---
_id: '11160'
abstract:
- lang: eng
text: Mutations in the chromodomain helicase DNA-binding 8 (CHD8) gene are a frequent
cause of autism spectrum disorder (ASD). While its phenotypic spectrum often encompasses
macrocephaly, implicating cortical abnormalities, how CHD8 haploinsufficiency
affects neurodevelopmental is unclear. Here, employing human cerebral organoids,
we find that CHD8 haploinsufficiency disrupted neurodevelopmental trajectories
with an accelerated and delayed generation of, respectively, inhibitory and excitatory
neurons that yields, at days 60 and 120, symmetrically opposite expansions in
their proportions. This imbalance is consistent with an enlargement of cerebral
organoids as an in vitro correlate of patients’ macrocephaly. Through an isogenic
design of patient-specific mutations and mosaic organoids, we define genotype-phenotype
relationships and uncover their cell-autonomous nature. Our results define cell-type-specific
CHD8-dependent molecular defects related to an abnormal program of proliferation
and alternative splicing. By identifying cell-type-specific effects of CHD8 mutations,
our study uncovers reproducible developmental alterations that may be employed
for neurodevelopmental disease modeling.
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
acknowledgement: We thank Farnaz Freeman for technical assistance. This research was
supported by the Scientific Service Units (SSU) of IST Austria through resources
provided by the Bioimaging Facility (BIF) and the Life Science Facility (LSF). This
work supported by the European Union’s Horizon 2020 research and innovation program
(ERC) grant 715508 to G.N. (REVERSEAUTISM) and grant 825759 to G.T. (ENDpoiNTs);
the Fondazione Cariplo 2017-0886 to A.L.T.; E-Rare-3 JTC 2018 IMPACT to M. Gabriele;
and the Austrian Science Fund FWF I 4205-B to G.N. Graphical abstract and figures
were created using BioRender.com.
article_number: '110615'
article_processing_charge: Yes
article_type: original
author:
- first_name: Carlo Emanuele
full_name: Villa, Carlo Emanuele
last_name: Villa
- first_name: Cristina
full_name: Cheroni, Cristina
last_name: Cheroni
- first_name: Christoph
full_name: Dotter, Christoph
id: 4C66542E-F248-11E8-B48F-1D18A9856A87
last_name: Dotter
orcid: 0000-0002-9033-9096
- first_name: Alejandro
full_name: López-Tóbon, Alejandro
last_name: López-Tóbon
- first_name: Bárbara
full_name: Oliveira, Bárbara
id: 3B03AA1A-F248-11E8-B48F-1D18A9856A87
last_name: Oliveira
- first_name: Roberto
full_name: Sacco, Roberto
id: 42C9F57E-F248-11E8-B48F-1D18A9856A87
last_name: Sacco
- first_name: Aysan Çerağ
full_name: Yahya, Aysan Çerağ
id: 365A65F8-F248-11E8-B48F-1D18A9856A87
last_name: Yahya
- first_name: Jasmin
full_name: Morandell, Jasmin
id: 4739D480-F248-11E8-B48F-1D18A9856A87
last_name: Morandell
- first_name: Michele
full_name: Gabriele, Michele
last_name: Gabriele
- first_name: Mojtaba
full_name: Tavakoli, Mojtaba
id: 3A0A06F4-F248-11E8-B48F-1D18A9856A87
last_name: Tavakoli
orcid: 0000-0002-7667-6854
- first_name: Julia
full_name: Lyudchik, Julia
id: 46E28B80-F248-11E8-B48F-1D18A9856A87
last_name: Lyudchik
- first_name: Christoph M
full_name: Sommer, Christoph M
id: 4DF26D8C-F248-11E8-B48F-1D18A9856A87
last_name: Sommer
orcid: 0000-0003-1216-9105
- first_name: Mariano
full_name: Gabitto, Mariano
last_name: Gabitto
- first_name: Johann G
full_name: Danzl, Johann G
id: 42EFD3B6-F248-11E8-B48F-1D18A9856A87
last_name: Danzl
orcid: 0000-0001-8559-3973
- first_name: Giuseppe
full_name: Testa, Giuseppe
last_name: Testa
- first_name: Gaia
full_name: Novarino, Gaia
id: 3E57A680-F248-11E8-B48F-1D18A9856A87
last_name: Novarino
orcid: 0000-0002-7673-7178
citation:
ama: Villa CE, Cheroni C, Dotter C, et al. CHD8 haploinsufficiency links autism
to transient alterations in excitatory and inhibitory trajectories. Cell Reports.
