suter, B., &
Jonas, P. M. (2021). How connectivity rules and synaptic properties shape the
efficacy of pattern separation in the entorhinal cortex–dentate gyrus–CA3 network.
Nature Computational Science. Springer Nature. https://doi.org/10.1038/s43588-021-00157-1
chicago: Guzmán, José, Alois Schlögl, Claudia Espinoza Martinez, Xiaomin Zhang,
Benjamin Suter, and Peter M Jonas. “How Connectivity Rules and Synaptic Properties
Shape the Efficacy of Pattern Separation in the Entorhinal Cortex–Dentate Gyrus–CA3
Network.” Nature Computational Science. Springer Nature, 2021. https://doi.org/10.1038/s43588-021-00157-1.
ieee: J. Guzmán, A. Schlögl, C. Espinoza Martinez, X. Zhang, B. Suter, and P. M.
Jonas, “How connectivity rules and synaptic properties shape the efficacy of pattern
separation in the entorhinal cortex–dentate gyrus–CA3 network,” Nature Computational
Science, vol. 1, no. 12. Springer Nature, pp. 830–842, 2021.
ista: Guzmán J, Schlögl A, Espinoza Martinez C, Zhang X, Suter B, Jonas PM. 2021.
How connectivity rules and synaptic properties shape the efficacy of pattern separation
in the entorhinal cortex–dentate gyrus–CA3 network. Nature Computational Science.
1(12), 830–842.
mla: Guzmán, José, et al. “How Connectivity Rules and Synaptic Properties Shape
the Efficacy of Pattern Separation in the Entorhinal Cortex–Dentate Gyrus–CA3
Network.” Nature Computational Science, vol. 1, no. 12, Springer Nature,
2021, pp. 830–42, doi:10.1038/s43588-021-00157-1.
short: J. Guzmán, A. Schlögl, C. Espinoza Martinez, X. Zhang, B. Suter, P.M. Jonas,
Nature Computational Science 1 (2021) 830–842.
date_created: 2022-03-04T08:32:36Z
date_published: 2021-12-16T00:00:00Z
date_updated: 2023-08-10T22:30:10Z
day: '16'
ddc:
- '610'
department:
- _id: PeJo
doi: 10.1038/s43588-021-00157-1
ec_funded: 1
file:
- access_level: open_access
checksum: 9fec5b667909ef52be96d502e4f8c2ae
content_type: application/pdf
creator: patrickd
date_created: 2022-06-02T12:51:07Z
date_updated: 2022-06-18T22:30:03Z
embargo: 2022-06-17
file_id: '11430'
file_name: Guzmanetal2021.pdf
file_size: 1699466
relation: main_file
- access_level: open_access
checksum: 52a005b13a114e3c3a28fa6bbe8b1a8d
content_type: application/pdf
creator: patrickd
date_created: 2022-06-02T12:53:47Z
date_updated: 2022-06-18T22:30:03Z
embargo: 2022-06-17
file_id: '11431'
file_name: Guzmanetal2021Suppl.pdf
file_size: 3005651
relation: supplementary_material
title: Supplementary Material
file_date_updated: 2022-06-18T22:30:03Z
has_accepted_license: '1'
intvolume: ' 1'
issue: '12'
keyword:
- general medicine
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.biorxiv.org/content/10.1101/647800
month: '12'
oa: 1
oa_version: Submitted Version
page: 830-842
project:
- _id: 25B7EB9E-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '692692'
name: Biophysics and circuit function of a giant cortical glumatergic synapse
- _id: 25C5A090-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Z00312
name: The Wittgenstein Prize
publication: Nature Computational Science
publication_identifier:
issn:
- 2662-8457
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- relation: press_release
url: https://ista.ac.at/en/news/spot-the-difference/
record:
- id: '10110'
relation: software
status: public
scopus_import: '1'
status: public
title: How connectivity rules and synaptic properties shape the efficacy of pattern
separation in the entorhinal cortex–dentate gyrus–CA3 network
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 1
year: '2021'
...
---
_id: '8931'
abstract:
- lang: eng
text: "Auxin is a major plant growth regulator, but current models on auxin perception
and signaling cannot explain the whole plethora of auxin effects, in particular
those associated with rapid responses. A possible candidate for a component of
additional auxin perception mechanisms is the AUXIN BINDING PROTEIN 1 (ABP1),
whose function in planta remains unclear.\r\nHere we combined expression analysis
with gain- and loss-of-function approaches to analyze the role of ABP1 in plant
development. ABP1 shows a broad expression largely overlapping with, but not regulated
by, transcriptional auxin response activity. Furthermore, ABP1 activity is not
essential for the transcriptional auxin signaling. Genetic in planta analysis
revealed that abp1 loss-of-function mutants show largely normal development with
minor defects in bolting. On the other hand, ABP1 gain-of-function alleles show
a broad range of growth and developmental defects, including root and hypocotyl
growth and bending, lateral root and leaf development, bolting, as well as response
to heat stress. At the cellular level, ABP1 gain-of-function leads to impaired
auxin effect on PIN polar distribution and affects BFA-sensitive PIN intracellular
aggregation.\r\nThe gain-of-function analysis suggests a broad, but still mechanistically
unclear involvement of ABP1 in plant development, possibly masked in abp1 loss-of-function
mutants by a functional redundancy."
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
acknowledgement: We would like to acknowledge Bioimaging and Life Science Facilities
at IST Austria for continuous support and also the Plant Sciences Core Facility
of CEITEC Masaryk University for their support with obtaining a part of the scientific
data. We gratefully acknowledge Lindy Abas for help with ABP1::GFP-ABP1 construct
design. This project has received funding from the European Research Council (ERC)
under the European Union’s Horizon 2020 research and innovation program [grant agreement
no. 742985] and Austrian Science Fund (FWF) [I 3630-B25] to J.F.; DOC Fellowship
of the Austrian Academy of Sciences to L.L.; the European Structural and Investment
Funds, Operational Programme Research, Development and Education - Project „MSCAfellow@MUNI“
[CZ.02.2.69/0.0/0.0/17_050/0008496] to M.P.. This project was also supported by
the Czech Science Foundation [GA 20-20860Y] to M.Z and MEYS CR [project no.CZ.02.1.01/0.0/0.0/16_019/0000738]
to M. Č.
article_number: '110750'
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Zuzana
full_name: Gelová, Zuzana
id: 0AE74790-0E0B-11E9-ABC7-1ACFE5697425
last_name: Gelová
orcid: 0000-0003-4783-1752
- first_name: Michelle C
full_name: Gallei, Michelle C
id: 35A03822-F248-11E8-B48F-1D18A9856A87
last_name: Gallei
orcid: 0000-0003-1286-7368
- first_name: Markéta
full_name: Pernisová, Markéta
last_name: Pernisová
- first_name: Géraldine
full_name: Brunoud, Géraldine
last_name: Brunoud
- first_name: Xixi
full_name: Zhang, Xixi
id: 61A66458-47E9-11EA-85BA-8AEAAF14E49A
last_name: Zhang
orcid: 0000-0001-7048-4627
- first_name: Matous
full_name: Glanc, Matous
id: 1AE1EA24-02D0-11E9-9BAA-DAF4881429F2
last_name: Glanc
orcid: 0000-0003-0619-7783
- first_name: Lanxin
full_name: Li, Lanxin
id: 367EF8FA-F248-11E8-B48F-1D18A9856A87
last_name: Li
orcid: 0000-0002-5607-272X
- first_name: Jaroslav
full_name: Michalko, Jaroslav
id: 483727CA-F248-11E8-B48F-1D18A9856A87
last_name: Michalko
- first_name: Zlata
full_name: Pavlovicova, Zlata
last_name: Pavlovicova
- first_name: Inge
full_name: Verstraeten, Inge
id: 362BF7FE-F248-11E8-B48F-1D18A9856A87
last_name: Verstraeten
orcid: 0000-0001-7241-2328
- first_name: Huibin
full_name: Han, Huibin
id: 31435098-F248-11E8-B48F-1D18A9856A87
last_name: Han
- first_name: Jakub
full_name: Hajny, Jakub
id: 4800CC20-F248-11E8-B48F-1D18A9856A87
last_name: Hajny
orcid: 0000-0003-2140-7195
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Milada
full_name: Čovanová, Milada
last_name: Čovanová
- first_name: Marta
full_name: Zwiewka, Marta
last_name: Zwiewka
- first_name: Lukas
full_name: Hörmayer, Lukas
id: 2EEE7A2A-F248-11E8-B48F-1D18A9856A87
last_name: Hörmayer
orcid: 0000-0001-8295-2926
- first_name: Matyas
full_name: Fendrych, Matyas
id: 43905548-F248-11E8-B48F-1D18A9856A87
last_name: Fendrych
orcid: 0000-0002-9767-8699
- first_name: Tongda
full_name: Xu, Tongda
last_name: Xu
- first_name: Teva
full_name: Vernoux, Teva
last_name: Vernoux
- first_name: Jiří
full_name: Friml, Jiří
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
citation:
ama: Gelová Z, Gallei MC, Pernisová M, et al. Developmental roles of auxin binding
protein 1 in Arabidopsis thaliana. Plant Science. 2021;303. doi:10.1016/j.plantsci.2020.110750
apa: Gelová, Z., Gallei, M. C., Pernisová, M., Brunoud, G., Zhang, X., Glanc, M.,
… Friml, J. (2021). Developmental roles of auxin binding protein 1 in Arabidopsis
thaliana. Plant Science. Elsevier. https://doi.org/10.1016/j.plantsci.2020.110750
chicago: Gelová, Zuzana, Michelle C Gallei, Markéta Pernisová, Géraldine Brunoud,
Xixi Zhang, Matous Glanc, Lanxin Li, et al. “Developmental Roles of Auxin Binding
Protein 1 in Arabidopsis Thaliana.” Plant Science. Elsevier, 2021. https://doi.org/10.1016/j.plantsci.2020.110750.
ieee: Z. Gelová et al., “Developmental roles of auxin binding protein 1 in
Arabidopsis thaliana,” Plant Science, vol. 303. Elsevier, 2021.
ista: Gelová Z, Gallei MC, Pernisová M, Brunoud G, Zhang X, Glanc M, Li L, Michalko
J, Pavlovicova Z, Verstraeten I, Han H, Hajny J, Hauschild R, Čovanová M, Zwiewka
M, Hörmayer L, Fendrych M, Xu T, Vernoux T, Friml J. 2021. Developmental roles
of auxin binding protein 1 in Arabidopsis thaliana. Plant Science. 303, 110750.
mla: Gelová, Zuzana, et al. “Developmental Roles of Auxin Binding Protein 1 in Arabidopsis
Thaliana.” Plant Science, vol. 303, 110750, Elsevier, 2021, doi:10.1016/j.plantsci.2020.110750.
short: Z. Gelová, M.C. Gallei, M. Pernisová, G. Brunoud, X. Zhang, M. Glanc, L.
