---
_id: '9607'
abstract:
- lang: eng
text: While high risk of failure is an inherent part of developing innovative therapies,
it can be reduced by adherence to evidence-based rigorous research practices.
Numerous analyses conducted to date have clearly identified measures that need
to be taken to improve research rigor. Supported through the European Union's
Innovative Medicines Initiative, the EQIPD consortium has developed a novel preclinical
research quality system that can be applied in both public and private sectors
and is free for anyone to use. The EQIPD Quality System was designed to be suited
to boost innovation by ensuring the generation of robust and reliable preclinical
data while being lean, effective and not becoming a burden that could negatively
impact the freedom to explore scientific questions. EQIPD defines research quality
as the extent to which research data are fit for their intended use. Fitness,
in this context, is defined by the stakeholders, who are the scientists directly
involved in the research, but also their funders, sponsors, publishers, research
tool manufacturers and collaboration partners such as peers in a multi-site research
project. The essence of the EQIPD Quality System is the set of 18 core requirements
that can be addressed flexibly, according to user-specific needs and following
a user-defined trajectory. The EQIPD Quality System proposes guidance on expectations
for quality-related measures, defines criteria for adequate processes (i.e., performance
standards) and provides examples of how such measures can be developed and implemented.
However, it does not prescribe any pre-determined solutions. EQIPD has also developed
tools (for optional use) to support users in implementing the system and assessment
services for those research units that successfully implement the quality system
and seek formal accreditation. Building upon the feedback from users and continuous
improvement, a sustainable EQIPD Quality System will ultimately serve the entire
community of scientists conducting non-regulated preclinical research, by helping
them generate reliable data that are fit for their intended use.
acknowledgement: This project has received funding from the Innovative Medicines Initiative
2 Joint Undertaking under grant agreement No 777364. This Joint Undertaking receives
support from the European Union’s Horizon 2020 research and innovation programme
and EFPIA. The authors are very grateful to Martin Heinrich (Abbvie, Ludwigshafen,
Germany) for the exceptional IT support and programming the EQIPD Planning Tool
and the Creator Tool and to Dr Shai Silberberg (NINDS, USA), Dr. Renza Roncarati
(PAASP Italy) and Dr Judith Homberg (Radboud University, Nijmegen) for highly stimulating
contributions to the discussions and comments on earlier versions of this manuscript.
We also wish to express our thanks to Dr. Sara Stöber (concentris research management
GmbH, Fürstenfeldbruck, Germany) for excellent and continuous support of this project.
Creation of the EQIPD Stakeholder group was supported by Noldus Information Technology
bv (Wageningen, the Netherlands).
article_processing_charge: No
article_type: original
author:
- first_name: Anton
full_name: Bespalov, Anton
last_name: Bespalov
- first_name: René
full_name: Bernard, René
last_name: Bernard
- first_name: Anja
full_name: Gilis, Anja
last_name: Gilis
- first_name: Björn
full_name: Gerlach, Björn
last_name: Gerlach
- first_name: Javier
full_name: Guillén, Javier
last_name: Guillén
- first_name: Vincent
full_name: Castagné, Vincent
last_name: Castagné
- first_name: Isabel A.
full_name: Lefevre, Isabel A.
last_name: Lefevre
- first_name: Fiona
full_name: Ducrey, Fiona
last_name: Ducrey
- first_name: Lee
full_name: Monk, Lee
last_name: Monk
- first_name: Sandrine
full_name: Bongiovanni, Sandrine
last_name: Bongiovanni
- first_name: Bruce
full_name: Altevogt, Bruce
last_name: Altevogt
- first_name: María
full_name: Arroyo-Araujo, María
last_name: Arroyo-Araujo
- first_name: Lior
full_name: Bikovski, Lior
last_name: Bikovski
- first_name: Natasja
full_name: De Bruin, Natasja
last_name: De Bruin
- first_name: Esmeralda
full_name: Castaños-Vélez, Esmeralda
last_name: Castaños-Vélez
- first_name: Alexander
full_name: Dityatev, Alexander
last_name: Dityatev
- first_name: Christoph H.
full_name: Emmerich, Christoph H.
last_name: Emmerich
- first_name: Raafat
full_name: Fares, Raafat
last_name: Fares
- first_name: Chantelle
full_name: Ferland-Beckham, Chantelle
last_name: Ferland-Beckham
- first_name: Christelle
full_name: Froger-Colléaux, Christelle
last_name: Froger-Colléaux
- first_name: Valerie
full_name: Gailus-Durner, Valerie
last_name: Gailus-Durner
- first_name: Sabine M.
full_name: Hölter, Sabine M.
last_name: Hölter
- first_name: Martine Cj
full_name: Hofmann, Martine Cj
last_name: Hofmann
- first_name: Patricia
full_name: Kabitzke, Patricia
last_name: Kabitzke
- first_name: Martien Jh
full_name: Kas, Martien Jh
last_name: Kas
- first_name: Claudia
full_name: Kurreck, Claudia
last_name: Kurreck
- first_name: Paul
full_name: Moser, Paul
last_name: Moser
- first_name: Malgorzata
full_name: Pietraszek, Malgorzata
last_name: Pietraszek
- first_name: Piotr
full_name: Popik, Piotr
last_name: Popik
- first_name: Heidrun
full_name: Potschka, Heidrun
last_name: Potschka
- first_name: Ernesto
full_name: Prado Montes De Oca, Ernesto
last_name: Prado Montes De Oca
- first_name: Leonardo
full_name: Restivo, Leonardo
last_name: Restivo
- first_name: Gernot
full_name: Riedel, Gernot
last_name: Riedel
- first_name: Merel
full_name: Ritskes-Hoitinga, Merel
last_name: Ritskes-Hoitinga
- first_name: Janko
full_name: Samardzic, Janko
last_name: Samardzic
- first_name: Michael
full_name: Schunn, Michael
id: 4272DB4A-F248-11E8-B48F-1D18A9856A87
last_name: Schunn
orcid: 0000-0003-4326-5300
- first_name: Claudia
full_name: Stöger, Claudia
last_name: Stöger
- first_name: Vootele
full_name: Voikar, Vootele
last_name: Voikar
- first_name: Jan
full_name: Vollert, Jan
last_name: Vollert
- first_name: Kimberley E.
full_name: Wever, Kimberley E.
last_name: Wever
- first_name: Kathleen
full_name: Wuyts, Kathleen
last_name: Wuyts
- first_name: Malcolm R.
full_name: Macleod, Malcolm R.
last_name: Macleod
- first_name: Ulrich
full_name: Dirnagl, Ulrich
last_name: Dirnagl
- first_name: Thomas
full_name: Steckler, Thomas
last_name: Steckler
citation:
ama: Bespalov A, Bernard R, Gilis A, et al. Introduction to the EQIPD quality system.
eLife. 2021;10. doi:10.7554/eLife.63294
apa: Bespalov, A., Bernard, R., Gilis, A., Gerlach, B., Guillén, J., Castagné, V.,
… Steckler, T. (2021). Introduction to the EQIPD quality system. ELife.
eLife Sciences Publications. https://doi.org/10.7554/eLife.63294
chicago: Bespalov, Anton, René Bernard, Anja Gilis, Björn Gerlach, Javier Guillén,
Vincent Castagné, Isabel A. Lefevre, et al. “Introduction to the EQIPD Quality
System.” ELife. eLife Sciences Publications, 2021. https://doi.org/10.7554/eLife.63294.
ieee: A. Bespalov et al., “Introduction to the EQIPD quality system,” eLife,
vol. 10. eLife Sciences Publications, 2021.
ista: Bespalov A, Bernard R, Gilis A, Gerlach B, Guillén J, Castagné V, Lefevre
IA, Ducrey F, Monk L, Bongiovanni S, Altevogt B, Arroyo-Araujo M, Bikovski L,
De Bruin N, Castaños-Vélez E, Dityatev A, Emmerich CH, Fares R, Ferland-Beckham
C, Froger-Colléaux C, Gailus-Durner V, Hölter SM, Hofmann MC, Kabitzke P, Kas
MJ, Kurreck C, Moser P, Pietraszek M, Popik P, Potschka H, Prado Montes De Oca
E, Restivo L, Riedel G, Ritskes-Hoitinga M, Samardzic J, Schunn M, Stöger C, Voikar
V, Vollert J, Wever KE, Wuyts K, Macleod MR, Dirnagl U, Steckler T. 2021. Introduction
to the EQIPD quality system. eLife. 10.
mla: Bespalov, Anton, et al. “Introduction to the EQIPD Quality System.” ELife,
vol. 10, eLife Sciences Publications, 2021, doi:10.7554/eLife.63294.
short: A. Bespalov, R. Bernard, A. Gilis, B. Gerlach, J. Guillén, V. Castagné, I.A.
Lefevre, F. Ducrey, L. Monk, S. Bongiovanni, B. Altevogt, M. Arroyo-Araujo, L.
Bikovski, N. De Bruin, E. Castaños-Vélez, A. Dityatev, C.H. Emmerich, R. Fares,
C. Ferland-Beckham, C. Froger-Colléaux, V. Gailus-Durner, S.M. Hölter, M.C. Hofmann,
P. Kabitzke, M.J. Kas, C. Kurreck, P. Moser, M. Pietraszek, P. Popik, H. Potschka,
E. Prado Montes De Oca, L. Restivo, G. Riedel, M. Ritskes-Hoitinga, J. Samardzic,
M. Schunn, C. Stöger, V. Voikar, J. Vollert, K.E. Wever, K. Wuyts, M.R. Macleod,
U. Dirnagl, T. Steckler, ELife 10 (2021).
date_created: 2021-06-27T22:01:49Z
date_published: 2021-05-24T00:00:00Z
date_updated: 2026-04-02T13:55:57Z
day: '24'
ddc:
- '570'
department:
- _id: PreCl
doi: 10.7554/eLife.63294
external_id:
isi:
- '000661272000001'
pmid:
- '34028353'
file:
- access_level: open_access
checksum: 885b746051a7a6b6e24e3d2781a48fde
content_type: application/pdf
creator: asandaue
date_created: 2021-06-28T11:35:30Z
date_updated: 2021-06-28T11:35:30Z
file_id: '9609'
file_name: 2021_ELife_Bespalov.pdf
file_size: 2500720
relation: main_file
success: 1
file_date_updated: 2021-06-28T11:35:30Z
has_accepted_license: '1'
intvolume: ' 10'
isi: 1
language:
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license: https://creativecommons.org/licenses/by/4.0/
month: '05'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Introduction to the EQIPD quality system
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: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 10
year: '2021'
...