2022;39(1). doi:10.1016/j.celrep.2022.110615
apa: Villa, C. E., Cheroni, C., Dotter, C., López-Tóbon, A., Oliveira, B., Sacco,
R., … Novarino, G. (2022). CHD8 haploinsufficiency links autism to transient alterations
in excitatory and inhibitory trajectories. Cell Reports. Elsevier. https://doi.org/10.1016/j.celrep.2022.110615
chicago: Villa, Carlo Emanuele, Cristina Cheroni, Christoph Dotter, Alejandro López-Tóbon,
Bárbara Oliveira, Roberto Sacco, Aysan Çerağ Yahya, et al. “CHD8 Haploinsufficiency
Links Autism to Transient Alterations in Excitatory and Inhibitory Trajectories.”
Cell Reports. Elsevier, 2022. https://doi.org/10.1016/j.celrep.2022.110615.
ieee: C. E. Villa et al., “CHD8 haploinsufficiency links autism to transient
alterations in excitatory and inhibitory trajectories,” Cell Reports, vol.
39, no. 1. Elsevier, 2022.
ista: Villa CE, Cheroni C, Dotter C, López-Tóbon A, Oliveira B, Sacco R, Yahya AÇ,
Morandell J, Gabriele M, Tavakoli M, Lyudchik J, Sommer CM, Gabitto M, Danzl JG,
Testa G, Novarino G. 2022. CHD8 haploinsufficiency links autism to transient alterations
in excitatory and inhibitory trajectories. Cell Reports. 39(1), 110615.
mla: Villa, Carlo Emanuele, et al. “CHD8 Haploinsufficiency Links Autism to Transient
Alterations in Excitatory and Inhibitory Trajectories.” Cell Reports, vol.
39, no. 1, 110615, Elsevier, 2022, doi:10.1016/j.celrep.2022.110615.
short: C.E. Villa, C. Cheroni, C. Dotter, A. López-Tóbon, B. Oliveira, R. Sacco,
A.Ç. Yahya, J. Morandell, M. Gabriele, M. Tavakoli, J. Lyudchik, C.M. Sommer,
M. Gabitto, J.G. Danzl, G. Testa, G. Novarino, Cell Reports 39 (2022).
corr_author: '1'
date_created: 2022-04-15T09:03:10Z
date_published: 2022-04-05T00:00:00Z
date_updated: 2026-04-26T22:30:31Z
day: '05'
ddc:
- '570'
department:
- _id: JoDa
- _id: GaNo
doi: 10.1016/j.celrep.2022.110615
ec_funded: 1
external_id:
isi:
- '000785983900003'
pmid:
- '35385734'
file:
- access_level: open_access
checksum: b4e8d68f0268dec499af333e6fd5d8e1
content_type: application/pdf
creator: dernst
date_created: 2022-04-15T09:06:25Z
date_updated: 2022-04-15T09:06:25Z
file_id: '11164'
file_name: 2022_CellReports_Villa.pdf
file_size: '7808644'
relation: main_file
success: 1
file_date_updated: 2022-04-15T09:06:25Z
has_accepted_license: '1'
intvolume: ' 39'
isi: 1
issue: '1'
keyword:
- General Biochemistry
- Genetics and Molecular Biology
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 25444568-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '715508'
name: Probing the Reversibility of Autism Spectrum Disorders by Employing in vivo
and in vitro Models
- _id: 2690FEAC-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: I04205
name: Identification of converging Molecular Pathways Across Chromatinopathies as
Targets for Therapy
publication: Cell Reports
publication_identifier:
issn:
- 2211-1247
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
record:
- id: '18681'
relation: dissertation_contains
status: public
- id: '18674'
relation: dissertation_contains
status: public
- id: '12364'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: CHD8 haploinsufficiency links autism to transient alterations in excitatory
and inhibitory trajectories
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 39
year: '2022'
...
---
_id: '7128'
abstract:
- lang: eng
text: Loss of functional cardiomyocytes is a major determinant of heart failure
after myocardial infarction. Previous high throughput screening studies have identified
a few microRNAs (miRNAs) that can induce cardiomyocyte proliferation and stimulate
cardiac regeneration in mice. Here, we show that all of the most effective of
these miRNAs activate nuclear localization of the master transcriptional cofactor
Yes-associated protein (YAP) and induce expression of YAP-responsive genes. In
particular, miR-199a-3p directly targets two mRNAs coding for proteins impinging
on the Hippo pathway, the upstream YAP inhibitory kinase TAOK1, and the E3 ubiquitin
ligase β-TrCP, which leads to YAP degradation. Several of the pro-proliferative
miRNAs (including miR-199a-3p) also inhibit filamentous actin depolymerization
by targeting Cofilin2, a process that by itself activates YAP nuclear translocation.