Li, J. Michalko, Z. Pavlovicova, I. Verstraeten, H. Han, J. Hajny, R. Hauschild,
M. Čovanová, M. Zwiewka, L. Hörmayer, M. Fendrych, T. Xu, T. Vernoux, J. Friml,
Plant Science 303 (2021).
date_created: 2020-12-09T14:48:28Z
date_published: 2021-02-01T00:00:00Z
date_updated: 2024-10-29T10:22:43Z
day: '01'
ddc:
- '580'
department:
- _id: JiFr
- _id: Bio
doi: 10.1016/j.plantsci.2020.110750
ec_funded: 1
external_id:
isi:
- '000614154500001'
pmid:
- '33487339'
file:
- access_level: open_access
checksum: a7f2562bdca62d67dfa88e271b62a629
content_type: application/pdf
creator: dernst
date_created: 2021-02-04T07:49:25Z
date_updated: 2021-02-04T07:49:25Z
file_id: '9083'
file_name: 2021_PlantScience_Gelova.pdf
file_size: 12563728
relation: main_file
success: 1
file_date_updated: 2021-02-04T07:49:25Z
has_accepted_license: '1'
intvolume: ' 303'
isi: 1
keyword:
- Agronomy and Crop Science
- Plant Science
- Genetics
- General Medicine
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 261099A6-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '742985'
name: Tracing Evolution of Auxin Transport and Polarity in Plants
- _id: 26538374-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: I03630
name: Molecular mechanisms of endocytic cargo recognition in plants
- _id: 26B4D67E-B435-11E9-9278-68D0E5697425
grant_number: '25351'
name: 'A Case Study of Plant Growth Regulation: Molecular Mechanism of Auxin-mediated
Rapid Growth Inhibition in Arabidopsis Root'
publication: Plant Science
publication_identifier:
issn:
- 0168-9452
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
record:
- id: '11626'
relation: dissertation_contains
status: public
- id: '10083'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Developmental roles of auxin binding protein 1 in Arabidopsis thaliana
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 303
year: '2021'
...
---
_id: '9387'
abstract:
- lang: eng
text: We report the complete analysis of a deterministic model of deleterious mutations
and negative selection against them at two haploid loci without recombination.
As long as mutation is a weaker force than selection, mutant alleles remain rare
at the only stable equilibrium, and otherwise, a variety of dynamics are possible.
If the mutation-free genotype is absent, generally the only stable equilibrium
is the one that corresponds to fixation of the mutant allele at the locus where
it is less deleterious. This result suggests that fixation of a deleterious allele
that follows a click of the Muller’s ratchet is governed by natural selection,
instead of random drift.
acknowledgement: This work was supported by the Russian Science Foundation grant N
16-14-10173.
article_number: '110729'
article_processing_charge: No
article_type: original
author:
- first_name: Kseniia
full_name: Khudiakova, Kseniia
id: 4E6DC800-AE37-11E9-AC72-31CAE5697425
last_name: Khudiakova
orcid: 0000-0002-6246-1465
- first_name: Tatiana Yu.
full_name: Neretina, Tatiana Yu.
last_name: Neretina
- first_name: Alexey S.
full_name: Kondrashov, Alexey S.
last_name: Kondrashov
citation:
ama: Khudiakova K, Neretina TY, Kondrashov AS. Two linked loci under mutation-selection
balance and Muller’s ratchet. Journal of Theoretical Biology. 2021;524.
doi:10.1016/j.jtbi.2021.110729
apa: Khudiakova, K., Neretina, T. Y., & Kondrashov, A. S. (2021). Two linked
loci under mutation-selection balance and Muller’s ratchet. Journal of Theoretical
Biology. Elsevier . https://doi.org/10.1016/j.jtbi.2021.110729
chicago: Khudiakova, Kseniia, Tatiana Yu. Neretina, and Alexey S. Kondrashov. “Two
Linked Loci under Mutation-Selection Balance and Muller’s Ratchet.” Journal
of Theoretical Biology. Elsevier , 2021. https://doi.org/10.1016/j.jtbi.2021.110729.
ieee: K. Khudiakova, T. Y. Neretina, and A. S. Kondrashov, “Two linked loci under
mutation-selection balance and Muller’s ratchet,” Journal of Theoretical Biology,
vol. 524. Elsevier , 2021.
ista: Khudiakova K, Neretina TY, Kondrashov AS. 2021. Two linked loci under mutation-selection
balance and Muller’s ratchet. Journal of Theoretical Biology. 524, 110729.
mla: Khudiakova, Kseniia, et al. “Two Linked Loci under Mutation-Selection Balance
and Muller’s Ratchet.” Journal of Theoretical Biology, vol. 524, 110729,
Elsevier , 2021, doi:10.1016/j.jtbi.2021.110729.
short: K. Khudiakova, T.Y. Neretina, A.S. Kondrashov, Journal of Theoretical Biology
524 (2021).
date_created: 2021-05-12T05:58:42Z
date_published: 2021-04-24T00:00:00Z
date_updated: 2023-08-08T13:32:40Z
day: '24'
department:
- _id: GradSch
doi: 10.1016/j.jtbi.2021.110729
external_id:
isi:
- '000659161500002'
intvolume: ' 524'
isi: 1
keyword:
- General Biochemistry
- Genetics and Molecular Biology
- Modelling and Simulation
- Statistics and Probability
- General Immunology and Microbiology
- Applied Mathematics
- General Agricultural and Biological Sciences
- General Medicine
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.biorxiv.org/content/10.1101/477489v1
month: '04'
oa: 1
oa_version: Preprint
publication: Journal of Theoretical Biology
publication_identifier:
issn:
- 0022-5193
publication_status: published
publisher: 'Elsevier '
quality_controlled: '1'
status: public
title: Two linked loci under mutation-selection balance and Muller’s ratchet
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 524
year: '2021'
...
---
_id: '10301'
abstract:
- lang: eng
text: De novo protein synthesis is required for synapse modifications underlying
stable memory encoding. Yet neurons are highly compartmentalized cells and how
protein synthesis can be regulated at the synapse level is unknown. Here, we characterize
neuronal signaling complexes formed by the postsynaptic scaffold GIT1, the mechanistic
target of rapamycin (mTOR) kinase, and Raptor that couple synaptic stimuli to
mTOR-dependent protein synthesis; and identify NMDA receptors containing GluN3A
subunits as key negative regulators of GIT1 binding to mTOR. Disruption of GIT1/mTOR
complexes by enhancing GluN3A expression or silencing GIT1 inhibits synaptic mTOR
activation and restricts the mTOR-dependent translation of specific activity-regulated
mRNAs. Conversely, GluN3A removal enables complex formation, potentiates mTOR-dependent
protein synthesis, and facilitates the consolidation of associative and spatial
memories in mice. The memory enhancement becomes evident with light or spaced
training, can be achieved by selectively deleting GluN3A from excitatory neurons
during adulthood, and does not compromise other aspects of cognition such as memory
flexibility or extinction. Our findings provide mechanistic insight into synaptic
translational control and reveal a potentially selective target for cognitive
enhancement.
acknowledgement: We thank Stuart Lipton and Nobuki Nakanishi for providing the Grin3a
knockout mice, Beverly Davidson for the AAV-caRheb, Jose Esteban for help with behavioral
and biochemical experiments, and Noelia Campillo, Rebeca Martínez-Turrillas, and
Ana Navarro for expert technical help. Work was funded by the UTE project CIMA;
fellowships from the Fundación Tatiana Pérez de Guzmán el Bueno, FEBS, and IBRO
(to M.J.C.D.), Generalitat Valenciana (to O.E.-Z.), Juan de la Cierva (to L.G.R.),
FPI-MINECO (to E.R.V., to S.N.) and Intertalentum postdoctoral program (to V.B.);
ANR (GluBrain3A) and ERC Advanced Grants (#693021) (to P.P.); Ramón y Cajal program
RYC2014-15784, RETOS-MINECO SAF2016-76565-R, ERANET-Neuron JTC 2019 ISCIII AC19/00077
FEDER funds (to R.A.); RETOS-MINECO SAF2017-87928-R (to A.B.); an NIH grant (NS76637)
and UTHSC College of Medicine funds (to S.J.T.); and NARSAD Independent Investigator
Award and grants from the MINECO (CSD2008-00005, SAF2013-48983R, SAF2016-80895-R),
Generalitat Valenciana (PROMETEO 2019/020)(to I.P.O.) and Severo-Ochoa Excellence
Awards (SEV-2013-0317, SEV-2017-0723).