---
_id: '9244'
abstract:
- lang: eng
text: 'Organ function depends on tissues adopting the correct architecture. However,
insights into organ architecture are currently hampered by an absence of standardized
quantitative 3D analysis. We aimed to develop a robust technology to visualize,
digitalize, and segment the architecture of two tubular systems in 3D: double
resin casting micro computed tomography (DUCT). As proof of principle, we applied
DUCT to a mouse model for Alagille syndrome (Jag1Ndr/Ndr mice), characterized
by intrahepatic bile duct paucity, that can spontaneously generate a biliary system
in adulthood. DUCT identified increased central biliary branching and peripheral
bile duct tortuosity as two compensatory processes occurring in distinct regions
of Jag1Ndr/Ndr liver, leading to full reconstitution of wild-type biliary volume
and phenotypic recovery. DUCT is thus a powerful new technology for 3D analysis,
which can reveal novel phenotypes and provide a standardized method of defining
liver architecture in mouse models.'
acknowledgement: "Work in ERA lab is supported by the Swedish Research Council, the
Center of Innovative Medicine (CIMED) Grant, Karolinska Institutet, and the Heart
and Lung Foundation, and\r\nthe Daniel Alagille Award from the European Association
for the Study of the Liver. One project in ERA lab is funded by ModeRNA, unrelated
to this project. The funders have no role in the design or interpretation of the
work. SH has been supported by a KI-MU PhD student program, and by a Wera Ekstro¨m
Foundation Scholarship. We are grateful for support from Tornspiran foundation to
NVH. JK: This research was carried out under the project CEITEC 2020 (LQ1601) with
financial support from the Ministry of Education, Youth and Sports of the Czech
Republic under the National Sustainability Programme II and CzechNanoLab Research
Infrastructure supported by MEYS CR (LM2018110) . UL: The financial support from
the Swedish Research Council and ICMC (Integrated CardioMetabolic Center) is acknowledged.
JJ: The work was supported by the Grant Agency of Masaryk University (project no.
MUNI/A/1565/2018). We thank Kari Huppert and Stacey Huppert for their expertise
and help regarding bile duct cannulation and their laboratory hospitality. We also
thank Nadja Schultz and Charlotte L Mattsson for their help with common bile duct
cannulation. We thank Daniel Holl for his help with trachea cannulation. We thank
Nikos Papadogiannakis for his assistance with mild Alagille biopsy samples and discussion.
We thank Karolinska Biomedicum Imaging Core, especially Shigeaki Kanatani for his
help with image analysis. We thank Jan Masek and Carolina Gutierrez for their scientific
input in manuscript writing. We thank Peter Ranefall and the BioImage Informatics
(SciLife national facility) for their help writing parts of the MATLAB pipeline.\r\nThe
TROMA-III antibody developed by Rolf Kemler was obtained from the Developmental
Studies Hybridoma (DSHB) Bank developed under the auspices of NICHD and maintained
by The University of Iowa, Department of Biological Sciences, Iowa City, IA52242.
We thank Goncalo M Brito for all illustrations. This work was supported by the European
Union (European Research Council Starting grant 851288 to E.H.)."
article_number: e60916
article_processing_charge: No
article_type: original
author:
- first_name: Simona
full_name: Hankeova, Simona
last_name: Hankeova
- first_name: Jakub
full_name: Salplachta, Jakub
last_name: Salplachta
- first_name: Tomas
full_name: Zikmund, Tomas
last_name: Zikmund
- first_name: Michaela
full_name: Kavkova, Michaela
last_name: Kavkova
- first_name: Noémi
full_name: Van Hul, Noémi
last_name: Van Hul
- first_name: Adam
full_name: Brinek, Adam
last_name: Brinek
- first_name: Veronika
full_name: Smekalova, Veronika
last_name: Smekalova
- first_name: Jakub
full_name: Laznovsky, Jakub
last_name: Laznovsky
- first_name: Feven
full_name: Dawit, Feven
last_name: Dawit
- first_name: Josef
full_name: Jaros, Josef
last_name: Jaros
- first_name: Vítězslav
full_name: Bryja, Vítězslav
last_name: Bryja
- first_name: Urban
full_name: Lendahl, Urban
last_name: Lendahl
- first_name: Ewa
full_name: Ellis, Ewa
last_name: Ellis
- first_name: Antal
full_name: Nemeth, Antal
last_name: Nemeth
- first_name: Björn
full_name: Fischler, Björn
last_name: Fischler
- first_name: Edouard B
full_name: Hannezo, Edouard B
id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
last_name: Hannezo
orcid: 0000-0001-6005-1561
- first_name: Jozef
full_name: Kaiser, Jozef
last_name: Kaiser
- first_name: Emma Rachel
full_name: Andersson, Emma Rachel
last_name: Andersson
citation:
ama: Hankeova S, Salplachta J, Zikmund T, et al. DUCT reveals architectural mechanisms
contributing to bile duct recovery in a mouse model for alagille syndrome. eLife.
2021;10. doi:10.7554/eLife.60916
apa: Hankeova, S., Salplachta, J., Zikmund, T., Kavkova, M., Van Hul, N., Brinek,
A., … Andersson, E. R. (2021). DUCT reveals architectural mechanisms contributing
to bile duct recovery in a mouse model for alagille syndrome. ELife. eLife
Sciences Publications. https://doi.org/10.7554/eLife.60916
chicago: Hankeova, Simona, Jakub Salplachta, Tomas Zikmund, Michaela Kavkova, Noémi
Van Hul, Adam Brinek, Veronika Smekalova, et al. “DUCT Reveals Architectural Mechanisms
Contributing to Bile Duct Recovery in a Mouse Model for Alagille Syndrome.” ELife.
eLife Sciences Publications, 2021. https://doi.org/10.7554/eLife.60916.
ieee: S. Hankeova et al., “DUCT reveals architectural mechanisms contributing
to bile duct recovery in a mouse model for alagille syndrome,” eLife, vol.
10. eLife Sciences Publications, 2021.
ista: Hankeova S, Salplachta J, Zikmund T, Kavkova M, Van Hul N, Brinek A, Smekalova
V, Laznovsky J, Dawit F, Jaros J, Bryja V, Lendahl U, Ellis E, Nemeth A, Fischler
B, Hannezo EB, Kaiser J, Andersson ER. 2021. DUCT reveals architectural mechanisms
contributing to bile duct recovery in a mouse model for alagille syndrome. eLife.
10, e60916.
mla: Hankeova, Simona, et al. “DUCT Reveals Architectural Mechanisms Contributing
to Bile Duct Recovery in a Mouse Model for Alagille Syndrome.” ELife, vol.
10, e60916, eLife Sciences Publications, 2021, doi:10.7554/eLife.60916.
short: S. Hankeova, J. Salplachta, T. Zikmund, M. Kavkova, N. Van Hul, A. Brinek,
V. Smekalova, J. Laznovsky, F. Dawit, J. Jaros, V. Bryja, U. Lendahl, E. Ellis,
A. Nemeth, B. Fischler, E.B. Hannezo, J. Kaiser, E.R. Andersson, ELife 10 (2021).
date_created: 2021-03-14T23:01:34Z
date_published: 2021-02-26T00:00:00Z
date_updated: 2026-04-02T14:00:00Z
day: '26'
ddc:
- '570'
department:
- _id: EdHa
doi: 10.7554/eLife.60916
ec_funded: 1
external_id:
isi:
- '000625357100001'
pmid:
- '33635272'
file:
- access_level: open_access
checksum: 20ccf4dfe46c48cf986794c8bf4fd1cb
content_type: application/pdf
creator: dernst
date_created: 2021-03-22T08:50:33Z
date_updated: 2021-03-22T08:50:33Z
file_id: '9271'
file_name: 2021_eLife_Hankeova.pdf
file_size: 9259690
relation: main_file
success: 1
file_date_updated: 2021-03-22T08:50:33Z
has_accepted_license: '1'
intvolume: ' 10'
isi: 1
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 05943252-7A3F-11EA-A408-12923DDC885E
call_identifier: H2020
grant_number: '851288'
name: Design Principles of Branching Morphogenesis
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: DUCT reveals architectural mechanisms contributing to bile duct recovery in
a mouse model for alagille 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: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 10
year: '2021'
...
---
_id: '9437'
abstract:
- lang: eng
text: The synaptic connection from medial habenula (MHb) to interpeduncular nucleus
(IPN) is critical for emotion-related behaviors and uniquely expresses R-type
Ca2+ channels (Cav2.3) and auxiliary GABAB receptor (GBR) subunits, the K+-channel
tetramerization domain-containing proteins (KCTDs). Activation of GBRs facilitates
or inhibits transmitter release from MHb terminals depending on the IPN subnucleus,
but the role of KCTDs is unknown. We therefore examined the localization and function
of Cav2.3, GBRs, and KCTDs in this pathway in mice. We show in heterologous cells
that KCTD8 and KCTD12b directly bind to Cav2.3 and that KCTD8 potentiates Cav2.3
currents in the absence of GBRs. In the rostral IPN, KCTD8, KCTD12b, and Cav2.3
co-localize at the presynaptic active zone. Genetic deletion indicated a bidirectional
modulation of Cav2.3-mediated release by these KCTDs with a compensatory increase
of KCTD8 in the active zone in KCTD12b-deficient mice. The interaction of Cav2.3
with KCTDs therefore scales synaptic strength independent of GBR activation.
acknowledgement: We are grateful to Akari Hagiwara and Toshihisa Ohtsuka for CAST
antibody, and Masahiko Watanabe for neurexin antibody. We thank David Adams for
kindly providing the stable Cav2.3 cell line. Cav2.3 KO mice were kindly provided
by Tsutomu Tanabe. This project has received funding from the European Research
Council (ERC) and European Commission (EC), under the European Union’s Horizon 2020
research and innovation programme (ERC grant agreement no. 694539 to Ryuichi Shigemoto,
no. 692692 to Peter Jonas, and the Marie Skłodowska-Curie grant agreement no. 665385
to Cihan Önal), the Swiss National Science Foundation Grant 31003A-172881 to Bernhard
Bettler and Deutsche Forschungsgemeinschaft (For 2143) and BIOSS-2 to Akos Kulik.