Thus, activation of YAP and modulation of the actin cytoskeleton are major components
of the pro-proliferative action of miR-199a-3p and other miRNAs that induce cardiomyocyte
proliferation.
article_processing_charge: Yes
article_type: original
author:
- first_name: Consuelo
full_name: Torrini, Consuelo
last_name: Torrini
- first_name: Ryan J
full_name: Cubero, Ryan J
id: 850B2E12-9CD4-11E9-837F-E719E6697425
last_name: Cubero
orcid: 0000-0003-0002-1867
- first_name: Ellen
full_name: Dirkx, Ellen
last_name: Dirkx
- first_name: Luca
full_name: Braga, Luca
last_name: Braga
- first_name: Hashim
full_name: Ali, Hashim
last_name: Ali
- first_name: Giulia
full_name: Prosdocimo, Giulia
last_name: Prosdocimo
- first_name: Maria Ines
full_name: Gutierrez, Maria Ines
last_name: Gutierrez
- first_name: Chiara
full_name: Collesi, Chiara
last_name: Collesi
- first_name: Danilo
full_name: Licastro, Danilo
last_name: Licastro
- first_name: Lorena
full_name: Zentilin, Lorena
last_name: Zentilin
- first_name: Miguel
full_name: Mano, Miguel
last_name: Mano
- first_name: Serena
full_name: Zacchigna, Serena
last_name: Zacchigna
- first_name: Michele
full_name: Vendruscolo, Michele
last_name: Vendruscolo
- first_name: Matteo
full_name: Marsili, Matteo
last_name: Marsili
- first_name: Areejit
full_name: Samal, Areejit
last_name: Samal
- first_name: Mauro
full_name: Giacca, Mauro
last_name: Giacca
citation:
ama: Torrini C, Cubero RJ, Dirkx E, et al. Common regulatory pathways mediate activity
of microRNAs inducing cardiomyocyte proliferation. Cell Reports. 2019;27(9):2759-2771.e5.
doi:10.1016/j.celrep.2019.05.005
apa: Torrini, C., Cubero, R. J., Dirkx, E., Braga, L., Ali, H., Prosdocimo, G.,
… Giacca, M. (2019). Common regulatory pathways mediate activity of microRNAs
inducing cardiomyocyte proliferation. Cell Reports. Elsevier. https://doi.org/10.1016/j.celrep.2019.05.005
chicago: Torrini, Consuelo, Ryan J Cubero, Ellen Dirkx, Luca Braga, Hashim Ali,
Giulia Prosdocimo, Maria Ines Gutierrez, et al. “Common Regulatory Pathways Mediate
Activity of MicroRNAs Inducing Cardiomyocyte Proliferation.” Cell Reports.
Elsevier, 2019. https://doi.org/10.1016/j.celrep.2019.05.005.
ieee: C. Torrini et al., “Common regulatory pathways mediate activity of
microRNAs inducing cardiomyocyte proliferation,” Cell Reports, vol. 27,
no. 9. Elsevier, p. 2759–2771.e5, 2019.
ista: Torrini C, Cubero RJ, Dirkx E, Braga L, Ali H, Prosdocimo G, Gutierrez MI,
Collesi C, Licastro D, Zentilin L, Mano M, Zacchigna S, Vendruscolo M, Marsili
M, Samal A, Giacca M. 2019. Common regulatory pathways mediate activity of microRNAs
inducing cardiomyocyte proliferation. Cell Reports. 27(9), 2759–2771.e5.
mla: Torrini, Consuelo, et al. “Common Regulatory Pathways Mediate Activity of MicroRNAs
Inducing Cardiomyocyte Proliferation.” Cell Reports, vol. 27, no. 9, Elsevier,
2019, p. 2759–2771.e5, doi:10.1016/j.celrep.2019.05.005.
short: C. Torrini, R.J. Cubero, E. Dirkx, L. Braga, H. Ali, G. Prosdocimo, M.I.
Gutierrez, C. Collesi, D. Licastro, L. Zentilin, M. Mano, S. Zacchigna, M. Vendruscolo,