article_number: e71575
article_processing_charge: No
article_type: original
author:
- first_name: María J
full_name: Conde-Dusman, María J
last_name: Conde-Dusman
- first_name: Partha N
full_name: Dey, Partha N
last_name: Dey
- first_name: Óscar
full_name: Elía-Zudaire, Óscar
last_name: Elía-Zudaire
- first_name: Luis E
full_name: Garcia Rabaneda, Luis E
id: 33D1B084-F248-11E8-B48F-1D18A9856A87
last_name: Garcia Rabaneda
- first_name: Carmen
full_name: García-Lira, Carmen
last_name: García-Lira
- first_name: Teddy
full_name: Grand, Teddy
last_name: Grand
- first_name: Victor
full_name: Briz, Victor
last_name: Briz
- first_name: Eric R
full_name: Velasco, Eric R
last_name: Velasco
- first_name: Raül
full_name: Andero Galí, Raül
last_name: Andero Galí
- first_name: Sergio
full_name: Niñerola, Sergio
last_name: Niñerola
- first_name: Angel
full_name: Barco, Angel
last_name: Barco
- first_name: Pierre
full_name: Paoletti, Pierre
last_name: Paoletti
- first_name: John F
full_name: Wesseling, John F
last_name: Wesseling
- first_name: Fabrizio
full_name: Gardoni, Fabrizio
last_name: Gardoni
- first_name: Steven J
full_name: Tavalin, Steven J
last_name: Tavalin
- first_name: Isabel
full_name: Perez-Otaño, Isabel
last_name: Perez-Otaño
citation:
ama: Conde-Dusman MJ, Dey PN, Elía-Zudaire Ó, et al. Control of protein synthesis
and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly.
eLife. 2021;10. doi:10.7554/elife.71575
apa: Conde-Dusman, M. J., Dey, P. N., Elía-Zudaire, Ó., Garcia Rabaneda, L. E.,
García-Lira, C., Grand, T., … Perez-Otaño, I. (2021). Control of protein synthesis
and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly.
ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.71575
chicago: Conde-Dusman, María J, Partha N Dey, Óscar Elía-Zudaire, Luis E Garcia
Rabaneda, Carmen García-Lira, Teddy Grand, Victor Briz, et al. “Control of Protein
Synthesis and Memory by GluN3A-NMDA Receptors through Inhibition of GIT1/MTORC1
Assembly.” ELife. eLife Sciences Publications, 2021. https://doi.org/10.7554/elife.71575.
ieee: M. J. Conde-Dusman et al., “Control of protein synthesis and memory
by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly,” eLife,
vol. 10. eLife Sciences Publications, 2021.
ista: Conde-Dusman MJ, Dey PN, Elía-Zudaire Ó, Garcia Rabaneda LE, García-Lira C,
Grand T, Briz V, Velasco ER, Andero Galí R, Niñerola S, Barco A, Paoletti P, Wesseling
JF, Gardoni F, Tavalin SJ, Perez-Otaño I. 2021. Control of protein synthesis and
memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly. eLife.
10, e71575.
mla: Conde-Dusman, María J., et al. “Control of Protein Synthesis and Memory by
GluN3A-NMDA Receptors through Inhibition of GIT1/MTORC1 Assembly.” ELife,
vol. 10, e71575, eLife Sciences Publications, 2021, doi:10.7554/elife.71575.
short: M.J. Conde-Dusman, P.N. Dey, Ó. Elía-Zudaire, L.E. Garcia Rabaneda, C. García-Lira,
T. Grand, V. Briz, E.R. Velasco, R. Andero Galí, S. Niñerola, A. Barco, P. Paoletti,
J.F. Wesseling, F. Gardoni, S.J. Tavalin, I. Perez-Otaño, ELife 10 (2021).
date_created: 2021-11-18T06:59:45Z
date_published: 2021-11-17T00:00:00Z
date_updated: 2023-08-14T11:50:50Z
day: '17'
ddc:
- '570'
department:
- _id: GaNo
doi: 10.7554/elife.71575
external_id:
isi:
- '000720945900001'
file:
- access_level: open_access
checksum: 59318e9e41507cec83c2f4070e6ad540
content_type: application/pdf
creator: lgarciar
date_created: 2021-11-18T07:02:02Z
date_updated: 2021-11-18T07:02:02Z
file_id: '10302'
file_name: elife-71575-v1.pdf
file_size: 2477302
relation: main_file
success: 1
file_date_updated: 2021-11-18T07:02:02Z
has_accepted_license: '1'
intvolume: ' 10'
isi: 1
keyword:
- general immunology and microbiology
- general biochemistry
- genetics and molecular biology
- general medicine
- general neuroscience
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
status: public
title: Control of protein synthesis and memory by GluN3A-NMDA receptors through inhibition
of GIT1/mTORC1 assembly
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 10
year: '2021'
...
---
_id: '11055'
abstract:
- lang: eng
text: Vascular dysfunctions are a common feature of multiple age-related diseases.
However, modeling healthy and pathological aging of the human vasculature represents
an unresolved experimental challenge. Here, we generated induced vascular endothelial
cells (iVECs) and smooth muscle cells (iSMCs) by direct reprogramming of healthy
human fibroblasts from donors of different ages and Hutchinson-Gilford Progeria
Syndrome (HGPS) patients. iVECs induced from old donors revealed upregulation
of GSTM1 and PALD1, genes linked to oxidative stress, inflammation and endothelial
junction stability, as vascular aging markers. A functional assay performed on
PALD1 KD VECs demonstrated a recovery in vascular permeability. We found that
iSMCs from HGPS donors overexpressed bone morphogenetic protein (BMP)−4, which
plays a key role in both vascular calcification and endothelial barrier damage
observed in HGPS. Strikingly, BMP4 concentrations are higher in serum from HGPS
vs. age-matched mice. Furthermore, targeting BMP4 with blocking antibody recovered
the functionality of the vascular barrier in vitro, hence representing a potential
future therapeutic strategy to limit cardiovascular dysfunction in HGPS. These
results show that iVECs and iSMCs retain disease-related signatures, allowing
modeling of vascular aging and HGPS in vitro.
article_number: e54383
article_processing_charge: No
article_type: original
author:
- first_name: Simone
full_name: Bersini, Simone
last_name: Bersini
- first_name: Roberta
full_name: Schulte, Roberta
last_name: Schulte
- first_name: Ling
full_name: Huang, Ling
last_name: Huang
- first_name: Hannah
full_name: Tsai, Hannah
last_name: Tsai
- 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: Bersini S, Schulte R, Huang L, Tsai H, Hetzer M. Direct reprogramming of human
smooth muscle and vascular endothelial cells reveals defects associated with aging
and Hutchinson-Gilford progeria syndrome. eLife. 2020;9. doi:10.7554/elife.54383
apa: Bersini, S., Schulte, R., Huang, L., Tsai, H., & Hetzer, M. (2020). Direct
reprogramming of human smooth muscle and vascular endothelial cells reveals defects
associated with aging and Hutchinson-Gilford progeria syndrome. ELife.
eLife Sciences Publications. https://doi.org/10.7554/elife.54383
chicago: Bersini, Simone, Roberta Schulte, Ling Huang, Hannah Tsai, and Martin Hetzer.
“Direct Reprogramming of Human Smooth Muscle and Vascular Endothelial Cells Reveals
Defects Associated with Aging and Hutchinson-Gilford Progeria Syndrome.” ELife.
eLife Sciences Publications, 2020. https://doi.org/10.7554/elife.54383.
ieee: S. Bersini, R. Schulte, L. Huang, H. Tsai, and M. Hetzer, “Direct reprogramming
of human smooth muscle and vascular endothelial cells reveals defects associated
with aging and Hutchinson-Gilford progeria syndrome,” eLife, vol. 9. eLife
Sciences Publications, 2020.
ista: Bersini S, Schulte R, Huang L, Tsai H, Hetzer M. 2020. Direct reprogramming
of human smooth muscle and vascular endothelial cells reveals defects associated
with aging and Hutchinson-Gilford progeria syndrome. eLife. 9, e54383.
mla: Bersini, Simone, et al. “Direct Reprogramming of Human Smooth Muscle and Vascular
Endothelial Cells Reveals Defects Associated with Aging and Hutchinson-Gilford
Progeria Syndrome.” ELife, vol. 9, e54383, eLife Sciences Publications,
2020, doi:10.7554/elife.54383.
short: S. Bersini, R. Schulte, L. Huang, H. Tsai, M. Hetzer, ELife 9 (2020).
date_created: 2022-04-07T07:43:48Z
date_published: 2020-09-08T00:00:00Z
date_updated: 2022-07-18T08:30:37Z
day: '08'
ddc:
- '570'
doi: 10.7554/elife.54383
extern: '1'
external_id:
pmid:
- '32896271'
file:
- access_level: open_access
checksum: f8b3821349a194050be02570d8fe7d4b
content_type: application/pdf
creator: dernst
date_created: 2022-04-08T06:53:10Z
date_updated: 2022-04-08T06:53:10Z
file_id: '11132'
file_name: 2020_eLife_Bersini.pdf
file_size: 4399825
relation: main_file
success: 1
file_date_updated: 2022-04-08T06:53:10Z
has_accepted_license: '1'
intvolume: ' 9'
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Medicine
- General Neuroscience
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Direct reprogramming of human smooth muscle and vascular endothelial cells
reveals defects associated with aging and Hutchinson-Gilford progeria syndrome
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: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 9
year: '2020'
...
---
_id: '15055'
abstract:
- lang: eng
text: Markov decision processes (MDPs) are the defacto framework for sequential
decision making in the presence of stochastic uncertainty. A classical optimization
criterion for MDPs is to maximize the expected discounted-sum payoff, which ignores
low probability catastrophic events with highly negative impact on the system.
On the other hand, risk-averse policies require the probability of undesirable
events to be below a given threshold, but they do not account for optimization
of the expected payoff. We consider MDPs with discounted-sum payoff with failure
states which represent catastrophic outcomes. The objective of risk-constrained
planning is to maximize the expected discounted-sum payoff among risk-averse policies
that ensure the probability to encounter a failure state is below a desired threshold.