article_number: e68274
article_processing_charge: No
article_type: original
author:
- first_name: Pradeep
full_name: Bhandari, Pradeep
id: 45EDD1BC-F248-11E8-B48F-1D18A9856A87
last_name: Bhandari
orcid: 0000-0003-0863-4481
- first_name: David H
full_name: Vandael, David H
id: 3AE48E0A-F248-11E8-B48F-1D18A9856A87
last_name: Vandael
orcid: 0000-0001-7577-1676
- first_name: Diego
full_name: Fernández-Fernández, Diego
last_name: Fernández-Fernández
- first_name: Thorsten
full_name: Fritzius, Thorsten
last_name: Fritzius
- first_name: David
full_name: Kleindienst, David
id: 42E121A4-F248-11E8-B48F-1D18A9856A87
last_name: Kleindienst
- first_name: Hüseyin C
full_name: Önal, Hüseyin C
id: 4659D740-F248-11E8-B48F-1D18A9856A87
last_name: Önal
orcid: 0000-0002-2771-2011
- first_name: Jacqueline-Claire
full_name: Montanaro-Punzengruber, Jacqueline-Claire
id: 3786AB44-F248-11E8-B48F-1D18A9856A87
last_name: Montanaro-Punzengruber
- first_name: Martin
full_name: Gassmann, Martin
last_name: Gassmann
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
- first_name: Akos
full_name: Kulik, Akos
last_name: Kulik
- first_name: Bernhard
full_name: Bettler, Bernhard
last_name: Bettler
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Peter
full_name: Koppensteiner, Peter
id: 3B8B25A8-F248-11E8-B48F-1D18A9856A87
last_name: Koppensteiner
orcid: 0000-0002-3509-1948
citation:
ama: Bhandari P, Vandael DH, Fernández-Fernández D, et al. GABAB receptor auxiliary
subunits modulate Cav2.3-mediated release from medial habenula terminals. eLife.
2021;10. doi:10.7554/ELIFE.68274
apa: Bhandari, P., Vandael, D. H., Fernández-Fernández, D., Fritzius, T., Kleindienst,
D., Önal, C., … Koppensteiner, P. (2021). GABAB receptor auxiliary subunits modulate
Cav2.3-mediated release from medial habenula terminals. ELife. eLife Sciences
Publications. https://doi.org/10.7554/ELIFE.68274
chicago: Bhandari, Pradeep, David H Vandael, Diego Fernández-Fernández, Thorsten
Fritzius, David Kleindienst, Cihan Önal, Jacqueline-Claire Montanaro-Punzengruber,
et al. “GABAB Receptor Auxiliary Subunits Modulate Cav2.3-Mediated Release from
Medial Habenula Terminals.” ELife. eLife Sciences Publications, 2021. https://doi.org/10.7554/ELIFE.68274.
ieee: P. Bhandari et al., “GABAB receptor auxiliary subunits modulate Cav2.3-mediated
release from medial habenula terminals,” eLife, vol. 10. eLife Sciences
Publications, 2021.
ista: Bhandari P, Vandael DH, Fernández-Fernández D, Fritzius T, Kleindienst D,
Önal C, Montanaro-Punzengruber J-C, Gassmann M, Jonas PM, Kulik A, Bettler B,
Shigemoto R, Koppensteiner P. 2021. GABAB receptor auxiliary subunits modulate
Cav2.3-mediated release from medial habenula terminals. eLife. 10, e68274.
mla: Bhandari, Pradeep, et al. “GABAB Receptor Auxiliary Subunits Modulate Cav2.3-Mediated
Release from Medial Habenula Terminals.” ELife, vol. 10, e68274, eLife
Sciences Publications, 2021, doi:10.7554/ELIFE.68274.
short: P. Bhandari, D.H. Vandael, D. Fernández-Fernández, T. Fritzius, D. Kleindienst,
C. Önal, J.-C. Montanaro-Punzengruber, M. Gassmann, P.M. Jonas, A. Kulik, B. Bettler,
R. Shigemoto, P. Koppensteiner, ELife 10 (2021).
date_created: 2021-05-30T22:01:23Z
date_published: 2021-04-29T00:00:00Z
date_updated: 2026-04-30T22:30:40Z
day: '29'
ddc:
- '570'
department:
- _id: RySh
- _id: PeJo
doi: 10.7554/ELIFE.68274
ec_funded: 1
external_id:
isi:
- '000651761700001'
pmid:
- '33913808'
file:
- access_level: open_access
checksum: 6ebcb79999f889766f7cd79ee134ad28
content_type: application/pdf
creator: cziletti
date_created: 2021-05-31T09:43:09Z
date_updated: 2021-05-31T09:43:09Z
file_id: '9440'
file_name: 2021_eLife_Bhandari.pdf
file_size: 8174719
relation: main_file
success: 1
file_date_updated: 2021-05-31T09:43:09Z
has_accepted_license: '1'
intvolume: ' 10'
isi: 1
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 25CA28EA-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '694539'
name: 'In situ analysis of single channel subunit composition in neurons: physiological
implication in synaptic plasticity and behaviour'
- _id: 25B7EB9E-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '692692'
name: Biophysics and circuit function of a giant cortical glutamatergic synapse
- _id: 2564DBCA-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '665385'
name: International IST Doctoral Program
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
related_material:
link:
- relation: earlier_version
url: https://doi.org/10.1101/2020.04.16.045112
record:
- id: '19271'
relation: dissertation_contains
status: public
- id: '9562'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: GABAB receptor auxiliary subunits modulate Cav2.3-mediated release from medial
habenula terminals
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: 10
year: '2021'
...
---
_id: '8127'
abstract:
- lang: eng
text: Mechanistic modeling in neuroscience aims to explain observed phenomena in
terms of underlying causes. However, determining which model parameters agree
with complex and stochastic neural data presents a significant challenge. We address
this challenge with a machine learning tool which uses deep neural density estimators—trained
using model simulations—to carry out Bayesian inference and retrieve the full
space of parameters compatible with raw data or selected data features. Our method
is scalable in parameters and data features and can rapidly analyze new data after
initial training. We demonstrate the power and flexibility of our approach on
receptive fields, ion channels, and Hodgkin–Huxley models. We also characterize
the space of circuit configurations giving rise to rhythmic activity in the crustacean
stomatogastric ganglion, and use these results to derive hypotheses for underlying
compensation mechanisms. Our approach will help close the gap between data-driven
and theory-driven models of neural dynamics.
acknowledgement: We thank Mahmood S Hoseini and Michael Stryker for sharing their
data for Figure 2, and Philipp Berens, Sean Bittner, Jan Boelts, John Cunningham,
Richard Gao, Scott Linderman, Eve Marder, Iain Murray, George Papamakarios, Astrid
Prinz, Auguste Schulz and Srinivas Turaga for discussions and/or comments on the
manuscript. This work was supported by the German Research Foundation (DFG) through
SFB 1233 ‘Robust Vision’, (276693517), SFB 1089 ‘Synaptic Microcircuits’, SPP 2041
‘Computational Connectomics’ and Germany's Excellence Strategy – EXC-Number 2064/1
– Project number 390727645 and the German Federal Ministry of Education and Research
(BMBF, project ‘ADIMEM’, FKZ 01IS18052 A-D) to JHM, a Sir Henry Dale Fellowship
by the Wellcome Trust and the Royal Society (WT100000; WFP and TPV), a Wellcome
Trust Senior Research Fellowship (214316/Z/18/Z; TPV), a ERC Consolidator Grant
(SYNAPSEEK; WPF and CC), and a UK Research and Innovation, Biotechnology and Biological
Sciences Research Council (CC, UKRI-BBSRC BB/N019512/1). We gratefully acknowledge
the Leibniz Supercomputing Centre for funding this project by providing computing
time on its Linux-Cluster.
article_number: e56261
article_processing_charge: No
article_type: original
author:
- first_name: Pedro J.
full_name: Gonçalves, Pedro J.
last_name: Gonçalves
orcid: 0000-0002-6987-4836
- first_name: Jan-Matthis
full_name: Lueckmann, Jan-Matthis
last_name: Lueckmann
orcid: 0000-0003-4320-4663
- first_name: Michael
full_name: Deistler, Michael
last_name: Deistler
orcid: 0000-0002-3573-0404
- first_name: Marcel
full_name: Nonnenmacher, Marcel
last_name: Nonnenmacher
orcid: 0000-0001-6044-6627
- first_name: Kaan
full_name: Öcal, Kaan
last_name: Öcal
orcid: 0000-0002-8528-6858
- first_name: Giacomo
full_name: Bassetto, Giacomo
last_name: Bassetto
- first_name: Chaitanya
full_name: Chintaluri, Chaitanya
id: BA06AFEE-A4BA-11EA-AE5C-14673DDC885E
last_name: Chintaluri
orcid: 0000-0003-4252-1608
- first_name: William F.
full_name: Podlaski, William F.
last_name: Podlaski
orcid: 0000-0001-6619-7502
- first_name: Sara A.
full_name: Haddad, Sara A.
last_name: Haddad
orcid: 0000-0003-0807-0823
- first_name: Tim P
full_name: Vogels, Tim P
id: CB6FF8D2-008F-11EA-8E08-2637E6697425
last_name: Vogels
orcid: 0000-0003-3295-6181
- first_name: David S.
full_name: Greenberg, David S.
last_name: Greenberg
- first_name: Jakob H.
full_name: Macke, Jakob H.
last_name: Macke
orcid: 0000-0001-5154-8912
citation:
ama: Gonçalves PJ, Lueckmann J-M, Deistler M, et al. Training deep neural density
estimators to identify mechanistic models of neural dynamics. eLife. 2020;9.
doi:10.7554/eLife.56261
apa: Gonçalves, P. J., Lueckmann, J.-M., Deistler, M., Nonnenmacher, M., Öcal, K.,
Bassetto, G., … Macke, J. H. (2020). Training deep neural density estimators to
identify mechanistic models of neural dynamics. ELife. eLife Sciences Publications.
https://doi.org/10.7554/eLife.56261
chicago: Gonçalves, Pedro J., Jan-Matthis Lueckmann, Michael Deistler, Marcel Nonnenmacher,
Kaan Öcal, Giacomo Bassetto, Chaitanya Chintaluri, et al. “Training Deep Neural
Density Estimators to Identify Mechanistic Models of Neural Dynamics.” ELife.
eLife Sciences Publications, 2020. https://doi.org/10.7554/eLife.56261.
ieee: P. J. Gonçalves et al., “Training deep neural density estimators to
identify mechanistic models of neural dynamics,” eLife, vol. 9. eLife Sciences
Publications, 2020.
ista: Gonçalves PJ, Lueckmann J-M, Deistler M, Nonnenmacher M, Öcal K, Bassetto
G, Chintaluri C, Podlaski WF, Haddad SA, Vogels TP, Greenberg DS, Macke JH. 2020.