M. Marsili, A. Samal, M. Giacca, Cell Reports 27 (2019) 2759–2771.e5.
date_created: 2019-11-26T22:30:07Z
date_published: 2019-05-28T00:00:00Z
date_updated: 2021-01-12T08:11:56Z
day: '28'
ddc:
- '576'
doi: 10.1016/j.celrep.2019.05.005
extern: '1'
external_id:
pmid:
- '31141697'
file:
- access_level: open_access
checksum: c5d855d07263bfec718673385d0ea2d7
content_type: application/pdf
creator: rcubero
date_created: 2019-11-26T22:30:43Z
date_updated: 2020-07-14T12:47:50Z
file_id: '7129'
file_name: torrini_cellreports_2019.pdf
file_size: 4650750
relation: main_file
file_date_updated: 2020-07-14T12:47:50Z
has_accepted_license: '1'
intvolume: ' 27'
issue: '9'
keyword:
- cardiomyocyte
- cell cycle
- Cofilin2
- cytoskeleton
- Hippo
- microRNA
- regeneration
- YAP
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-nd/4.0/
month: '05'
oa: 1
oa_version: Published Version
page: 2759-2771.e5
pmid: 1
publication: Cell Reports
publication_identifier:
issn:
- 2211-1247
publication_status: published
publisher: Elsevier
quality_controlled: '1'
status: public
title: Common regulatory pathways mediate activity of microRNAs inducing cardiomyocyte
proliferation
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 27
year: '2019'
...
---
_id: '672'
abstract:
- lang: eng
text: Trafficking cells frequently transmigrate through epithelial and endothelial
monolayers. How monolayers cooperate with the penetrating cells to support their
transit is poorly understood. We studied dendritic cell (DC) entry into lymphatic
capillaries as a model system for transendothelial migration. We find that the
chemokine CCL21, which is the decisive guidance cue for intravasation, mainly
localizes in the trans-Golgi network and intracellular vesicles of lymphatic endothelial
cells. Upon DC transmigration, these Golgi deposits disperse and CCL21 becomes
extracellularly enriched at the sites of endothelial cell-cell junctions. When
we reconstitute the transmigration process in vitro, we find that secretion of
CCL21-positive vesicles is triggered by a DC contact-induced calcium signal, and
selective calcium chelation in lymphatic endothelium attenuates transmigration.
Altogether, our data demonstrate a chemokine-mediated feedback between DCs and
lymphatic endothelium, which facilitates transendothelial migration.
article_processing_charge: Yes
author:
- first_name: Kari
full_name: Vaahtomeri, Kari
id: 368EE576-F248-11E8-B48F-1D18A9856A87
last_name: Vaahtomeri
orcid: 0000-0001-7829-3518
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
- first_name: Matthias
full_name: Mehling, Matthias
id: 3C23B994-F248-11E8-B48F-1D18A9856A87
last_name: Mehling
orcid: 0000-0001-8599-1226
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Vaahtomeri K, Brown M, Hauschild R, et al. Locally triggered release of the
chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia.
Cell Reports. 2017;19(5):902-909. doi:10.1016/j.celrep.2017.04.027
apa: Vaahtomeri, K., Brown, M., Hauschild, R., de Vries, I., Leithner, A. F., Mehling,
M., … Sixt, M. K. (2017). Locally triggered release of the chemokine CCL21 promotes
dendritic cell transmigration across lymphatic endothelia. Cell Reports.
Cell Press. https://doi.org/10.1016/j.celrep.2017.04.027
chicago: Vaahtomeri, Kari, Markus Brown, Robert Hauschild, Ingrid de Vries, Alexander
F Leithner, Matthias Mehling, Walter Kaufmann, and Michael K Sixt. “Locally Triggered
Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic
Endothelia.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.04.027.
ieee: K. Vaahtomeri et al., “Locally triggered release of the chemokine CCL21
promotes dendritic cell transmigration across lymphatic endothelia,” Cell Reports,
vol. 19, no. 5. Cell Press, pp. 902–909, 2017.
ista: Vaahtomeri K, Brown M, Hauschild R, de Vries I, Leithner AF, Mehling M, Kaufmann
W, Sixt MK. 2017. Locally triggered release of the chemokine CCL21 promotes dendritic
cell transmigration across lymphatic endothelia. Cell Reports. 19(5), 902–909.
mla: Vaahtomeri, Kari, et al. “Locally Triggered Release of the Chemokine CCL21
Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” Cell Reports,
vol. 19, no. 5, Cell Press, 2017, pp. 902–09, doi:10.1016/j.celrep.2017.04.027.