Our main contribution is an efficient risk-constrained planning algorithm that
combines UCT-like search with a predictor learned through interaction with the
MDP (in the style of AlphaZero) and with a risk-constrained action selection via
linear programming. We demonstrate the effectiveness of our approach with experiments
on classical MDPs from the literature, including benchmarks with an order of 106
states.
acknowledgement: Krishnendu Chatterjee is supported by the Austrian Science Fund (FWF)
NFN Grant No. S11407-N23 (RiSE/SHiNE), and COST Action GAMENET. Tomas Brazdil is
supported by the Grant Agency of Masaryk University grant no. MUNI/G/0739/2017 and
by the Czech Science Foundation grant No. 18-11193S. Petr Novotny and Jirı Vahala
are supported by the Czech Science Foundation grant No. GJ19-15134Y.
article_processing_charge: No
article_type: original
arxiv: 1
author:
- first_name: Tomáš
full_name: Brázdil, Tomáš
last_name: Brázdil
- first_name: Krishnendu
full_name: Chatterjee, Krishnendu
id: 2E5DCA20-F248-11E8-B48F-1D18A9856A87
last_name: Chatterjee
orcid: 0000-0002-4561-241X
- first_name: Petr
full_name: Novotný, Petr
last_name: Novotný
- first_name: Jiří
full_name: Vahala, Jiří
last_name: Vahala
citation:
ama: Brázdil T, Chatterjee K, Novotný P, Vahala J. Reinforcement learning of risk-constrained
policies in Markov decision processes. Proceedings of the 34th AAAI Conference
on Artificial Intelligence. 2020;34(06):9794-9801. doi:10.1609/aaai.v34i06.6531
apa: 'Brázdil, T., Chatterjee, K., Novotný, P., & Vahala, J. (2020). Reinforcement
learning of risk-constrained policies in Markov decision processes. Proceedings
of the 34th AAAI Conference on Artificial Intelligence. New York, NY, United
States: Association for the Advancement of Artificial Intelligence. https://doi.org/10.1609/aaai.v34i06.6531'
chicago: Brázdil, Tomáš, Krishnendu Chatterjee, Petr Novotný, and Jiří Vahala. “Reinforcement
Learning of Risk-Constrained Policies in Markov Decision Processes.” Proceedings
of the 34th AAAI Conference on Artificial Intelligence. Association for the
Advancement of Artificial Intelligence, 2020. https://doi.org/10.1609/aaai.v34i06.6531.
ieee: T. Brázdil, K. Chatterjee, P. Novotný, and J. Vahala, “Reinforcement learning
of risk-constrained policies in Markov decision processes,” Proceedings of
the 34th AAAI Conference on Artificial Intelligence, vol. 34, no. 06. Association
for the Advancement of Artificial Intelligence, pp. 9794–9801, 2020.
ista: Brázdil T, Chatterjee K, Novotný P, Vahala J. 2020. Reinforcement learning
of risk-constrained policies in Markov decision processes. Proceedings of the
34th AAAI Conference on Artificial Intelligence. 34(06), 9794–9801.
mla: Brázdil, Tomáš, et al. “Reinforcement Learning of Risk-Constrained Policies
in Markov Decision Processes.” Proceedings of the 34th AAAI Conference on Artificial
Intelligence, vol. 34, no. 06, Association for the Advancement of Artificial
Intelligence, 2020, pp. 9794–801, doi:10.1609/aaai.v34i06.6531.
short: T. Brázdil, K. Chatterjee, P. Novotný, J. Vahala, Proceedings of the 34th
AAAI Conference on Artificial Intelligence 34 (2020) 9794–9801.
conference:
end_date: 2020-02-12
location: New York, NY, United States
name: 'AAAI: Conference on Artificial Intelligence'
start_date: 2020-02-07
date_created: 2024-03-04T08:07:22Z
date_published: 2020-04-03T00:00:00Z
date_updated: 2024-03-04T08:30:16Z
day: '03'
department:
- _id: KrCh
doi: 10.1609/aaai.v34i06.6531
external_id:
arxiv:
- '2002.12086'
intvolume: ' 34'
issue: '06'
keyword:
- General Medicine
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.48550/arXiv.2002.12086
month: '04'
oa: 1
oa_version: Preprint
page: 9794-9801
project:
- _id: 25863FF4-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: S11407
name: Game Theory
publication: Proceedings of the 34th AAAI Conference on Artificial Intelligence
publication_identifier:
issn:
- 2374-3468
publication_status: published
publisher: Association for the Advancement of Artificial Intelligence
quality_controlled: '1'
status: public
title: Reinforcement learning of risk-constrained policies in Markov decision processes
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 34
year: '2020'
...
---
_id: '15063'
abstract:
- lang: eng
text: We consider the least singular value of a large random matrix with real or
complex i.i.d. Gaussian entries shifted by a constant z∈C. We prove an optimal
lower tail estimate on this singular value in the critical regime where z is around
the spectral edge, thus improving the classical bound of Sankar, Spielman and
Teng (SIAM J. Matrix Anal. Appl. 28:2 (2006), 446–476) for the particular shift-perturbation
in the edge regime. Lacking Brézin–Hikami formulas in the real case, we rely on
the superbosonization formula (Comm. Math. Phys. 283:2 (2008), 343–395).
acknowledgement: Partially supported by ERC Advanced Grant No. 338804. This project
has received funding from the European Union’s Horizon 2020 research and innovation
programme under the Marie Sklodowska-Curie Grant Agreement No. 66538
article_processing_charge: No
article_type: original
arxiv: 1
author:
- first_name: Giorgio
full_name: Cipolloni, Giorgio
id: 42198EFA-F248-11E8-B48F-1D18A9856A87
last_name: Cipolloni
orcid: 0000-0002-4901-7992
- first_name: László
full_name: Erdös, László
id: 4DBD5372-F248-11E8-B48F-1D18A9856A87
last_name: Erdös
orcid: 0000-0001-5366-9603
- first_name: Dominik J
full_name: Schröder, Dominik J
id: 408ED176-F248-11E8-B48F-1D18A9856A87
last_name: Schröder
orcid: 0000-0002-2904-1856
citation:
ama: Cipolloni G, Erdös L, Schröder DJ. Optimal lower bound on the least singular
value of the shifted Ginibre ensemble. Probability and Mathematical Physics.
2020;1(1):101-146. doi:10.2140/pmp.2020.1.101
apa: Cipolloni, G., Erdös, L., & Schröder, D. J. (2020). Optimal lower bound
on the least singular value of the shifted Ginibre ensemble. Probability and
Mathematical Physics. Mathematical Sciences Publishers. https://doi.org/10.2140/pmp.2020.1.101
chicago: Cipolloni, Giorgio, László Erdös, and Dominik J Schröder. “Optimal Lower
Bound on the Least Singular Value of the Shifted Ginibre Ensemble.” Probability
and Mathematical Physics. Mathematical Sciences Publishers, 2020. https://doi.org/10.2140/pmp.2020.1.101.
ieee: G. Cipolloni, L. Erdös, and D. J. Schröder, “Optimal lower bound on the least
singular value of the shifted Ginibre ensemble,” Probability and Mathematical
Physics, vol. 1, no. 1. Mathematical Sciences Publishers, pp. 101–146, 2020.
ista: Cipolloni G, Erdös L, Schröder DJ. 2020. Optimal lower bound on the least
singular value of the shifted Ginibre ensemble. Probability and Mathematical Physics.
1(1), 101–146.
mla: Cipolloni, Giorgio, et al. “Optimal Lower Bound on the Least Singular Value
of the Shifted Ginibre Ensemble.” Probability and Mathematical Physics,
vol. 1, no. 1, Mathematical Sciences Publishers, 2020, pp. 101–46, doi:10.2140/pmp.2020.1.101.
short: G. Cipolloni, L. Erdös, D.J. Schröder, Probability and Mathematical Physics
1 (2020) 101–146.
date_created: 2024-03-04T10:27:57Z
date_published: 2020-11-16T00:00:00Z
date_updated: 2024-03-04T10:33:15Z
day: '16'
department:
- _id: LaEr
doi: 10.2140/pmp.2020.1.101
ec_funded: 1
external_id:
arxiv:
- '1908.01653'
intvolume: ' 1'
issue: '1'
keyword:
- General Medicine
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.48550/arXiv.1908.01653
month: '11'
oa: 1
oa_version: Preprint
page: 101-146
project:
- _id: 258DCDE6-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '338804'
name: Random matrices, universality and disordered quantum systems
- _id: 2564DBCA-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '665385'
name: International IST Doctoral Program
publication: Probability and Mathematical Physics
publication_identifier:
issn:
- 2690-1005
- 2690-0998
publication_status: published
publisher: Mathematical Sciences Publishers
quality_controlled: '1'
scopus_import: '1'
status: public
title: Optimal lower bound on the least singular value of the shifted Ginibre ensemble
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 1
year: '2020'
...
---
_id: '13361'
abstract:
- lang: eng
text: "In nature, light is harvested by photoactive proteins to drive a range of
biological processes, including photosynthesis, phototaxis, vision, and ultimately
life. Bacteriorhodopsin, for example, is a protein embedded within archaeal cell
membranes that binds the chromophore retinal within its hydrophobic pocket. Exposure
to light triggers regioselective photoisomerization of the confined retinal, which
in turn initiates a cascade of conformational changes within the protein, triggering
proton flux against the concentration gradient, providing the microorganisms with
the energy to live. We are inspired by these functions in nature to harness light
energy using synthetic photoswitches under confinement. Like retinal, synthetic
photoswitches require some degree of conformational flexibility to isomerize.