Training deep neural density estimators to identify mechanistic models of neural
dynamics. eLife. 9, e56261.
mla: Gonçalves, Pedro J., et al. “Training Deep Neural Density Estimators to Identify
Mechanistic Models of Neural Dynamics.” ELife, vol. 9, e56261, eLife Sciences
Publications, 2020, doi:10.7554/eLife.56261.
short: P.J. Gonçalves, J.-M. Lueckmann, M. Deistler, M. Nonnenmacher, K. Öcal, G.
Bassetto, C. Chintaluri, W.F. Podlaski, S.A. Haddad, T.P. Vogels, D.S. Greenberg,
J.H. Macke, ELife 9 (2020).
date_created: 2020-07-16T12:26:04Z
date_published: 2020-09-17T00:00:00Z
date_updated: 2025-04-14T07:54:31Z
day: '17'
ddc:
- '570'
department:
- _id: TiVo
doi: 10.7554/eLife.56261
ec_funded: 1
external_id:
isi:
- '000584989400001'
pmid:
- '32940606'
file:
- access_level: open_access
checksum: c4300ddcd93ed03fc9c6cdf1f77890be
content_type: application/pdf
creator: cziletti
date_created: 2020-10-27T11:37:32Z
date_updated: 2020-10-27T11:37:32Z
file_id: '8709'
file_name: 2020_eLife_Gonçalves.pdf
file_size: 17355867
relation: main_file
success: 1
file_date_updated: 2020-10-27T11:37:32Z
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 0aacfa84-070f-11eb-9043-d7eb2c709234
call_identifier: H2020
grant_number: '819603'
name: Learning the shape of synaptic plasticity rules for neuronal architectures
and function through machine learning.
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Training deep neural density estimators to identify mechanistic models of neural
dynamics
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: 9
year: '2020'
...
---
_id: '7490'
abstract:
- lang: eng
text: In plants, clathrin mediated endocytosis (CME) represents the major route
for cargo internalisation from the cell surface. It has been assumed to operate
in an evolutionary conserved manner as in yeast and animals. Here we report characterisation
of ultrastructure, dynamics and mechanisms of plant CME as allowed by our advancement
in electron microscopy and quantitative live imaging techniques. Arabidopsis CME
appears to follow the constant curvature model and the bona fide CME population
generates vesicles of a predominantly hexagonal-basket type; larger and with faster
kinetics than in other models. Contrary to the existing paradigm, actin is dispensable
for CME events at the plasma membrane but plays a unique role in collecting endocytic
vesicles, sorting of internalised cargos and directional endosome movement that
itself actively promote CME events. Internalized vesicles display a strongly delayed
and sequential uncoating. These unique features highlight the independent evolution
of the plant CME mechanism during the autonomous rise of multicellularity in eukaryotes.
acknowledged_ssus:
- _id: LifeSc
- _id: Bio
- _id: EM-Fac
article_number: e52067
article_processing_charge: No
article_type: original
author:
- first_name: Madhumitha
full_name: Narasimhan, Madhumitha
id: 44BF24D0-F248-11E8-B48F-1D18A9856A87
last_name: Narasimhan
orcid: 0000-0002-8600-0671
- first_name: Alexander J
full_name: Johnson, Alexander J
id: 46A62C3A-F248-11E8-B48F-1D18A9856A87
last_name: Johnson
orcid: 0000-0002-2739-8843
- first_name: Roshan
full_name: Prizak, Roshan
id: 4456104E-F248-11E8-B48F-1D18A9856A87
last_name: Prizak
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Shutang
full_name: Tan, Shutang
id: 2DE75584-F248-11E8-B48F-1D18A9856A87
last_name: Tan
orcid: 0000-0002-0471-8285
- first_name: Barbara E
full_name: Casillas Perez, Barbara E
id: 351ED2AA-F248-11E8-B48F-1D18A9856A87
last_name: Casillas Perez
- first_name: Jiří
full_name: Friml, Jiří
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
citation:
ama: Narasimhan M, Johnson AJ, Prizak R, et al. Evolutionarily unique mechanistic
framework of clathrin-mediated endocytosis in plants. eLife. 2020;9. doi:10.7554/eLife.52067
apa: Narasimhan, M., Johnson, A. J., Prizak, R., Kaufmann, W., Tan, S., Casillas
Perez, B. E., & Friml, J. (2020). Evolutionarily unique mechanistic framework
of clathrin-mediated endocytosis in plants. ELife. eLife Sciences Publications.
https://doi.org/10.7554/eLife.52067
chicago: Narasimhan, Madhumitha, Alexander J Johnson, Roshan Prizak, Walter Kaufmann,
Shutang Tan, Barbara E Casillas Perez, and Jiří Friml. “Evolutionarily Unique
Mechanistic Framework of Clathrin-Mediated Endocytosis in Plants.” ELife.
eLife Sciences Publications, 2020. https://doi.org/10.7554/eLife.52067.
ieee: M. Narasimhan et al., “Evolutionarily unique mechanistic framework
of clathrin-mediated endocytosis in plants,” eLife, vol. 9. eLife Sciences
Publications, 2020.
ista: Narasimhan M, Johnson AJ, Prizak R, Kaufmann W, Tan S, Casillas Perez BE,
Friml J. 2020. Evolutionarily unique mechanistic framework of clathrin-mediated
endocytosis in plants. eLife. 9, e52067.
mla: Narasimhan, Madhumitha, et al. “Evolutionarily Unique Mechanistic Framework
of Clathrin-Mediated Endocytosis in Plants.” ELife, vol. 9, e52067, eLife
Sciences Publications, 2020, doi:10.7554/eLife.52067.
short: M. Narasimhan, A.J. Johnson, R. Prizak, W. Kaufmann, S. Tan, B.E. Casillas
Perez, J. Friml, ELife 9 (2020).
date_created: 2020-02-16T23:00:50Z
date_published: 2020-01-23T00:00:00Z
date_updated: 2025-04-14T07:45:03Z
day: '23'
ddc:
- '570'
- '580'
department:
- _id: JiFr
- _id: GaTk
- _id: EM-Fac
- _id: SyCr
doi: 10.7554/eLife.52067
ec_funded: 1
external_id:
isi:
- '000514104100001'
pmid:
- '31971511'
file:
- access_level: open_access
checksum: 2052daa4be5019534f3a42f200a09f32
content_type: application/pdf
creator: dernst
date_created: 2020-02-18T07:21:16Z
date_updated: 2020-07-14T12:47:59Z
file_id: '7494'
file_name: 2020_eLife_Narasimhan.pdf
file_size: 7247468
relation: main_file
file_date_updated: 2020-07-14T12:47:59Z
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
language:
- iso: eng
month: '01'
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
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Evolutionarily unique mechanistic framework of clathrin-mediated endocytosis
in plants
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: 9
year: '2020'
...
---
_id: '7878'
abstract:
- lang: eng
text: Type 1 metabotropic glutamate receptors (mGluR1s) are key elements in neuronal
signaling. While their function is well documented in slices, requirements for
their activation in vivo are poorly understood. We examine this question in adult
mice in vivo using 2-photon imaging of cerebellar molecular layer interneurons
(MLIs) expressing GCaMP. In anesthetized mice, parallel fiber activation evokes
beam-like Cai rises in postsynaptic MLIs which depend on co-activation of mGluR1s
and ionotropic glutamate receptors (iGluRs). In awake mice, blocking mGluR1 decreases
Cai rises associated with locomotion. In vitro studies and freeze-fracture electron
microscopy show that the iGluR-mGluR1 interaction is synergistic and favored by
close association of the two classes of receptors. Altogether our results suggest
that mGluR1s, acting in synergy with iGluRs, potently contribute to processing
cerebellar neuronal signaling under physiological conditions.
article_number: e56839
article_processing_charge: No
article_type: original
author:
- first_name: Jin
full_name: Bao, Jin
last_name: Bao
- first_name: Michael
full_name: Graupner, Michael
last_name: Graupner
- first_name: Guadalupe
full_name: Astorga, Guadalupe
last_name: Astorga
- first_name: Thibault
full_name: Collin, Thibault
last_name: Collin
- first_name: Abdelali
full_name: Jalil, Abdelali
last_name: Jalil
- first_name: Dwi Wahyu
full_name: Indriati, Dwi Wahyu
last_name: Indriati
- first_name: Jonathan
full_name: Bradley, Jonathan
last_name: Bradley
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Isabel
full_name: Llano, Isabel
last_name: Llano
citation:
ama: Bao J, Graupner M, Astorga G, et al. Synergism of type 1 metabotropic and ionotropic
glutamate receptors in cerebellar molecular layer interneurons in vivo. eLife.
2020;9. doi:10.7554/eLife.56839
apa: Bao, J., Graupner, M., Astorga, G., Collin, T., Jalil, A., Indriati, D. W.,
… Llano, I. (2020). Synergism of type 1 metabotropic and ionotropic glutamate
receptors in cerebellar molecular layer interneurons in vivo. ELife. eLife
Sciences Publications. https://doi.org/10.7554/eLife.56839
chicago: Bao, Jin, Michael Graupner, Guadalupe Astorga, Thibault Collin, Abdelali
Jalil, Dwi Wahyu Indriati, Jonathan Bradley, Ryuichi Shigemoto, and Isabel Llano.
“Synergism of Type 1 Metabotropic and Ionotropic Glutamate Receptors in Cerebellar
Molecular Layer Interneurons in Vivo.” ELife. eLife Sciences Publications,
2020. https://doi.org/10.7554/eLife.56839.
ieee: J. Bao et al., “Synergism of type 1 metabotropic and ionotropic glutamate
receptors in cerebellar molecular layer interneurons in vivo,” eLife, vol.
9. eLife Sciences Publications, 2020.
ista: Bao J, Graupner M, Astorga G, Collin T, Jalil A, Indriati DW, Bradley J, Shigemoto
R, Llano I. 2020. Synergism of type 1 metabotropic and ionotropic glutamate receptors
in cerebellar molecular layer interneurons in vivo. eLife. 9, e56839.
mla: Bao, Jin, et al. “Synergism of Type 1 Metabotropic and Ionotropic Glutamate
Receptors in Cerebellar Molecular Layer Interneurons in Vivo.” ELife, vol.