short: K. Vaahtomeri, M. Brown, R. Hauschild, I. de Vries, A.F. Leithner, M. Mehling,
W. Kaufmann, M.K. Sixt, Cell Reports 19 (2017) 902–909.
corr_author: '1'
date_created: 2018-12-11T11:47:50Z
date_published: 2017-05-02T00:00:00Z
date_updated: 2025-09-10T14:27:34Z
day: '02'
ddc:
- '570'
department:
- _id: MiSi
- _id: Bio
- _id: EM-Fac
doi: 10.1016/j.celrep.2017.04.027
ec_funded: 1
external_id:
isi:
- '000402124100002'
file:
- access_level: open_access
checksum: 8fdddaab1f1d76a6ec9ca94dcb6b07a2
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:54Z
date_updated: 2020-07-14T12:47:38Z
file_id: '5109'
file_name: IST-2017-900-v1+1_1-s2.0-S2211124717305211-main.pdf
file_size: 2248814
relation: main_file
file_date_updated: 2020-07-14T12:47:38Z
has_accepted_license: '1'
intvolume: ' 19'
isi: 1
issue: '5'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: 902 - 909
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and force transduction of migrating leukocytes
publication: Cell Reports
publication_identifier:
issn:
- 2211-1247
publication_status: published
publisher: Cell Press
publist_id: '7052'
pubrep_id: '900'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration
across lymphatic endothelia
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 19
year: '2017'
...
---
_id: '677'
abstract:
- lang: eng
text: The INO80 complex (INO80-C) is an evolutionarily conserved nucleosome remodeler
that acts in transcription, replication, and genome stability. It is required
for resistance against genotoxic agents and is involved in the repair of DNA double-strand
breaks (DSBs) by homologous recombination (HR). However, the causes of the HR
defect in INO80-C mutant cells are controversial. Here, we unite previous findings
using a system to study HR with high spatial resolution in budding yeast. We find
that INO80-C has at least two distinct functions during HR—DNA end resection and
presynaptic filament formation. Importantly, the second function is linked to
the histone variant H2A.Z. In the absence of H2A.Z, presynaptic filament formation
and HR are restored in INO80-C-deficient mutants, suggesting that presynaptic
filament formation is the crucial INO80-C function during HR.
article_processing_charge: No
author:
- first_name: Claudio
full_name: Lademann, Claudio
last_name: Lademann
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Boris
full_name: Pfander, Boris
last_name: Pfander
- first_name: Stefan
full_name: Jentsch, Stefan
last_name: Jentsch
citation:
ama: Lademann C, Renkawitz J, Pfander B, Jentsch S. The INO80 complex removes H2A.Z
to promote presynaptic filament formation during homologous recombination. Cell
Reports. 2017;19(7):1294-1303. doi:10.1016/j.celrep.2017.04.051
apa: Lademann, C., Renkawitz, J., Pfander, B., & Jentsch, S. (2017). The INO80
complex removes H2A.Z to promote presynaptic filament formation during homologous
recombination. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2017.04.051
chicago: Lademann, Claudio, Jörg Renkawitz, Boris Pfander, and Stefan Jentsch. “The
INO80 Complex Removes H2A.Z to Promote Presynaptic Filament Formation during Homologous
Recombination.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.04.051.
ieee: C. Lademann, J. Renkawitz, B. Pfander, and S. Jentsch, “The INO80 complex
removes H2A.Z to promote presynaptic filament formation during homologous recombination,”
Cell Reports, vol. 19, no. 7. Cell Press, pp. 1294–1303, 2017.
ista: Lademann C, Renkawitz J, Pfander B, Jentsch S. 2017. The INO80 complex removes
H2A.Z to promote presynaptic filament formation during homologous recombination.
Cell Reports. 19(7), 1294–1303.
mla: Lademann, Claudio, et al. “The INO80 Complex Removes H2A.Z to Promote Presynaptic
Filament Formation during Homologous Recombination.” Cell Reports, vol.
19, no. 7, Cell Press, 2017, pp. 1294–303, doi:10.1016/j.celrep.2017.04.051.
short: C. Lademann, J. Renkawitz, B. Pfander, S. Jentsch, Cell Reports 19 (2017)
1294–1303.
date_created: 2018-12-11T11:47:52Z
date_published: 2017-05-16T00:00:00Z
date_updated: 2025-09-10T14:23:55Z
day: '16'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1016/j.celrep.2017.04.051
external_id:
isi:
- '000402125100002'
file:
- access_level: open_access
checksum: efc7287d9c6354983cb151880e9ad72a
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:15:48Z
date_updated: 2020-07-14T12:47:40Z
file_id: '5171'
file_name: IST-2017-899-v1+1_1-s2.0-S2211124717305454-main.pdf
file_size: 3005610
relation: main_file
file_date_updated: 2020-07-14T12:47:40Z
has_accepted_license: '1'
intvolume: ' 19'
isi: 1
issue: '7'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: 1294 - 1303
publication: Cell Reports
publication_identifier:
issn:
- 2211-1247
publication_status: published
publisher: Cell Press
publist_id: '7046'
pubrep_id: '899'
quality_controlled: '1'
scopus_import: '1'
status: public
title: The INO80 complex removes H2A.Z to promote presynaptic filament formation during
homologous recombination
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 19
year: '2017'
...