In nature, the conformational change associated with retinal isomerization is
accommodated by the structural flexibility of the opsin host, yet it results in
steric communication between the chromophore and the protein. Similarly, we strive
to design systems wherein isomerization of confined photoswitches results in steric
communication between a photoswitch and its confining environment. To achieve
this aim, a balance must be struck between molecular crowding and conformational
freedom under confinement: too much crowding prevents switching, whereas too much
freedom resembles switching of isolated molecules in solution, preventing communication.\r\n\r\nIn
this Account, we discuss five classes of synthetic light-switchable compounds—diarylethenes,
anthracenes, azobenzenes, spiropyrans, and donor–acceptor Stenhouse adducts—comparing
their behaviors under confinement and in solution. The environments employed to
confine these photoswitches are diverse, ranging from planar surfaces to nanosized
cavities within coordination cages, nanoporous frameworks, and nanoparticle aggregates.
The trends that emerge are primarily dependent on the nature of the photoswitch
and not on the material used for confinement. In general, we find that photoswitches
requiring less conformational freedom for switching are, as expected, more straightforward
to isomerize reversibly under confinement. Because these compounds undergo only
small structural changes upon isomerization, however, switching does not propagate
into communication with their environment. Conversely, photoswitches that require
more conformational freedom are more challenging to switch under confinement but
also can influence system-wide behavior.\r\n\r\nAlthough we are primarily interested
in the effects of geometric constraints on photoswitching under confinement, additional
effects inevitably emerge when a compound is removed from solution and placed
within a new, more crowded environment. For instance, we have found that compounds
that convert to zwitterionic isomers upon light irradiation often experience stabilization
of these forms under confinement. This effect results from the mutual stabilization
of zwitterions that are brought into close proximity on surfaces or within cavities.
Furthermore, photoswitches can experience preorganization under confinement, influencing
the selectivity and efficiency of their photoreactions. Because intermolecular
interactions arising from confinement cannot be considered independently from
the effects of geometric constraints, we describe all confinement effects concurrently
throughout this Account."
article_processing_charge: No
article_type: original
author:
- first_name: Angela B.
full_name: Grommet, Angela B.
last_name: Grommet
- first_name: Lucia M.
full_name: Lee, Lucia M.
last_name: Lee
- first_name: Rafal
full_name: Klajn, Rafal
id: 8e84690e-1e48-11ed-a02b-a1e6fb8bb53b
last_name: Klajn
citation:
ama: Grommet AB, Lee LM, Klajn R. Molecular photoswitching in confined spaces. Accounts
of Chemical Research. 2020;53(11):2600-2610. doi:10.1021/acs.accounts.0c00434
apa: Grommet, A. B., Lee, L. M., & Klajn, R. (2020). Molecular photoswitching
in confined spaces. Accounts of Chemical Research. American Chemical Society.
https://doi.org/10.1021/acs.accounts.0c00434
chicago: Grommet, Angela B., Lucia M. Lee, and Rafal Klajn. “Molecular Photoswitching
in Confined Spaces.” Accounts of Chemical Research. American Chemical Society,
2020. https://doi.org/10.1021/acs.accounts.0c00434.
ieee: A. B. Grommet, L. M. Lee, and R. Klajn, “Molecular photoswitching in confined
spaces,” Accounts of Chemical Research, vol. 53, no. 11. American Chemical
Society, pp. 2600–2610, 2020.
ista: Grommet AB, Lee LM, Klajn R. 2020. Molecular photoswitching in confined spaces.
Accounts of Chemical Research. 53(11), 2600–2610.
mla: Grommet, Angela B., et al. “Molecular Photoswitching in Confined Spaces.” Accounts
of Chemical Research, vol. 53, no. 11, American Chemical Society, 2020, pp.
2600–10, doi:10.1021/acs.accounts.0c00434.
short: A.B. Grommet, L.M. Lee, R. Klajn, Accounts of Chemical Research 53 (2020)
2600–2610.
date_created: 2023-08-01T09:35:50Z
date_published: 2020-11-17T00:00:00Z
date_updated: 2023-08-07T10:06:46Z
day: '17'
doi: 10.1021/acs.accounts.0c00434
extern: '1'
external_id:
pmid:
- '32969638'
intvolume: ' 53'
issue: '11'
keyword:
- General Medicine
- General Chemistry
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1021/acs.accounts.0c00434
month: '11'
oa: 1
oa_version: Published Version
page: 2600-2610
pmid: 1
publication: Accounts of Chemical Research
publication_identifier:
eissn:
- 1520-4898
issn:
- 0001-4842
publication_status: published
publisher: American Chemical Society
quality_controlled: '1'
scopus_import: '1'
status: public
title: Molecular photoswitching in confined spaces
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 53
year: '2020'
...
---
_id: '11060'
abstract:
- lang: eng
text: The inner nuclear membrane (INM) is a subdomain of the endoplasmic reticulum
(ER) that is gated by the nuclear pore complex. It is unknown whether proteins
of the INM and ER are degraded through shared or distinct pathways in mammalian
cells. We applied dynamic proteomics to profile protein half-lives and report
that INM and ER residents turn over at similar rates, indicating that the INM’s
unique topology is not a barrier to turnover. Using a microscopy approach, we
observed that the proteasome can degrade INM proteins in situ. However, we also
uncovered evidence for selective, vesicular transport-mediated turnover of a single
INM protein, emerin, that is potentiated by ER stress. Emerin is rapidly cleared
from the INM by a mechanism that requires emerin’s LEM domain to mediate vesicular
trafficking to lysosomes. This work demonstrates that the INM can be dynamically
remodeled in response to environmental inputs.
article_number: e49796
article_processing_charge: No
article_type: original
author:
- first_name: Abigail
full_name: Buchwalter, Abigail
last_name: Buchwalter
- first_name: Roberta
full_name: Schulte, Roberta
last_name: Schulte
- first_name: Hsiao
full_name: Tsai, Hsiao
last_name: Tsai
- first_name: Juliana
full_name: Capitanio, Juliana
last_name: Capitanio
- 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: Buchwalter A, Schulte R, Tsai H, Capitanio J, Hetzer M. Selective clearance
of the inner nuclear membrane protein emerin by vesicular transport during ER
stress. eLife. 2019;8. doi:10.7554/elife.49796
apa: Buchwalter, A., Schulte, R., Tsai, H., Capitanio, J., & Hetzer, M. (2019).
Selective clearance of the inner nuclear membrane protein emerin by vesicular
transport during ER stress. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.49796
chicago: Buchwalter, Abigail, Roberta Schulte, Hsiao Tsai, Juliana Capitanio, and
Martin Hetzer. “Selective Clearance of the Inner Nuclear Membrane Protein Emerin
by Vesicular Transport during ER Stress.” ELife. eLife Sciences Publications,
2019. https://doi.org/10.7554/elife.49796.
ieee: A. Buchwalter, R. Schulte, H. Tsai, J. Capitanio, and M. Hetzer, “Selective
clearance of the inner nuclear membrane protein emerin by vesicular transport
during ER stress,” eLife, vol. 8. eLife Sciences Publications, 2019.
ista: Buchwalter A, Schulte R, Tsai H, Capitanio J, Hetzer M. 2019. Selective clearance
of the inner nuclear membrane protein emerin by vesicular transport during ER
stress. eLife. 8, e49796.
mla: Buchwalter, Abigail, et al. “Selective Clearance of the Inner Nuclear Membrane
Protein Emerin by Vesicular Transport during ER Stress.” ELife, vol. 8,
e49796, eLife Sciences Publications, 2019, doi:10.7554/elife.49796.
short: A. Buchwalter, R. Schulte, H. Tsai, J. Capitanio, M. Hetzer, ELife 8 (2019).
date_created: 2022-04-07T07:45:02Z
date_published: 2019-10-10T00:00:00Z
date_updated: 2023-05-31T06:36:22Z
day: '10'
ddc:
- '570'
doi: 10.7554/elife.49796
extern: '1'
external_id:
pmid:
- '31599721'
file:
- access_level: open_access
checksum: 1e8672a1e9c3dc0a2d3d0dad89673616
content_type: application/pdf
creator: dernst
date_created: 2022-04-08T08:18:01Z
date_updated: 2022-04-08T08:18:01Z
file_id: '11138'
file_name: 2019_eLife_Buchwalter.pdf
file_size: 6984654
relation: main_file
success: 1
file_date_updated: 2022-04-08T08:18:01Z
has_accepted_license: '1'
intvolume: ' 8'
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Medicine
- General Neuroscience
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
related_material:
record:
- id: '13079'
relation: research_data
status: public
scopus_import: '1'
status: public
title: Selective clearance of the inner nuclear membrane protein emerin by vesicular
transport during ER stress
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: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 8
year: '2019'
...
---
_id: '12192'
abstract:
- lang: eng
text: Transposable elements (TEs), the movement of which can damage the genome,
are epigenetically silenced in eukaryotes. Intriguingly, TEs are activated in
the sperm companion cell – vegetative cell (VC) – of the flowering plant Arabidopsis
thaliana. However, the extent and mechanism of this activation are unknown. Here
we show that about 100 heterochromatic TEs are activated in VCs, mostly by DEMETER-catalyzed
DNA demethylation. We further demonstrate that DEMETER access to some of these
TEs is permitted by the natural depletion of linker histone H1 in VCs. Ectopically
expressed H1 suppresses TEs in VCs by reducing DNA demethylation and via a methylation-independent
mechanism. We demonstrate that H1 is required for heterochromatin condensation
in plant cells and show that H1 overexpression creates heterochromatic foci in
the VC progenitor cell. Taken together, our results demonstrate that the natural
depletion of H1 during male gametogenesis facilitates DEMETER-directed DNA demethylation,
heterochromatin relaxation, and TE activation.
acknowledgement: We thank David Twell for the pDONR-P4-P1R-pLAT52 and pDONR-P2R-P3-mRFP
vectors, the John Innes Centre Bioimaging Facility (Elaine Barclay and Grant Calder)
for their assistance with microscopy, and the Norwich BioScience Institute Partnership
Computing infrastructure for Science Group for High Performance Computing resources.