9, e56839, eLife Sciences Publications, 2020, doi:10.7554/eLife.56839.
short: J. Bao, M. Graupner, G. Astorga, T. Collin, A. Jalil, D.W. Indriati, J. Bradley,
R. Shigemoto, I. Llano, ELife 9 (2020).
date_created: 2020-05-24T22:00:58Z
date_published: 2020-05-13T00:00:00Z
date_updated: 2026-04-02T14:28:17Z
day: '13'
ddc:
- '570'
department:
- _id: RySh
doi: 10.7554/eLife.56839
external_id:
isi:
- '000535191600001'
pmid:
- '32401196'
file:
- access_level: open_access
checksum: 8ea99bb6660cc407dbdb00c173b01683
content_type: application/pdf
creator: dernst
date_created: 2020-05-26T09:34:54Z
date_updated: 2020-07-14T12:48:04Z
file_id: '7891'
file_name: 2020_eLife_Bao.pdf
file_size: 4832050
relation: main_file
file_date_updated: 2020-07-14T12:48:04Z
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Synergism of type 1 metabotropic and ionotropic glutamate receptors in cerebellar
molecular layer interneurons in vivo
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: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 9
year: '2020'
...
---
_id: '7909'
abstract:
- lang: eng
text: Cell migration entails networks and bundles of actin filaments termed lamellipodia
and microspikes or filopodia, respectively, as well as focal adhesions, all of
which recruit Ena/VASP family members hitherto thought to antagonize efficient
cell motility. However, we find these proteins to act as positive regulators of
migration in different murine cell lines. CRISPR/Cas9-mediated loss of Ena/VASP
proteins reduced lamellipodial actin assembly and perturbed lamellipodial architecture,
as evidenced by changed network geometry as well as reduction of filament length
and number that was accompanied by abnormal Arp2/3 complex and heterodimeric capping
protein accumulation. Loss of Ena/VASP function also abolished the formation of
microspikes normally embedded in lamellipodia, but not of filopodia capable of
emanating without lamellipodia. Ena/VASP-deficiency also impaired integrin-mediated
adhesion accompanied by reduced traction forces exerted through these structures.
Our data thus uncover novel Ena/VASP functions of these actin polymerases that
are fully consistent with their promotion of cell migration.
article_number: e55351
article_processing_charge: No
article_type: original
author:
- first_name: Julia
full_name: Damiano-Guercio, Julia
last_name: Damiano-Guercio
- first_name: Laëtitia
full_name: Kurzawa, Laëtitia
last_name: Kurzawa
- first_name: Jan
full_name: Müller, Jan
id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D
last_name: Müller
- first_name: Georgi A
full_name: Dimchev, Georgi A
id: 38C393BE-F248-11E8-B48F-1D18A9856A87
last_name: Dimchev
orcid: 0000-0001-8370-6161
- first_name: Matthias
full_name: Schaks, Matthias
last_name: Schaks
- first_name: Maria
full_name: Nemethova, Maria
id: 34E27F1C-F248-11E8-B48F-1D18A9856A87
last_name: Nemethova
- first_name: Thomas
full_name: Pokrant, Thomas
last_name: Pokrant
- first_name: Stefan
full_name: Brühmann, Stefan
last_name: Brühmann
- first_name: Joern
full_name: Linkner, Joern
last_name: Linkner
- first_name: Laurent
full_name: Blanchoin, Laurent
last_name: Blanchoin
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Klemens
full_name: Rottner, Klemens
last_name: Rottner
- first_name: Jan
full_name: Faix, Jan
last_name: Faix
citation:
ama: Damiano-Guercio J, Kurzawa L, Müller J, et al. Loss of Ena/VASP interferes
with lamellipodium architecture, motility and integrin-dependent adhesion. eLife.
2020;9. doi:10.7554/eLife.55351
apa: Damiano-Guercio, J., Kurzawa, L., Müller, J., Dimchev, G. A., Schaks, M., Nemethova,
M., … Faix, J. (2020). Loss of Ena/VASP interferes with lamellipodium architecture,
motility and integrin-dependent adhesion. ELife. eLife Sciences Publications.
https://doi.org/10.7554/eLife.55351
chicago: Damiano-Guercio, Julia, Laëtitia Kurzawa, Jan Müller, Georgi A Dimchev,
Matthias Schaks, Maria Nemethova, Thomas Pokrant, et al. “Loss of Ena/VASP Interferes
with Lamellipodium Architecture, Motility and Integrin-Dependent Adhesion.” ELife.
eLife Sciences Publications, 2020. https://doi.org/10.7554/eLife.55351.
ieee: J. Damiano-Guercio et al., “Loss of Ena/VASP interferes with lamellipodium
architecture, motility and integrin-dependent adhesion,” eLife, vol. 9.
eLife Sciences Publications, 2020.
ista: Damiano-Guercio J, Kurzawa L, Müller J, Dimchev GA, Schaks M, Nemethova M,
Pokrant T, Brühmann S, Linkner J, Blanchoin L, Sixt MK, Rottner K, Faix J. 2020.
Loss of Ena/VASP interferes with lamellipodium architecture, motility and integrin-dependent
adhesion. eLife. 9, e55351.
mla: Damiano-Guercio, Julia, et al. “Loss of Ena/VASP Interferes with Lamellipodium
Architecture, Motility and Integrin-Dependent Adhesion.” ELife, vol. 9,
e55351, eLife Sciences Publications, 2020, doi:10.7554/eLife.55351.
short: J. Damiano-Guercio, L. Kurzawa, J. Müller, G.A. Dimchev, M. Schaks, M. Nemethova,
T. Pokrant, S. Brühmann, J. Linkner, L. Blanchoin, M.K. Sixt, K. Rottner, J. Faix,
ELife 9 (2020).
date_created: 2020-05-31T22:00:49Z
date_published: 2020-05-11T00:00:00Z
date_updated: 2026-04-02T14:32:12Z
day: '11'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.7554/eLife.55351
ec_funded: 1
external_id:
isi:
- '000537208000001'
pmid:
- '32391788'
file:
- access_level: open_access
checksum: d33bd4441b9a0195718ce1ba5d2c48a6
content_type: application/pdf
creator: dernst
date_created: 2020-06-02T10:35:37Z
date_updated: 2020-07-14T12:48:05Z
file_id: '7914'
file_name: 2020_eLife_Damiano_Guercio.pdf
file_size: 10535713
relation: main_file
file_date_updated: 2020-07-14T12:48:05Z
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular Navigation Along Spatial Gradients
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Loss of Ena/VASP interferes with lamellipodium architecture, motility and integrin-dependent
adhesion
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: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 9
year: '2020'
...
---
_id: '7466'
abstract:
- lang: eng
text: Unpaired ligands are secreted signals that act via a GP130-like receptor,
domeless, to activate JAK/STAT signalling in Drosophila. Like many mammalian cytokines,
unpaireds can be activated by infection and other stresses and can promote insulin
resistance in target tissues. However, the importance of this effect in non-inflammatory
physiology is unknown. Here, we identify a requirement for unpaired-JAK signalling
as a metabolic regulator in healthy adult Drosophila muscle. Adult muscles show
basal JAK-STAT signalling activity in the absence of any immune challenge. Plasmatocytes
(Drosophila macrophages) are an important source of this tonic signal. Loss of
the dome receptor on adult muscles significantly reduces lifespan and causes local
and systemic metabolic pathology. These pathologies result from hyperactivation
of AKT and consequent deregulation of metabolism. Thus, we identify a cytokine
signal that must be received in muscle to control AKT activity and metabolic homeostasis.
article_number: e51595
article_processing_charge: No
article_type: original
author:
- first_name: Katrin
full_name: Kierdorf, Katrin
last_name: Kierdorf
- first_name: Fabian
full_name: Hersperger, Fabian
last_name: Hersperger
- first_name: Jessica
full_name: Sharrock, Jessica
last_name: Sharrock
- first_name: Crystal M.
full_name: Vincent, Crystal M.
last_name: Vincent
- first_name: Pinar
full_name: Ustaoglu, Pinar
last_name: Ustaoglu
- first_name: Jiawen
full_name: Dou, Jiawen
last_name: Dou
- first_name: Attila
full_name: György, Attila
id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87
last_name: György
orcid: 0000-0002-1819-198X
- first_name: Olaf
full_name: Groß, Olaf
last_name: Groß
- first_name: Daria E
full_name: Siekhaus, Daria E
id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
last_name: Siekhaus
orcid: 0000-0001-8323-8353
- first_name: Marc S.
full_name: Dionne, Marc S.
last_name: Dionne
citation:
ama: Kierdorf K, Hersperger F, Sharrock J, et al. Muscle function and homeostasis
require cytokine inhibition of AKT activity in Drosophila. eLife. 2020;9.
doi:10.7554/eLife.51595
apa: Kierdorf, K., Hersperger, F., Sharrock, J., Vincent, C. M., Ustaoglu, P., Dou,
J., … Dionne, M. S. (2020). Muscle function and homeostasis require cytokine inhibition
of AKT activity in Drosophila. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.51595
chicago: Kierdorf, Katrin, Fabian Hersperger, Jessica Sharrock, Crystal M. Vincent,
Pinar Ustaoglu, Jiawen Dou, Attila György, Olaf Groß, Daria E Siekhaus, and Marc
S. Dionne. “Muscle Function and Homeostasis Require Cytokine Inhibition of AKT
Activity in Drosophila.” ELife. eLife Sciences Publications, 2020. https://doi.org/10.7554/eLife.51595.
ieee: K. Kierdorf et al., “Muscle function and homeostasis require cytokine
inhibition of AKT activity in Drosophila,” eLife, vol. 9. eLife Sciences
Publications, 2020.
ista: Kierdorf K, Hersperger F, Sharrock J, Vincent CM, Ustaoglu P, Dou J, György
A, Groß O, Siekhaus DE, Dionne MS. 2020. Muscle function and homeostasis require
cytokine inhibition of AKT activity in Drosophila. eLife. 9, e51595.
mla: Kierdorf, Katrin, et al. “Muscle Function and Homeostasis Require Cytokine
Inhibition of AKT Activity in Drosophila.” ELife, vol. 9, e51595, eLife
Sciences Publications, 2020, doi:10.7554/eLife.51595.
short: K. Kierdorf, F. Hersperger, J. Sharrock, C.M. Vincent, P. Ustaoglu, J. Dou,
A. György, O. Groß, D.E. Siekhaus, M.S. Dionne, ELife 9 (2020).
date_created: 2020-02-09T23:00:51Z
date_published: 2020-01-20T00:00:00Z
date_updated: 2026-04-03T09:24:34Z
day: '20'
ddc:
- '570'
department:
- _id: DaSi
doi: 10.7554/eLife.51595
external_id:
isi:
- '000512304800001'
file:
- access_level: open_access
checksum: 3a072be843f416c7a7d532a51dc0addb
content_type: application/pdf
creator: dernst
date_created: 2020-02-10T08:53:16Z
date_updated: 2020-07-14T12:47:59Z
file_id: '7470'
file_name: 2020_eLife_Kierdorf.pdf
file_size: 4959933
relation: main_file
file_date_updated: 2020-07-14T12:47:59Z
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
project:
- _id: 253B6E48-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P29638
name: The role of Drosophila TNF alpha in immune cell invasion
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Muscle function and homeostasis require cytokine inhibition of AKT activity
in Drosophila
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: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 9
year: '2020'
...