---
_id: '1117'
abstract:
- lang: eng
text: 'GABAergic synapses in brain circuits generate inhibitory output signals with
submillisecond latency and temporal precision. Whether the molecular identity
of the release sensor contributes to these signaling properties remains unclear.
Here, we examined the Ca^2+ sensor of exocytosis at GABAergic basket cell (BC)
to Purkinje cell (PC) synapses in cerebellum. Immunolabeling suggested that BC
terminals selectively expressed synaptotagmin 2 (Syt2), whereas synaptotagmin
1 (Syt1) was enriched in excitatory terminals. Genetic elimination of Syt2 reduced
action potential-evoked release to ∼10%, identifying Syt2 as the major Ca^2+ sensor
at BC-PC synapses. Differential adenovirus-mediated rescue revealed that Syt2
triggered release with shorter latency and higher temporal precision and mediated
faster vesicle pool replenishment than Syt1. Furthermore, deletion of Syt2 severely
reduced and delayed disynaptic inhibition following parallel fiber stimulation.
Thus, the selective use of Syt2 as release sensor at BC-PC synapses ensures fast
and efficient feedforward inhibition in cerebellar microcircuits. #bioimagingfacility-author'
acknowledged_ssus:
- _id: Bio
- _id: PreCl
article_processing_charge: No
author:
- first_name: Chong
full_name: Chen, Chong
id: 3DFD581A-F248-11E8-B48F-1D18A9856A87
last_name: Chen
- first_name: Itaru
full_name: Arai, Itaru
id: 32A73F6C-F248-11E8-B48F-1D18A9856A87
last_name: Arai
- first_name: Rachel
full_name: Satterield, Rachel
last_name: Satterield
- first_name: Samuel
full_name: Young, Samuel
last_name: Young
- 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: Chen C, Arai itaru, Satterield R, Young S, Jonas PM. Synaptotagmin 2 is the
fast Ca2+ sensor at a central inhibitory synapse. Cell Reports. 2017;18(3):723-736.
doi:10.1016/j.celrep.2016.12.067
apa: Chen, C., Arai, itaru, Satterield, R., Young, S., & Jonas, P. M. (2017).
Synaptotagmin 2 is the fast Ca2+ sensor at a central inhibitory synapse. Cell
Reports. Cell Press. https://doi.org/10.1016/j.celrep.2016.12.067
chicago: Chen, Chong, itaru Arai, Rachel Satterield, Samuel Young, and Peter M Jonas.
“Synaptotagmin 2 Is the Fast Ca2+ Sensor at a Central Inhibitory Synapse.” Cell
Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2016.12.067.
ieee: C. Chen, itaru Arai, R. Satterield, S. Young, and P. M. Jonas, “Synaptotagmin
2 is the fast Ca2+ sensor at a central inhibitory synapse,” Cell Reports,
vol. 18, no. 3. Cell Press, pp. 723–736, 2017.
ista: Chen C, Arai itaru, Satterield R, Young S, Jonas PM. 2017. Synaptotagmin
2 is the fast Ca2+ sensor at a central inhibitory synapse. Cell Reports. 18(3),
723–736.
mla: Chen, Chong, et al. “Synaptotagmin 2 Is the Fast Ca2+ Sensor at a Central Inhibitory
Synapse.” Cell Reports, vol. 18, no. 3, Cell Press, 2017, pp. 723–36, doi:10.1016/j.celrep.2016.12.067.
short: C. Chen, itaru Arai, R. Satterield, S. Young, P.M. Jonas, Cell Reports 18
(2017) 723–736.
date_created: 2018-12-11T11:50:14Z
date_published: 2017-01-17T00:00:00Z
date_updated: 2026-04-08T14:09:28Z
day: '17'
ddc:
- '571'
department:
- _id: PeJo
doi: 10.1016/j.celrep.2016.12.067
ec_funded: 1
external_id:
isi:
- '000396470600013'
file:
- access_level: open_access
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:16:09Z
date_updated: 2018-12-12T10:16:09Z
file_id: '5195'
file_name: IST-2017-751-v1+1_1-s2.0-S2211124716317740-main.pdf
file_size: 4427591
relation: main_file
file_date_updated: 2018-12-12T10:16:09Z
has_accepted_license: '1'
intvolume: ' 18'
isi: 1
issue: '3'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
page: 723 - 736
project:
- _id: 25C26B1E-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P24909-B24
name: Mechanisms of transmitter release at GABAergic synapses
- _id: 25C0F108-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '268548'
name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons
publication: Cell Reports
publication_identifier:
issn:
- 2211-1247
publication_status: published
publisher: Cell Press
publist_id: '6245'
pubrep_id: '751'
quality_controlled: '1'
related_material:
record:
- id: '324'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Synaptotagmin 2 is the fast Ca2+ sensor at a central inhibitory synapse
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: 18
year: '2017'
...