This work was funded by a Biotechnology and Biological Sciences Research Council
(BBSRC) David Phillips Fellowship (BB/L025043/1; SH, JZ and XF), a European Research
Council Starting Grant ('SexMeth' 804981; XF) and a Grant to Exceptional Researchers
by the Gatsby Charitable Foundation (SH and XF).
article_number: '42530'
article_processing_charge: No
article_type: original
author:
- first_name: Shengbo
full_name: He, Shengbo
last_name: He
- first_name: Martin
full_name: Vickers, Martin
last_name: Vickers
- first_name: Jingyi
full_name: Zhang, Jingyi
last_name: Zhang
- first_name: Xiaoqi
full_name: Feng, Xiaoqi
id: e0164712-22ee-11ed-b12a-d80fcdf35958
last_name: Feng
orcid: 0000-0002-4008-1234
citation:
ama: He S, Vickers M, Zhang J, Feng X. Natural depletion of histone H1 in sex cells
causes DNA demethylation, heterochromatin decondensation and transposon activation.
eLife. 2019;8. doi:10.7554/elife.42530
apa: He, S., Vickers, M., Zhang, J., & Feng, X. (2019). Natural depletion of
histone H1 in sex cells causes DNA demethylation, heterochromatin decondensation
and transposon activation. ELife. eLife Sciences Publications, Ltd. https://doi.org/10.7554/elife.42530
chicago: He, Shengbo, Martin Vickers, Jingyi Zhang, and Xiaoqi Feng. “Natural Depletion
of Histone H1 in Sex Cells Causes DNA Demethylation, Heterochromatin Decondensation
and Transposon Activation.” ELife. eLife Sciences Publications, Ltd, 2019.
https://doi.org/10.7554/elife.42530.
ieee: S. He, M. Vickers, J. Zhang, and X. Feng, “Natural depletion of histone H1
in sex cells causes DNA demethylation, heterochromatin decondensation and transposon
activation,” eLife, vol. 8. eLife Sciences Publications, Ltd, 2019.
ista: He S, Vickers M, Zhang J, Feng X. 2019. Natural depletion of histone H1 in
sex cells causes DNA demethylation, heterochromatin decondensation and transposon
activation. eLife. 8, 42530.
mla: He, Shengbo, et al. “Natural Depletion of Histone H1 in Sex Cells Causes DNA
Demethylation, Heterochromatin Decondensation and Transposon Activation.” ELife,
vol. 8, 42530, eLife Sciences Publications, Ltd, 2019, doi:10.7554/elife.42530.
short: S. He, M. Vickers, J. Zhang, X. Feng, ELife 8 (2019).
date_created: 2023-01-16T09:17:21Z
date_published: 2019-05-28T00:00:00Z
date_updated: 2023-05-08T10:54:12Z
day: '28'
ddc:
- '580'
department:
- _id: XiFe
doi: 10.7554/elife.42530
extern: '1'
external_id:
unknown:
- '31135340'
file:
- access_level: open_access
checksum: ea6b89c20d59e5eb3646916fe5d568ad
content_type: application/pdf
creator: alisjak
date_created: 2023-02-07T09:42:46Z
date_updated: 2023-02-07T09:42:46Z
file_id: '12525'
file_name: 2019_elife_He.pdf
file_size: 2493837
relation: main_file
success: 1
file_date_updated: 2023-02-07T09:42:46Z
has_accepted_license: '1'
intvolume: ' 8'
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Medicine
- General Neuroscience
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6594752/
month: '05'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications, Ltd
quality_controlled: '1'
scopus_import: '1'
status: public
title: Natural depletion of histone H1 in sex cells causes DNA demethylation, heterochromatin
decondensation and transposon activation
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 8
year: '2019'
...
---
_id: '10880'
abstract:
- lang: eng
text: Acquisition of evolutionary novelties is a fundamental process for adapting
to the external environment and invading new niches and results in the diversification
of life, which we can see in the world today. How such novel phenotypic traits
are acquired in the course of evolution and are built up in developing embryos
has been a central question in biology. Whole-genome duplication (WGD) is a process
of genome doubling that supplies raw genetic materials and increases genome complexity.
Recently, it has been gradually revealed that WGD and subsequent fate changes
of duplicated genes can facilitate phenotypic evolution. Here, we review the current
understanding of the relationship between WGD and the acquisition of evolutionary
novelties. We show some examples of this link and discuss how WGD and subsequent
duplicated genes can facilitate phenotypic evolution as well as when such genomic
doubling can be advantageous for adaptation.
acknowledgement: This work was supported by JSPS overseas research fellowships (Y.M.)
and SENSHIN Medical Research Foundation (K.K.T.).
article_processing_charge: No
article_type: original
author:
- first_name: Moriyama
full_name: Yuuta, Moriyama
id: 4968E7C8-F248-11E8-B48F-1D18A9856A87
last_name: Yuuta
orcid: 0000-0002-2853-8051
- first_name: Kazuko
full_name: Koshiba-Takeuchi, Kazuko
last_name: Koshiba-Takeuchi
citation:
ama: Yuuta M, Koshiba-Takeuchi K. Significance of whole-genome duplications on the
emergence of evolutionary novelties. Briefings in Functional Genomics.
2018;17(5):329-338. doi:10.1093/bfgp/ely007
apa: Yuuta, M., & Koshiba-Takeuchi, K. (2018). Significance of whole-genome
duplications on the emergence of evolutionary novelties. Briefings in Functional
Genomics. Oxford University Press. https://doi.org/10.1093/bfgp/ely007
chicago: Yuuta, Moriyama, and Kazuko Koshiba-Takeuchi. “Significance of Whole-Genome
Duplications on the Emergence of Evolutionary Novelties.” Briefings in Functional
Genomics. Oxford University Press, 2018. https://doi.org/10.1093/bfgp/ely007.
ieee: M. Yuuta and K. Koshiba-Takeuchi, “Significance of whole-genome duplications
on the emergence of evolutionary novelties,” Briefings in Functional Genomics,
vol. 17, no. 5. Oxford University Press, pp. 329–338, 2018.
ista: Yuuta M, Koshiba-Takeuchi K. 2018. Significance of whole-genome duplications
on the emergence of evolutionary novelties. Briefings in Functional Genomics.
17(5), 329–338.
mla: Yuuta, Moriyama, and Kazuko Koshiba-Takeuchi. “Significance of Whole-Genome
Duplications on the Emergence of Evolutionary Novelties.” Briefings in Functional
Genomics, vol. 17, no. 5, Oxford University Press, 2018, pp. 329–38, doi:10.1093/bfgp/ely007.
short: M. Yuuta, K. Koshiba-Takeuchi, Briefings in Functional Genomics 17 (2018)
329–338.
date_created: 2022-03-18T12:40:35Z
date_published: 2018-09-01T00:00:00Z
date_updated: 2023-09-19T15:11:22Z
day: '01'
department:
- _id: CaHe
doi: 10.1093/bfgp/ely007
external_id:
isi:
- '000456054400004'
pmid:
- '29579140'
intvolume: ' 17'
isi: 1
issue: '5'
keyword:
- Genetics
- Molecular Biology
- Biochemistry
- General Medicine
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1093/bfgp/ely007
month: '09'
oa: 1
oa_version: Published Version
page: 329-338
pmid: 1
publication: Briefings in Functional Genomics
publication_identifier:
eissn:
- 2041-2657
issn:
- 2041-2649
publication_status: published
publisher: Oxford University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Significance of whole-genome duplications on the emergence of evolutionary
novelties
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 17
year: '2018'
...
---
_id: '8439'
abstract:
- lang: eng
text: Lipopolysaccharides (LPS) are complex glycolipids forming the outside layer
of Gram-negative bacteria. Their hydrophobic and heterogeneous nature greatly
hampers their structural study in an environment similar to the bacterial surface.
We have studied LPS purified from E. coli and pathogenic P. aeruginosa with long
O-antigen polysaccharides assembled in solution as vesicles or elongated micelles.
Solid-state NMR with magic-angle spinning permitted the identification of NMR
signals arising from regions with different flexibilities in the LPS, from the
lipid components to the O-antigen polysaccharides. Atomic scale data on the LPS
enabled the study of the interaction of gentamicin antibiotic bound to P. aeruginosa
LPS, for which we could confirm that a specific oligosaccharide is involved in
the antibiotic binding. The possibility to study LPS alone and bound to a ligand
when it is assembled in membrane-like structures opens great prospects for the
investigation of proteins and antibiotics that specifically target such an important
molecule at the surface of Gram-negative bacteria.
article_processing_charge: No
article_type: original
author:
- first_name: Cedric
full_name: Laguri, Cedric
last_name: Laguri
- first_name: Alba
full_name: Silipo, Alba
last_name: Silipo
- first_name: Alessandra M.
full_name: Martorana, Alessandra M.
last_name: Martorana
- first_name: Paul
full_name: Schanda, Paul
id: 7B541462-FAF6-11E9-A490-E8DFE5697425
last_name: Schanda
orcid: 0000-0002-9350-7606
- first_name: Roberta
full_name: Marchetti, Roberta
last_name: Marchetti
- first_name: Alessandra
full_name: Polissi, Alessandra
last_name: Polissi
- first_name: Antonio
full_name: Molinaro, Antonio
last_name: Molinaro
- first_name: Jean-Pierre
full_name: Simorre, Jean-Pierre
last_name: Simorre
citation:
ama: Laguri C, Silipo A, Martorana AM, et al. Solid state NMR studies of intact
lipopolysaccharide endotoxin. ACS Chemical Biology. 2018;13(8):2106-2113.
doi:10.1021/acschembio.8b00271
apa: Laguri, C., Silipo, A., Martorana, A. M., Schanda, P., Marchetti, R., Polissi,
A., … Simorre, J.-P. (2018). Solid state NMR studies of intact lipopolysaccharide
endotoxin. ACS Chemical Biology. American Chemical Society. https://doi.org/10.1021/acschembio.8b00271
chicago: Laguri, Cedric, Alba Silipo, Alessandra M. Martorana, Paul Schanda, Roberta
Marchetti, Alessandra Polissi, Antonio Molinaro, and Jean-Pierre Simorre. “Solid
State NMR Studies of Intact Lipopolysaccharide Endotoxin.” ACS Chemical Biology.