---
_id: '8740'
abstract:
- lang: eng
text: In vitro work revealed that excitatory synaptic inputs to hippocampal inhibitory
interneurons could undergo Hebbian, associative, or non-associative plasticity.
Both behavioral and learning-dependent reorganization of these connections has
also been demonstrated by measuring spike transmission probabilities in pyramidal
cell-interneuron spike cross-correlations that indicate monosynaptic connections.
Here we investigated the activity-dependent modification of these connections
during exploratory behavior in rats by optogenetically inhibiting pyramidal cell
and interneuron subpopulations. Light application and associated firing alteration
of pyramidal and interneuron populations led to lasting changes in pyramidal-interneuron
connection weights as indicated by spike transmission changes. Spike transmission
alterations were predicted by the light-mediated changes in the number of pre-
and postsynaptic spike pairing events and by firing rate changes of interneurons
but not pyramidal cells. This work demonstrates the presence of activity-dependent
associative and non-associative reorganization of pyramidal-interneuron connections
triggered by the optogenetic modification of the firing rate and spike synchrony
of cells.
acknowledgement: We thank Michele Nardin and Federico Stella for comments on an earlier
version of the manuscript. K Deisseroth for providing the pAAV-CaMKIIα::eNpHR3.0-YFP
plasmid through Addgene. E Boyden for providing AAV2/1.CaMKII::ArchT.GFP.WPRE.SV40
plasmid through Penn Vector Core. This work was supported by the Austrian Science
Fund (I02072 and I03713) and a Swiss National Science Foundation grant to PS. The
authors declare no conflicts of interest.
article_number: '61106'
article_processing_charge: No
article_type: original
author:
- first_name: Igor
full_name: Gridchyn, Igor
id: 4B60654C-F248-11E8-B48F-1D18A9856A87
last_name: Gridchyn
orcid: 0000-0002-1807-1929
- first_name: Philipp
full_name: Schönenberger, Philipp
id: 3B9D816C-F248-11E8-B48F-1D18A9856A87
last_name: Schönenberger
- first_name: Joseph
full_name: O'Neill, Joseph
id: 426376DC-F248-11E8-B48F-1D18A9856A87
last_name: O'Neill
- first_name: Jozsef L
full_name: Csicsvari, Jozsef L
id: 3FA14672-F248-11E8-B48F-1D18A9856A87
last_name: Csicsvari
orcid: 0000-0002-5193-4036
citation:
ama: Gridchyn I, Schönenberger P, O’Neill J, Csicsvari JL. Optogenetic inhibition-mediated
activity-dependent modification of CA1 pyramidal-interneuron connections during
behavior. eLife. 2020;9. doi:10.7554/eLife.61106
apa: Gridchyn, I., Schönenberger, P., O’Neill, J., & Csicsvari, J. L. (2020).
Optogenetic inhibition-mediated activity-dependent modification of CA1 pyramidal-interneuron
connections during behavior. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.61106
chicago: Gridchyn, Igor, Philipp Schönenberger, Joseph O’Neill, and Jozsef L Csicsvari.
“Optogenetic Inhibition-Mediated Activity-Dependent Modification of CA1 Pyramidal-Interneuron
Connections during Behavior.” ELife. eLife Sciences Publications, 2020.
https://doi.org/10.7554/eLife.61106.
ieee: I. Gridchyn, P. Schönenberger, J. O’Neill, and J. L. Csicsvari, “Optogenetic
inhibition-mediated activity-dependent modification of CA1 pyramidal-interneuron
connections during behavior,” eLife, vol. 9. eLife Sciences Publications,
2020.
ista: Gridchyn I, Schönenberger P, O’Neill J, Csicsvari JL. 2020. Optogenetic inhibition-mediated
activity-dependent modification of CA1 pyramidal-interneuron connections during
behavior. eLife. 9, 61106.
mla: Gridchyn, Igor, et al. “Optogenetic Inhibition-Mediated Activity-Dependent
Modification of CA1 Pyramidal-Interneuron Connections during Behavior.” ELife,
vol. 9, 61106, eLife Sciences Publications, 2020, doi:10.7554/eLife.61106.
short: I. Gridchyn, P. Schönenberger, J. O’Neill, J.L. Csicsvari, ELife 9 (2020).
corr_author: '1'
date_created: 2020-11-08T23:01:25Z
date_published: 2020-10-05T00:00:00Z
date_updated: 2026-04-07T08:37:11Z
day: '05'
ddc:
- '570'
department:
- _id: JoCs
doi: 10.7554/eLife.61106
external_id:
isi:
- '000584369000001'
pmid:
- '33016875'
file:
- access_level: open_access
checksum: 6a7b0543c440f4c000a1864e69377d95
content_type: application/pdf
creator: dernst
date_created: 2020-11-09T09:17:40Z
date_updated: 2020-11-09T09:17:40Z
file_id: '8749'
file_name: 2020_eLife_Gridchyn.pdf
file_size: 447669
relation: main_file
success: 1
file_date_updated: 2020-11-09T09:17:40Z
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 257D4372-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: I2072-B27
name: Interneuron plasticity during spatial learning
- _id: 2654F984-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: I 3713-B27
name: Interneuro plasticity during spatial learning
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
related_material:
record:
- id: '8563'
relation: research_data
status: public
scopus_import: '1'
status: public
title: Optogenetic inhibition-mediated activity-dependent modification of CA1 pyramidal-interneuron
connections during behavior
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: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 9
year: '2020'
...
---
_id: '8284'
abstract:
- lang: eng
text: Multiple resistance and pH adaptation (Mrp) antiporters are multi-subunit
Na+ (or K+)/H+ exchangers representing an ancestor of many essential redox-driven
proton pumps, such as respiratory complex I. The mechanism of coupling between
ion or electron transfer and proton translocation in this large protein family
is unknown. Here, we present the structure of the Mrp complex from Anoxybacillus
flavithermus solved by cryo-EM at 3.0 Å resolution. It is a dimer of seven-subunit
protomers with 50 trans-membrane helices each. Surface charge distribution within
each monomer is remarkably asymmetric, revealing probable proton and sodium translocation
pathways. On the basis of the structure we propose a mechanism where the coupling
between sodium and proton translocation is facilitated by a series of electrostatic
interactions between a cation and key charged residues. This mechanism is likely
to be applicable to the entire family of redox proton pumps, where electron transfer
to substrates replaces cation movements.
acknowledged_ssus:
- _id: EM-Fac
- _id: LifeSc
acknowledgement: This research was supported by the Scientific Service Units (SSU)
of IST Austria through resources provided by the Electron Microscopy Facility (EMF),
the Life Science Facility (LSF) and the IST high-performance computing cluster.
We thank Dr Victor-Valentin Hodirnau and Daniel Johann Gütl from IST Austria for
assistance with collecting cryo-EM data. We thank Prof. Masahiro Ito (Graduate School
of Life Sciences, Toyo University, Japan) for a kind provision of plasmid DNA encoding
Mrp from A. flavithermus WK1. JS is a recipient of a DOC Fellowship of the Austrian
Academy of Sciences at the Institute of Science and Technology, Austria.
article_number: e59407
article_processing_charge: No
article_type: original
author:
- first_name: Julia
full_name: Steiner, Julia
id: 3BB67EB0-F248-11E8-B48F-1D18A9856A87
last_name: Steiner
orcid: 0000-0003-0493-3775
- first_name: Leonid A
full_name: Sazanov, Leonid A
id: 338D39FE-F248-11E8-B48F-1D18A9856A87
last_name: Sazanov
orcid: 0000-0002-0977-7989
citation:
ama: Steiner J, Sazanov LA. Structure and mechanism of the Mrp complex, an ancient
cation/proton antiporter. eLife. 2020;9. doi:10.7554/eLife.59407
apa: Steiner, J., & Sazanov, L. A. (2020). Structure and mechanism of the Mrp
complex, an ancient cation/proton antiporter. ELife. eLife Sciences Publications.
https://doi.org/10.7554/eLife.59407
chicago: Steiner, Julia, and Leonid A Sazanov. “Structure and Mechanism of the Mrp
Complex, an Ancient Cation/Proton Antiporter.” ELife. eLife Sciences Publications,
2020. https://doi.org/10.7554/eLife.59407.
ieee: J. Steiner and L. A. Sazanov, “Structure and mechanism of the Mrp complex,
an ancient cation/proton antiporter,” eLife, vol. 9. eLife Sciences Publications,
2020.
ista: Steiner J, Sazanov LA. 2020. Structure and mechanism of the Mrp complex, an
ancient cation/proton antiporter. eLife. 9, e59407.
mla: Steiner, Julia, and Leonid A. Sazanov. “Structure and Mechanism of the Mrp
Complex, an Ancient Cation/Proton Antiporter.” ELife, vol. 9, e59407, eLife
Sciences Publications, 2020, doi:10.7554/eLife.59407.
short: J. Steiner, L.A. Sazanov, ELife 9 (2020).
date_created: 2020-08-24T06:24:04Z
date_published: 2020-07-31T00:00:00Z
date_updated: 2026-04-08T07:23:36Z
day: '31'
ddc:
- '570'
department:
- _id: LeSa
doi: 10.7554/eLife.59407
external_id:
isi:
- '000562123600001'
pmid:
- '32735215'
file:
- access_level: open_access
checksum: b3656d14d5ddbb9d26e3074eea2d0c15
content_type: application/pdf
creator: cziletti
date_created: 2020-08-24T13:31:53Z
date_updated: 2020-08-24T13:31:53Z
file_id: '8289'
file_name: 2020_eLife_Steiner.pdf
file_size: 7320493
relation: main_file
success: 1
file_date_updated: 2020-08-24T13:31:53Z
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 26169496-B435-11E9-9278-68D0E5697425
grant_number: '24741'
name: Revealing the functional mechanism of Mrp antiporter, an ancestor of complex
I
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/mystery-of-giant-proton-pump-solved/
record:
- id: '8353'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Structure and mechanism of the Mrp complex, an ancient cation/proton antiporter
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: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 9
year: '2020'
...