---
_id: '749'
abstract:
- lang: eng
text: 'Synaptotagmin 7 (Syt7) is thought to be a Ca2+ sensor that mediates asynchronous
transmitter release and facilitation at synapses. However, Syt7 is strongly expressed
in fast-spiking, parvalbumin-expressing GABAergic interneurons, and the output
synapses of these neurons produce only minimal asynchronous release and show depression
rather than facilitation. To resolve this apparent contradiction, we examined
the effects of genetic elimination of Syt7 on synaptic transmission at the GABAergic
basket cell (BC)-Purkinje cell (PC) synapse in cerebellum. Our results indicate
that at the BC-PC synapse, Syt7 contributes to asynchronous release, pool replenishment,
and facilitation. In combination, these three effects ensure efficient transmitter
release during high-frequency activity and guarantee frequency independence of
inhibition. Our results identify a distinct function of Syt7: ensuring the efficiency
of high-frequency inhibitory synaptic transmission'
acknowledged_ssus:
- _id: PreCl
article_processing_charge: No
author:
- first_name: Chong
full_name: Chen, Chong
id: 3DFD581A-F248-11E8-B48F-1D18A9856A87
last_name: Chen
- first_name: Rachel
full_name: Satterfield, Rachel
last_name: Satterfield
- first_name: Samuel
full_name: Young, Samuel
last_name: Young
- 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: Chen C, Satterfield R, Young S, Jonas PM. Triple function of Synaptotagmin
7 ensures efficiency of high-frequency transmission at central GABAergic synapses.
Cell Reports. 2017;21(8):2082-2089. doi:10.1016/j.celrep.2017.10.122
apa: Chen, C., Satterfield, R., Young, S., & Jonas, P. M. (2017). Triple function
of Synaptotagmin 7 ensures efficiency of high-frequency transmission at central
GABAergic synapses. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2017.10.122
chicago: Chen, Chong, Rachel Satterfield, Samuel Young, and Peter M Jonas. “Triple
Function of Synaptotagmin 7 Ensures Efficiency of High-Frequency Transmission
at Central GABAergic Synapses.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.10.122.
ieee: C. Chen, R. Satterfield, S. Young, and P. M. Jonas, “Triple function of Synaptotagmin
7 ensures efficiency of high-frequency transmission at central GABAergic synapses,”
Cell Reports, vol. 21, no. 8. Cell Press, pp. 2082–2089, 2017.
ista: Chen C, Satterfield R, Young S, Jonas PM. 2017. Triple function of Synaptotagmin
7 ensures efficiency of high-frequency transmission at central GABAergic synapses.
Cell Reports. 21(8), 2082–2089.
mla: Chen, Chong, et al. “Triple Function of Synaptotagmin 7 Ensures Efficiency
of High-Frequency Transmission at Central GABAergic Synapses.” Cell Reports,
vol. 21, no. 8, Cell Press, 2017, pp. 2082–89, doi:10.1016/j.celrep.2017.10.122.
short: C. Chen, R. Satterfield, S. Young, P.M. Jonas, Cell Reports 21 (2017) 2082–2089.
corr_author: '1'
date_created: 2018-12-11T11:48:18Z
date_published: 2017-11-21T00:00:00Z
date_updated: 2026-04-08T14:09:28Z
day: '21'
ddc:
- '570'
- '571'
department:
- _id: PeJo
doi: 10.1016/j.celrep.2017.10.122
ec_funded: 1
external_id:
isi:
- '000416216700007'
file:
- access_level: open_access
checksum: a6afa3764909bf6edafa07982d8e1cee
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:09:14Z
date_updated: 2020-07-14T12:47:59Z
file_id: '4737'
file_name: IST-2017-874-v1+1_PIIS2211124717316029.pdf
file_size: 2759195
relation: main_file
file_date_updated: 2020-07-14T12:47:59Z
has_accepted_license: '1'
intvolume: ' 21'
isi: 1
issue: '8'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
page: 2082 - 2089
project:
- _id: 25C26B1E-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P24909-B24
name: Mechanisms of transmitter release at GABAergic synapses
- _id: 25B7EB9E-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '692692'
name: Biophysics and circuit function of a giant cortical glutamatergic synapse
publication: Cell Reports
publication_identifier:
issn:
- 2211-1247
publication_status: published
publisher: Cell Press
publist_id: '6907'
pubrep_id: '874'
quality_controlled: '1'
related_material:
record:
- id: '324'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Triple function of Synaptotagmin 7 ensures efficiency of high-frequency transmission
at central GABAergic synapses
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: 21
year: '2017'
...