American Chemical Society, 2018. https://doi.org/10.1021/acschembio.8b00271.
ieee: C. Laguri et al., “Solid state NMR studies of intact lipopolysaccharide
endotoxin,” ACS Chemical Biology, vol. 13, no. 8. American Chemical Society,
pp. 2106–2113, 2018.
ista: Laguri C, Silipo A, Martorana AM, Schanda P, Marchetti R, Polissi A, Molinaro
A, Simorre J-P. 2018. Solid state NMR studies of intact lipopolysaccharide endotoxin.
ACS Chemical Biology. 13(8), 2106–2113.
mla: Laguri, Cedric, et al. “Solid State NMR Studies of Intact Lipopolysaccharide
Endotoxin.” ACS Chemical Biology, vol. 13, no. 8, American Chemical Society,
2018, pp. 2106–13, doi:10.1021/acschembio.8b00271.
short: C. Laguri, A. Silipo, A.M. Martorana, P. Schanda, R. Marchetti, A. Polissi,
A. Molinaro, J.-P. Simorre, ACS Chemical Biology 13 (2018) 2106–2113.
date_created: 2020-09-18T10:05:09Z
date_published: 2018-07-02T00:00:00Z
date_updated: 2021-01-12T08:19:16Z
day: '02'
doi: 10.1021/acschembio.8b00271
extern: '1'
intvolume: ' 13'
issue: '8'
keyword:
- Molecular Medicine
- Biochemistry
- General Medicine
language:
- iso: eng
month: '07'
oa_version: None
page: 2106-2113
publication: ACS Chemical Biology
publication_identifier:
issn:
- 1554-8929
- 1554-8937
publication_status: published
publisher: American Chemical Society
quality_controlled: '1'
status: public
title: Solid state NMR studies of intact lipopolysaccharide endotoxin
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 13
year: '2018'
...
---
_id: '10370'
abstract:
- lang: eng
text: Eukaryotic cells are densely packed with macromolecular complexes and intertwining
organelles, continually transported and reshaped. Intriguingly, organelles avoid
clashing and entangling with each other in such limited space. Mitochondria form
extensive networks constantly remodeled by fission and fusion. Here, we show that
mitochondrial fission is triggered by mechanical forces. Mechano-stimulation of
mitochondria – via encounter with motile intracellular pathogens, via external
pressure applied by an atomic force microscope, or via cell migration across uneven
microsurfaces – results in the recruitment of the mitochondrial fission machinery,
and subsequent division. We propose that MFF, owing to affinity for narrow mitochondria,
acts as a membrane-bound force sensor to recruit the fission machinery to mechanically
strained sites. Thus, mitochondria adapt to the environment by sensing and responding
to biomechanical cues. Our findings that mechanical triggers can be coupled to
biochemical responses in membrane dynamics may explain how organelles orderly
cohabit in the crowded cytoplasm.
article_number: e30292
article_processing_charge: No
article_type: original
author:
- first_name: Sebastian Carsten Johannes
full_name: Helle, Sebastian Carsten Johannes
last_name: Helle
- first_name: Qian
full_name: Feng, Qian
last_name: Feng
- first_name: Mathias J
full_name: Aebersold, Mathias J
last_name: Aebersold
- first_name: Luca
full_name: Hirt, Luca
last_name: Hirt
- first_name: Raphael R
full_name: Grüter, Raphael R
last_name: Grüter
- first_name: Afshin
full_name: Vahid, Afshin
last_name: Vahid
- first_name: Andrea
full_name: Sirianni, Andrea
last_name: Sirianni
- first_name: Serge
full_name: Mostowy, Serge
last_name: Mostowy
- first_name: Jess G
full_name: Snedeker, Jess G
last_name: Snedeker
- first_name: Anđela
full_name: Šarić, Anđela
id: bf63d406-f056-11eb-b41d-f263a6566d8b
last_name: Šarić
orcid: 0000-0002-7854-2139
- first_name: Timon
full_name: Idema, Timon
last_name: Idema
- first_name: Tomaso
full_name: Zambelli, Tomaso
last_name: Zambelli
- first_name: Benoît
full_name: Kornmann, Benoît
last_name: Kornmann
citation:
ama: Helle SCJ, Feng Q, Aebersold MJ, et al. Mechanical force induces mitochondrial
fission. eLife. 2017;6. doi:10.7554/elife.30292
apa: Helle, S. C. J., Feng, Q., Aebersold, M. J., Hirt, L., Grüter, R. R., Vahid,
A., … Kornmann, B. (2017). Mechanical force induces mitochondrial fission. ELife.
eLife Sciences Publications. https://doi.org/10.7554/elife.30292
chicago: Helle, Sebastian Carsten Johannes, Qian Feng, Mathias J Aebersold, Luca
Hirt, Raphael R Grüter, Afshin Vahid, Andrea Sirianni, et al. “Mechanical Force
Induces Mitochondrial Fission.” ELife. eLife Sciences Publications, 2017.
https://doi.org/10.7554/elife.30292.
ieee: S. C. J. Helle et al., “Mechanical force induces mitochondrial fission,”
eLife, vol. 6. eLife Sciences Publications, 2017.
ista: Helle SCJ, Feng Q, Aebersold MJ, Hirt L, Grüter RR, Vahid A, Sirianni A, Mostowy
S, Snedeker JG, Šarić A, Idema T, Zambelli T, Kornmann B. 2017. Mechanical force
induces mitochondrial fission. eLife. 6, e30292.
mla: Helle, Sebastian Carsten Johannes, et al. “Mechanical Force Induces Mitochondrial
Fission.” ELife, vol. 6, e30292, eLife Sciences Publications, 2017, doi:10.7554/elife.30292.
short: S.C.J. Helle, Q. Feng, M.J. Aebersold, L. Hirt, R.R. Grüter, A. Vahid, A.
Sirianni, S. Mostowy, J.G. Snedeker, A. Šarić, T. Idema, T. Zambelli, B. Kornmann,
ELife 6 (2017).
date_created: 2021-11-29T08:51:38Z
date_published: 2017-11-09T00:00:00Z
date_updated: 2021-11-29T09:28:14Z
day: '09'
ddc:
- '572'
doi: 10.7554/elife.30292
extern: '1'
external_id:
pmid:
- '29119945'
file:
- access_level: open_access
checksum: c35f42dcfb007f6d6c761a27e24c26d3
content_type: application/pdf
creator: cchlebak
date_created: 2021-11-29T09:07:41Z
date_updated: 2021-11-29T09:07:41Z
file_id: '10372'
file_name: 2017_eLife_Helle.pdf
file_size: 6120157
relation: main_file
success: 1
file_date_updated: 2021-11-29T09:07:41Z
has_accepted_license: '1'
intvolume: ' 6'
keyword:
- general immunology and microbiology
- general biochemistry
- genetics and molecular biology
- general medicine
- general neuroscience
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://elifesciences.org/articles/30292
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Mechanical force induces mitochondrial fission
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: 8b945eb4-e2f2-11eb-945a-df72226e66a9
volume: 6
year: '2017'
...
---
_id: '12196'
abstract:
- lang: eng
text: SNC1 (SUPPRESSOR OF NPR1, CONSTITUTIVE 1) is one of a suite of intracellular
Arabidopsis NOD-like receptor (NLR) proteins which, upon activation, result in
the induction of defense responses. However, the molecular mechanisms underlying
NLR activation and the subsequent provocation of immune responses are only partially
characterized. To identify negative regulators of NLR-mediated immunity, a forward
genetic screen was undertaken to search for enhancers of the dwarf, autoimmune
gain-of-function snc1 mutant. To avoid lethality resulting from severe dwarfism,
the screen was conducted using mos4 (modifier of snc1, 4) snc1 plants, which display
wild-type-like morphology and resistance. M2 progeny were screened for mutant,
snc1-enhancing (muse) mutants displaying a reversion to snc1-like phenotypes.
The muse9 mos4 snc1 triple mutant was found to exhibit dwarf morphology, elevated
expression of the pPR2-GUS defense marker reporter gene and enhanced resistance
to the oomycete pathogen Hyaloperonospora arabidopsidis Noco2. Via map-based cloning
and Illumina sequencing, it was determined that the muse9 mutation is in the gene
encoding the SWI/SNF chromatin remodeler SYD (SPLAYED), and was thus renamed syd-10.
The syd-10 single mutant has no observable alteration from wild-type-like resistance,
although the syd-4 T-DNA insertion allele displays enhanced resistance to the
bacterial pathogen Pseudomonas syringae pv. maculicola ES4326. Transcription of
SNC1 is increased in both syd-4 and syd-10. These data suggest that SYD plays
a subtle, specific role in the regulation of SNC1 expression and SNC1-mediated
immunity. SYD may work with other proteins at the chromatin level to repress SNC1
transcription; such regulation is important for fine-tuning the expression of
NLR-encoding genes to prevent unpropitious autoimmunity.
acknowledgement: "This work was supported by the National Sciences and Engineering
Research Council of Canada [Canada Graduate\r\nScholarship–Doctoral to K.J.; Discovery
Grant to X.L.]; the department of Botany at the University of f British Columbia\r\n[the
Dewar Cooper Memorial Fund to X.L.].The authors would like to thank Dr. Yuelin Zhang
and Ms. Yan Li for their assistance with next-generation sequencing, and Mr. Charles
Copeland for critical reading of the manuscript."
article_processing_charge: No
article_type: original
author:
- first_name: Kaeli C.M.
full_name: Johnson, Kaeli C.M.
last_name: Johnson
- first_name: Shitou
full_name: Xia, Shitou
last_name: Xia
- first_name: Xiaoqi
full_name: Feng, Xiaoqi
id: e0164712-22ee-11ed-b12a-d80fcdf35958
last_name: Feng
orcid: 0000-0002-4008-1234
- first_name: Xin
full_name: Li, Xin
last_name: Li
citation:
ama: Johnson KCM, Xia S, Feng X, Li X. The chromatin remodeler SPLAYED negatively
regulates SNC1-mediated immunity. Plant and Cell Physiology. 2015;56(8):1616-1623.
doi:10.1093/pcp/pcv087
apa: Johnson, K. C. M., Xia, S., Feng, X., & Li, X. (2015). The chromatin remodeler
SPLAYED negatively regulates SNC1-mediated immunity. Plant and Cell Physiology.