---
_id: '6230'
abstract:
- lang: eng
text: Great care is needed when interpreting claims about the genetic basis of human
variation based on data from genome-wide association studies.
article_number: e45380
article_processing_charge: No
author:
- first_name: Nicholas H
full_name: Barton, Nicholas H
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
orcid: 0000-0002-8548-5240
- first_name: Joachim
full_name: Hermisson, Joachim
last_name: Hermisson
- first_name: Magnus
full_name: Nordborg, Magnus
last_name: Nordborg
citation:
ama: Barton NH, Hermisson J, Nordborg M. Why structure matters. eLife. 2019;8.
doi:10.7554/eLife.45380
apa: Barton, N. H., Hermisson, J., & Nordborg, M. (2019). Why structure matters.
ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.45380
chicago: Barton, Nicholas H, Joachim Hermisson, and Magnus Nordborg. “Why Structure
Matters.” ELife. eLife Sciences Publications, 2019. https://doi.org/10.7554/eLife.45380.
ieee: N. H. Barton, J. Hermisson, and M. Nordborg, “Why structure matters,” eLife,
vol. 8. eLife Sciences Publications, 2019.
ista: Barton NH, Hermisson J, Nordborg M. 2019. Why structure matters. eLife. 8,
e45380.
mla: Barton, Nicholas H., et al. “Why Structure Matters.” ELife, vol. 8,
e45380, eLife Sciences Publications, 2019, doi:10.7554/eLife.45380.
short: N.H. Barton, J. Hermisson, M. Nordborg, ELife 8 (2019).
date_created: 2019-04-07T21:59:15Z
date_published: 2019-03-21T00:00:00Z
date_updated: 2026-04-02T14:03:15Z
day: '21'
ddc:
- '570'
department:
- _id: NiBa
doi: 10.7554/eLife.45380
external_id:
isi:
- '000461988300001'
file:
- access_level: open_access
checksum: 130d7544b57df4a6787e1263c2d7ea43
content_type: application/pdf
creator: dernst
date_created: 2019-04-11T11:43:38Z
date_updated: 2020-07-14T12:47:24Z
file_id: '6293'
file_name: 2019_eLife_Barton.pdf
file_size: 298466
relation: main_file
file_date_updated: 2020-07-14T12:47:24Z
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/body-height-bmi-disease-risk-co/
scopus_import: '1'
status: public
title: Why structure matters
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: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 8
year: '2019'
...
---
_id: '6868'
abstract:
- lang: eng
text: "Hyperpolarization-activated cyclic-nucleotide-gated (HCN) channels control
electrical rhythmicity and excitability in the heart and brain, but the function
of HCN channels at the subcellular level in axons remains poorly understood. Here,
we show that the action potential conduction velocity in both myelinated and unmyelinated
central axons can be bidirectionally modulated by a HCN channel blocker, cyclic
adenosine monophosphate (cAMP), and neuromodulators. Recordings from mouse cerebellar
mossy fiber boutons show that HCN channels ensure reliable high-frequency firing
and are strongly modulated by cAMP (EC50 40 mM; estimated endogenous cAMP concentration
13 mM). In addition, immunogold-electron microscopy revealed HCN2 as the dominating
subunit in cerebellar mossy fibers. Computational modeling indicated that HCN2
channels control conduction velocity primarily by altering the resting membrane
potential\r\nand are associated with significant metabolic costs. These results
suggest that the cAMP-HCN pathway provides neuromodulators with an opportunity
to finely tune energy consumption and temporal delays across axons in the brain."
article_number: e42766
article_processing_charge: No
article_type: original
author:
- first_name: Niklas
full_name: Byczkowicz, Niklas
last_name: Byczkowicz
- first_name: Abdelmoneim
full_name: Eshra, Abdelmoneim
last_name: Eshra
- first_name: Jacqueline-Claire
full_name: Montanaro-Punzengruber, Jacqueline-Claire
id: 3786AB44-F248-11E8-B48F-1D18A9856A87
last_name: Montanaro-Punzengruber
- first_name: Andrea
full_name: Trevisiol, Andrea
last_name: Trevisiol
- first_name: Johannes
full_name: Hirrlinger, Johannes
last_name: Hirrlinger
- first_name: Maarten Hp
full_name: Kole, Maarten Hp
last_name: Kole
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Stefan
full_name: Hallermann, Stefan
last_name: Hallermann
citation:
ama: Byczkowicz N, Eshra A, Montanaro-Punzengruber J-C, et al. HCN channel-mediated
neuromodulation can control action potential velocity and fidelity in central
axons. eLife. 2019;8. doi:10.7554/eLife.42766
apa: Byczkowicz, N., Eshra, A., Montanaro-Punzengruber, J.-C., Trevisiol, A., Hirrlinger,
J., Kole, M. H., … Hallermann, S. (2019). HCN channel-mediated neuromodulation
can control action potential velocity and fidelity in central axons. ELife.
eLife Sciences Publications. https://doi.org/10.7554/eLife.42766
chicago: Byczkowicz, Niklas, Abdelmoneim Eshra, Jacqueline-Claire Montanaro-Punzengruber,
Andrea Trevisiol, Johannes Hirrlinger, Maarten Hp Kole, Ryuichi Shigemoto, and
Stefan Hallermann. “HCN Channel-Mediated Neuromodulation Can Control Action Potential
Velocity and Fidelity in Central Axons.” ELife. eLife Sciences Publications,
2019. https://doi.org/10.7554/eLife.42766.
ieee: N. Byczkowicz et al., “HCN channel-mediated neuromodulation can control
action potential velocity and fidelity in central axons,” eLife, vol. 8.
eLife Sciences Publications, 2019.
ista: Byczkowicz N, Eshra A, Montanaro-Punzengruber J-C, Trevisiol A, Hirrlinger
J, Kole MH, Shigemoto R, Hallermann S. 2019. HCN channel-mediated neuromodulation
can control action potential velocity and fidelity in central axons. eLife. 8,
e42766.
mla: Byczkowicz, Niklas, et al. “HCN Channel-Mediated Neuromodulation Can Control
Action Potential Velocity and Fidelity in Central Axons.” ELife, vol. 8,
e42766, eLife Sciences Publications, 2019, doi:10.7554/eLife.42766.
short: N. Byczkowicz, A. Eshra, J.-C. Montanaro-Punzengruber, A. Trevisiol, J. Hirrlinger,
M.H. Kole, R. Shigemoto, S. Hallermann, ELife 8 (2019).
date_created: 2019-09-15T22:00:43Z
date_published: 2019-09-09T00:00:00Z
date_updated: 2026-04-03T09:40:28Z
day: '09'
ddc:
- '570'
department:
- _id: RySh
doi: 10.7554/eLife.42766
external_id:
isi:
- '000485663900001'
file:
- access_level: open_access
checksum: c350b7861ef0fb537cae8a3232aec016
content_type: application/pdf
creator: dernst
date_created: 2019-09-16T13:14:33Z
date_updated: 2020-07-14T12:47:42Z
file_id: '6880'
file_name: 2019_eLife_Byczkowicz.pdf
file_size: 4008137
relation: main_file
file_date_updated: 2020-07-14T12:47:42Z
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: HCN channel-mediated neuromodulation can control action potential velocity
and fidelity in central axons
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: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 8
year: '2019'
...
---
_id: '7340'
abstract:
- lang: eng
text: Coupling of endoplasmic reticulum stress to dimerisation‑dependent activation
of the UPR transducer IRE1 is incompletely understood. Whilst the luminal co-chaperone
ERdj4 promotes a complex between the Hsp70 BiP and IRE1's stress-sensing luminal
domain (IRE1LD) that favours the latter's monomeric inactive state and loss of
ERdj4 de-represses IRE1, evidence linking these cellular and in vitro observations
is presently lacking. We report that enforced loading of endogenous BiP onto endogenous
IRE1α repressed UPR signalling in CHO cells and deletions in the IRE1α locus that
de-repressed the UPR in cells, encode flexible regions of IRE1LD that mediated
BiP‑induced monomerisation in vitro. Changes in the hydrogen exchange mass spectrometry
profile of IRE1LD induced by ERdj4 and BiP confirmed monomerisation and were consistent
with active destabilisation of the IRE1LD dimer. Together, these observations
support a competition model whereby waning ER stress passively partitions ERdj4
and BiP to IRE1LD to initiate active repression of UPR signalling.
acknowledgement: We thank the CIMR flow cytometry core facility team (Reiner Schulte,
Chiara Cossetti and Gabriela Grondys-Kotarba) for assistance with FACS, the Huntington
lab for access to the Octet machine, Steffen Preissler for advice on data interpretation,
Roman Kityk and Nicole Luebbehusen for help and advice with HX-MS experiments.
article_number: e50793
article_processing_charge: No
article_type: original
author:
- first_name: Niko Paresh
full_name: Amin-Wetzel, Niko Paresh
id: E95D3014-9D8C-11E9-9C80-D2F8E5697425
last_name: Amin-Wetzel
- first_name: Lisa
full_name: Neidhardt, Lisa
last_name: Neidhardt
- first_name: Yahui
full_name: Yan, Yahui
last_name: Yan
- first_name: Matthias P.
full_name: Mayer, Matthias P.
last_name: Mayer
- first_name: David
full_name: Ron, David
last_name: Ron
citation:
ama: Amin-Wetzel NP, Neidhardt L, Yan Y, Mayer MP, Ron D. Unstructured regions in
IRE1α specify BiP-mediated destabilisation of the luminal domain dimer and repression
of the UPR. eLife. 2019;8. doi:10.7554/eLife.50793
apa: Amin-Wetzel, N. P., Neidhardt, L., Yan, Y., Mayer, M. P., & Ron, D. (2019).