Oxford University Press. https://doi.org/10.1093/pcp/pcv087
chicago: Johnson, Kaeli C.M., Shitou Xia, Xiaoqi Feng, and Xin Li. “The Chromatin
Remodeler SPLAYED Negatively Regulates SNC1-Mediated Immunity.” Plant and Cell
Physiology. Oxford University Press, 2015. https://doi.org/10.1093/pcp/pcv087.
ieee: K. C. M. Johnson, S. Xia, X. Feng, and X. Li, “The chromatin remodeler SPLAYED
negatively regulates SNC1-mediated immunity,” Plant and Cell Physiology,
vol. 56, no. 8. Oxford University Press, pp. 1616–1623, 2015.
ista: Johnson KCM, Xia S, Feng X, Li X. 2015. The chromatin remodeler SPLAYED negatively
regulates SNC1-mediated immunity. Plant and Cell Physiology. 56(8), 1616–1623.
mla: Johnson, Kaeli C. M., et al. “The Chromatin Remodeler SPLAYED Negatively Regulates
SNC1-Mediated Immunity.” Plant and Cell Physiology, vol. 56, no. 8, Oxford
University Press, 2015, pp. 1616–23, doi:10.1093/pcp/pcv087.
short: K.C.M. Johnson, S. Xia, X. Feng, X. Li, Plant and Cell Physiology 56 (2015)
1616–1623.
date_created: 2023-01-16T09:20:22Z
date_published: 2015-08-01T00:00:00Z
date_updated: 2023-05-08T11:03:23Z
department:
- _id: XiFe
doi: 10.1093/pcp/pcv087
extern: '1'
external_id:
pmid:
- '26063389'
intvolume: ' 56'
issue: '8'
keyword:
- Cell Biology
- Plant Science
- Physiology
- General Medicine
language:
- iso: eng
month: '08'
oa_version: None
page: 1616-1623
pmid: 1
publication: Plant and Cell Physiology
publication_identifier:
issn:
- 0032-0781
- 1471-9053
publication_status: published
publisher: Oxford University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: The chromatin remodeler SPLAYED negatively regulates SNC1-mediated immunity
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 56
year: '2015'
...
---
_id: '10814'
abstract:
- lang: eng
text: We review recent progress towards a rigorous understanding of the excitation
spectrum of bosonic quantum many-body systems. In particular, we explain how one
can rigorously establish the predictions resulting from the Bogoliubov approximation
in the mean field limit. The latter predicts that the spectrum is made up of elementary
excitations, whose energy behaves linearly in the momentum for small momentum.
This property is crucial for the superfluid behavior of the system. We also discuss
a list of open problems in this field.
article_processing_charge: No
article_type: original
author:
- first_name: Robert
full_name: Seiringer, Robert
id: 4AFD0470-F248-11E8-B48F-1D18A9856A87
last_name: Seiringer
orcid: 0000-0002-6781-0521
citation:
ama: Seiringer R. The excitation spectrum for Bose fluids with weak interactions.
Jahresbericht der Deutschen Mathematiker-Vereinigung. 2014;116:21-41. doi:10.1365/s13291-014-0083-9
apa: Seiringer, R. (2014). The excitation spectrum for Bose fluids with weak interactions.
Jahresbericht Der Deutschen Mathematiker-Vereinigung. Springer Nature.
https://doi.org/10.1365/s13291-014-0083-9
chicago: Seiringer, Robert. “The Excitation Spectrum for Bose Fluids with Weak Interactions.”
Jahresbericht Der Deutschen Mathematiker-Vereinigung. Springer Nature,
2014. https://doi.org/10.1365/s13291-014-0083-9.
ieee: R. Seiringer, “The excitation spectrum for Bose fluids with weak interactions,”
Jahresbericht der Deutschen Mathematiker-Vereinigung, vol. 116. Springer
Nature, pp. 21–41, 2014.
ista: Seiringer R. 2014. The excitation spectrum for Bose fluids with weak interactions.
Jahresbericht der Deutschen Mathematiker-Vereinigung. 116, 21–41.
mla: Seiringer, Robert. “The Excitation Spectrum for Bose Fluids with Weak Interactions.”
Jahresbericht Der Deutschen Mathematiker-Vereinigung, vol. 116, Springer
Nature, 2014, pp. 21–41, doi:10.1365/s13291-014-0083-9.
short: R. Seiringer, Jahresbericht Der Deutschen Mathematiker-Vereinigung 116 (2014)
21–41.
date_created: 2022-03-04T07:54:39Z
date_published: 2014-03-01T00:00:00Z
date_updated: 2023-09-05T14:19:47Z
day: '01'
department:
- _id: RoSe
doi: 10.1365/s13291-014-0083-9
intvolume: ' 116'
keyword:
- General Medicine
language:
- iso: eng
month: '03'
oa_version: None
page: 21-41
publication: Jahresbericht der Deutschen Mathematiker-Vereinigung
publication_identifier:
eissn:
- 1869-7135
issn:
- 0012-0456
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: The excitation spectrum for Bose fluids with weak interactions
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 116
year: '2014'
...
---
_id: '10815'
abstract:
- lang: eng
text: In the last several decades, developmental biology has clarified the molecular
mechanisms of embryogenesis and organogenesis. In particular, it has demonstrated
that the “tool-kit genes” essential for regulating developmental processes are
not only highly conserved among species, but are also used as systems at various
times and places in an organism to control distinct developmental events. Therefore,
mutations in many of these tool-kit genes may cause congenital diseases involving
morphological abnormalities. This link between genes and abnormal morphological
phenotypes underscores the importance of understanding how cells behave and contribute
to morphogenesis as a result of gene function. Recent improvements in live imaging
and in quantitative analyses of cellular dynamics will advance our understanding
of the cellular pathogenesis of congenital diseases associated with aberrant morphologies.
In these studies, it is critical to select an appropriate model organism for the
particular phenomenon of interest.
acknowledgement: The authors thank all the members of the Division of Morphogenesis,
National Institute for Basic Biology, for their contributions to the research, their
encouragement, and helpful discussions, particularly Dr M. Suzuki for his critical
reading of the manuscript. We also thank the Model Animal Research and Spectrography
and Bioimaging Facilities, NIBB Core Research Facilities, for technical support.
M.H. was supported by a research fellowship from the Japan Society for the Promotion
of Science (JSPS). Our work introduced in this review was supported by a Grant-in-Aid
for Scientific Research on Innovative Areas from the Ministry of Education, Culture,
Sports, Science, and Technology (MEXT), Japan, to N.U.
article_processing_charge: No
article_type: original
author:
- first_name: Masakazu
full_name: Hashimoto, Masakazu
last_name: Hashimoto
- first_name: Hitoshi
full_name: Morita, Hitoshi
id: 4C6E54C6-F248-11E8-B48F-1D18A9856A87
last_name: Morita
- first_name: Naoto
full_name: Ueno, Naoto
last_name: Ueno
citation:
ama: Hashimoto M, Morita H, Ueno N. Molecular and cellular mechanisms of development
underlying congenital diseases. Congenital Anomalies. 2014;54(1):1-7. doi:10.1111/cga.12039
apa: Hashimoto, M., Morita, H., & Ueno, N. (2014). Molecular and cellular mechanisms
of development underlying congenital diseases. Congenital Anomalies. Wiley.
https://doi.org/10.1111/cga.12039
chicago: Hashimoto, Masakazu, Hitoshi Morita, and Naoto Ueno. “Molecular and Cellular
Mechanisms of Development Underlying Congenital Diseases.” Congenital Anomalies.
Wiley, 2014. https://doi.org/10.1111/cga.12039.
ieee: M. Hashimoto, H. Morita, and N. Ueno, “Molecular and cellular mechanisms of
development underlying congenital diseases,” Congenital Anomalies, vol.
54, no. 1. Wiley, pp. 1–7, 2014.
ista: Hashimoto M, Morita H, Ueno N. 2014. Molecular and cellular mechanisms of
development underlying congenital diseases. Congenital Anomalies. 54(1), 1–7.
mla: Hashimoto, Masakazu, et al. “Molecular and Cellular Mechanisms of Development
Underlying Congenital Diseases.” Congenital Anomalies, vol. 54, no. 1,
Wiley, 2014, pp. 1–7, doi:10.1111/cga.12039.
short: M. Hashimoto, H. Morita, N. Ueno, Congenital Anomalies 54 (2014) 1–7.
date_created: 2022-03-04T08:17:25Z
date_published: 2014-02-01T00:00:00Z
date_updated: 2022-03-04T08:26:05Z
day: '01'
department:
- _id: CaHe
doi: 10.1111/cga.12039
external_id:
pmid:
- '24666178'
intvolume: ' 54'
issue: '1'
keyword:
- Developmental Biology
- Embryology
- General Medicine
- Pediatrics
- Perinatology
- and Child Health
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1111/cga.12039
month: '02'
oa: 1
oa_version: None
page: 1-7
pmid: 1
publication: Congenital Anomalies
publication_identifier:
issn:
- 0914-3505
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Molecular and cellular mechanisms of development underlying congenital diseases
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 54
year: '2014'
...