Unstructured regions in IRE1α specify BiP-mediated destabilisation of the luminal
domain dimer and repression of the UPR. ELife. eLife Sciences Publications.
https://doi.org/10.7554/eLife.50793
chicago: Amin-Wetzel, Niko Paresh, Lisa Neidhardt, Yahui Yan, Matthias P. Mayer,
and David Ron. “Unstructured Regions in IRE1α Specify BiP-Mediated Destabilisation
of the Luminal Domain Dimer and Repression of the UPR.” ELife. eLife Sciences
Publications, 2019. https://doi.org/10.7554/eLife.50793.
ieee: N. P. Amin-Wetzel, L. Neidhardt, Y. Yan, M. P. Mayer, and D. Ron, “Unstructured
regions in IRE1α specify BiP-mediated destabilisation of the luminal domain dimer
and repression of the UPR,” eLife, vol. 8. eLife Sciences Publications,
2019.
ista: Amin-Wetzel NP, Neidhardt L, Yan Y, Mayer MP, Ron D. 2019. Unstructured regions
in IRE1α specify BiP-mediated destabilisation of the luminal domain dimer and
repression of the UPR. eLife. 8, e50793.
mla: Amin-Wetzel, Niko Paresh, et al. “Unstructured Regions in IRE1α Specify BiP-Mediated
Destabilisation of the Luminal Domain Dimer and Repression of the UPR.” ELife,
vol. 8, e50793, eLife Sciences Publications, 2019, doi:10.7554/eLife.50793.
short: N.P. Amin-Wetzel, L. Neidhardt, Y. Yan, M.P. Mayer, D. Ron, ELife 8 (2019).
date_created: 2020-01-19T23:00:39Z
date_published: 2019-12-24T00:00:00Z
date_updated: 2026-04-03T09:44:20Z
day: '24'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.7554/eLife.50793
external_id:
isi:
- '000512303700001'
pmid:
- '31873072'
file:
- access_level: open_access
checksum: 29fcbcd8c1fc7f11a596ed7f14ea1c82
content_type: application/pdf
creator: dernst
date_created: 2020-11-19T11:37:41Z
date_updated: 2020-11-19T11:37:41Z
file_id: '8777'
file_name: 2019_eLife_AminWetzel.pdf
file_size: 4817384
relation: main_file
success: 1
file_date_updated: 2020-11-19T11:37:41Z
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Unstructured regions in IRE1α specify BiP-mediated destabilisation of the luminal
domain dimer and repression of the UPR
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: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 8
year: '2019'
...
---
_id: '7202'
abstract:
- lang: eng
text: The cerebral cortex contains multiple areas with distinctive cytoarchitectonical
patterns, but the cellular mechanisms underlying the emergence of this diversity
remain unclear. Here, we have investigated the neuronal output of individual progenitor
cells in the developing mouse neocortex using a combination of methods that together
circumvent the biases and limitations of individual approaches. Our experimental
results indicate that progenitor cells generate pyramidal cell lineages with a
wide range of sizes and laminar configurations. Mathematical modelling indicates
that these outcomes are compatible with a stochastic model of cortical neurogenesis
in which progenitor cells undergo a series of probabilistic decisions that lead
to the specification of very heterogeneous progenies. Our findings support a mechanism
for cortical neurogenesis whose flexibility would make it capable to generate
the diverse cytoarchitectures that characterize distinct neocortical areas.
article_number: e51381
article_processing_charge: No
article_type: original
author:
- first_name: Alfredo
full_name: Llorca, Alfredo
last_name: Llorca
- first_name: Gabriele
full_name: Ciceri, Gabriele
last_name: Ciceri
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Fong Kuan
full_name: Wong, Fong Kuan
last_name: Wong
- first_name: Giovanni
full_name: Diana, Giovanni
last_name: Diana
- first_name: Eleni
full_name: Serafeimidou-Pouliou, Eleni
last_name: Serafeimidou-Pouliou
- first_name: Marian
full_name: Fernández-Otero, Marian
last_name: Fernández-Otero
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Sebastian J.
full_name: Arnold, Sebastian J.
last_name: Arnold
- first_name: Martin
full_name: Meyer, Martin
last_name: Meyer
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Miguel
full_name: Maravall, Miguel
last_name: Maravall
- first_name: Oscar
full_name: Marín, Oscar
last_name: Marín
citation:
ama: Llorca A, Ciceri G, Beattie RJ, et al. A stochastic framework of neurogenesis
underlies the assembly of neocortical cytoarchitecture. eLife. 2019;8.
doi:10.7554/eLife.51381
apa: Llorca, A., Ciceri, G., Beattie, R. J., Wong, F. K., Diana, G., Serafeimidou-Pouliou,
E., … Marín, O. (2019). A stochastic framework of neurogenesis underlies the assembly
of neocortical cytoarchitecture. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.51381
chicago: Llorca, Alfredo, Gabriele Ciceri, Robert J Beattie, Fong Kuan Wong, Giovanni
Diana, Eleni Serafeimidou-Pouliou, Marian Fernández-Otero, et al. “A Stochastic
Framework of Neurogenesis Underlies the Assembly of Neocortical Cytoarchitecture.”
ELife. eLife Sciences Publications, 2019. https://doi.org/10.7554/eLife.51381.
ieee: A. Llorca et al., “A stochastic framework of neurogenesis underlies
the assembly of neocortical cytoarchitecture,” eLife, vol. 8. eLife Sciences
Publications, 2019.
ista: Llorca A, Ciceri G, Beattie RJ, Wong FK, Diana G, Serafeimidou-Pouliou E,
Fernández-Otero M, Streicher C, Arnold SJ, Meyer M, Hippenmeyer S, Maravall M,
Marín O. 2019. A stochastic framework of neurogenesis underlies the assembly of
neocortical cytoarchitecture. eLife. 8, e51381.
mla: Llorca, Alfredo, et al. “A Stochastic Framework of Neurogenesis Underlies the
Assembly of Neocortical Cytoarchitecture.” ELife, vol. 8, e51381, eLife
Sciences Publications, 2019, doi:10.7554/eLife.51381.
short: A. Llorca, G. Ciceri, R.J. Beattie, F.K. Wong, G. Diana, E. Serafeimidou-Pouliou,
M. Fernández-Otero, C. Streicher, S.J. Arnold, M. Meyer, S. Hippenmeyer, M. Maravall,
O. Marín, ELife 8 (2019).
date_created: 2019-12-22T23:00:42Z
date_published: 2019-11-18T00:00:00Z
date_updated: 2026-04-03T09:46:33Z
day: '18'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.7554/eLife.51381
ec_funded: 1
external_id:
isi:
- '000508156800001'
pmid:
- '31736464'
file:
- access_level: open_access
checksum: b460ecc33e1a68265e7adea775021f3a
content_type: application/pdf
creator: dernst
date_created: 2020-02-18T15:19:26Z
date_updated: 2020-07-14T12:47:53Z
file_id: '7503'
file_name: 2019_eLife_Llorca.pdf
file_size: 2960543
relation: main_file
file_date_updated: 2020-07-14T12:47:53Z
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 264E56E2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02416
name: Molecular Mechanisms Regulating Gliogenesis in the Neocortex
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: A stochastic framework of neurogenesis underlies the assembly of neocortical
cytoarchitecture
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: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 8
year: '2019'
...
---
_id: '9445'
abstract:
- lang: eng
text: Cytosine methylation regulates essential genome functions across eukaryotes,
but the fundamental question of whether nucleosomal or naked DNA is the preferred
substrate of plant and animal methyltransferases remains unresolved. Here, we
show that genetic inactivation of a single DDM1/Lsh family nucleosome remodeler
biases methylation toward inter-nucleosomal linker DNA in Arabidopsis thaliana
and mouse. We find that DDM1 enables methylation of DNA bound to the nucleosome,
suggesting that nucleosome-free DNA is the preferred substrate of eukaryotic methyltransferases
in vivo. Furthermore, we show that simultaneous mutation of DDM1 and linker histone
H1 in Arabidopsis reproduces the strong linker-specific methylation patterns of
species that diverged from flowering plants and animals over a billion years ago.
Our results indicate that in the absence of remodeling, nucleosomes are strong
barriers to DNA methyltransferases. Linker-specific methylation can evolve simply
by breaking the connection between nucleosome remodeling and DNA methylation.
article_number: e30674
article_processing_charge: No
article_type: original
author:
- first_name: David B
full_name: Lyons, David B
last_name: Lyons
- first_name: Daniel
full_name: Zilberman, Daniel
id: 6973db13-dd5f-11ea-814e-b3e5455e9ed1
last_name: Zilberman
orcid: 0000-0002-0123-8649
citation:
ama: Lyons DB, Zilberman D. DDM1 and Lsh remodelers allow methylation of DNA wrapped
in nucleosomes. eLife. 2017;6. doi:10.7554/elife.30674
apa: Lyons, D. B., & Zilberman, D. (2017). DDM1 and Lsh remodelers allow methylation
of DNA wrapped in nucleosomes. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.30674
chicago: Lyons, David B, and Daniel Zilberman. “DDM1 and Lsh Remodelers Allow Methylation
of DNA Wrapped in Nucleosomes.” ELife. eLife Sciences Publications, 2017.
https://doi.org/10.7554/elife.30674.
ieee: D. B. Lyons and D. Zilberman, “DDM1 and Lsh remodelers allow methylation of
DNA wrapped in nucleosomes,” eLife, vol. 6. eLife Sciences Publications,
2017.
ista: Lyons DB, Zilberman D. 2017. DDM1 and Lsh remodelers allow methylation of
DNA wrapped in nucleosomes. eLife. 6, e30674.
mla: Lyons, David B., and Daniel Zilberman. “DDM1 and Lsh Remodelers Allow Methylation
of DNA Wrapped in Nucleosomes.” ELife, vol. 6, e30674, eLife Sciences Publications,
2017, doi:10.7554/elife.30674.
short: D.B. Lyons, D. Zilberman, ELife 6 (2017).
date_created: 2021-06-02T14:28:58Z
date_published: 2017-11-15T00:00:00Z
date_updated: 2021-12-14T07:54:36Z
day: '15'
ddc:
- '570'
department:
- _id: DaZi
doi: 10.7554/elife.30674
extern: '1'
external_id:
pmid:
- '29140247'
file:
- access_level: open_access
checksum: 4cfcdd67511ae4aed3d993550e46e146
content_type: application/pdf
creator: cziletti
date_created: 2021-06-02T14:33:36Z
date_updated: 2021-06-02T14:33:36Z
file_id: '9446'
file_name: 2017_eLife_Lyons.pdf
file_size: 1603102
relation: main_file
success: 1
file_date_updated: 2021-06-02T14:33:36Z
has_accepted_license: '1'
intvolume: ' 6'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: DDM1 and Lsh remodelers allow methylation of DNA wrapped in nucleosomes
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'
...