---
DOAJ_listed: '1'
_id: '18365'
abstract:
- lang: eng
text: Yeast cells with DNA damage avoid respiration, presumably because products
of oxidative metabolism can be harmful to DNA. We show that DNA damage inhibits
the activity of the Snf1 (AMP-activated) protein kinase (AMPK), which activates
expression of genes required for respiration. Glucose and DNA damage upregulate
SUMOylation of Snf1, catalyzed by the SUMO E3 ligase Mms21, which inhibits SNF1
activity. The DNA damage checkpoint kinases Mec1/ATR and Tel1/ATM, as well as
the nutrient-sensing protein kinase A (PKA), regulate Mms21 activity toward Snf1.
Mec1 and Tel1 are required for two SNF1-regulated processes—glucose sensing and
ADH2 gene expression—even without exogenous genotoxic stress. Our results imply
that inhibition of Snf1 by SUMOylation is a mechanism by which cells lower their
respiration in response to DNA damage. This raises the possibility that activation
of DNA damage checkpoint mechanisms could contribute to aerobic fermentation (Warburg
effect), a hallmark of cancer cells.
article_processing_charge: No
author:
- first_name: Kobi J.
full_name: Simpson-Lavy, Kobi J.
last_name: Simpson-Lavy
- first_name: Alexander
full_name: Bronstein, Alexander
id: 58f3726e-7cba-11ef-ad8b-e6e8cb3904e6
last_name: Bronstein
orcid: 0000-0001-9699-8730
- first_name: Martin
full_name: Kupiec, Martin
last_name: Kupiec
- first_name: Mark
full_name: Johnston, Mark
last_name: Johnston
citation:
ama: Simpson-Lavy KJ, Bronstein AM, Kupiec M, Johnston M. Cross-talk between carbon
cetabolism and the DNA camage response in S. cerevisiae. Cell Reports.
2015;12(11):1865-1875. doi:10.1016/j.celrep.2015.08.025
apa: Simpson-Lavy, K. J., Bronstein, A. M., Kupiec, M., & Johnston, M. (2015).
Cross-talk between carbon cetabolism and the DNA camage response in S. cerevisiae.
Cell Reports. Elsevier. https://doi.org/10.1016/j.celrep.2015.08.025
chicago: Simpson-Lavy, Kobi J., Alex M. Bronstein, Martin Kupiec, and Mark Johnston.
“Cross-Talk between Carbon Cetabolism and the DNA Camage Response in S. Cerevisiae.”
Cell Reports. Elsevier, 2015. https://doi.org/10.1016/j.celrep.2015.08.025.
ieee: K. J. Simpson-Lavy, A. M. Bronstein, M. Kupiec, and M. Johnston, “Cross-talk
between carbon cetabolism and the DNA camage response in S. cerevisiae,” Cell
Reports, vol. 12, no. 11. Elsevier, pp. 1865–1875, 2015.
ista: Simpson-Lavy KJ, Bronstein AM, Kupiec M, Johnston M. 2015. Cross-talk between
carbon cetabolism and the DNA camage response in S. cerevisiae. Cell Reports.
12(11), 1865–1875.
mla: Simpson-Lavy, Kobi J., et al. “Cross-Talk between Carbon Cetabolism and the
DNA Camage Response in S. Cerevisiae.” Cell Reports, vol. 12, no. 11, Elsevier,
2015, pp. 1865–75, doi:10.1016/j.celrep.2015.08.025.
short: K.J. Simpson-Lavy, A.M. Bronstein, M. Kupiec, M. Johnston, Cell Reports 12
(2015) 1865–1875.
date_created: 2024-10-15T11:20:54Z
date_published: 2015-09-22T00:00:00Z
date_updated: 2024-12-18T12:23:56Z
day: '22'
doi: 10.1016/j.celrep.2015.08.025
extern: '1'
intvolume: ' 12'
issue: '11'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.celrep.2015.08.025
month: '09'
oa: 1
oa_version: Published Version
page: 1865-1875
publication: Cell Reports
publication_identifier:
issn:
- 2211-1247
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Cross-talk between carbon cetabolism and the DNA camage response in S. cerevisiae
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 12
year: '2015'
...
---
_id: '7598'
article_processing_charge: No
article_type: original
author:
- first_name: Shutang
full_name: Tan, Shutang
id: 2DE75584-F248-11E8-B48F-1D18A9856A87
last_name: Tan
orcid: 0000-0002-0471-8285
- first_name: Hong-Wei
full_name: Xue, Hong-Wei
last_name: Xue
citation:
ama: Tan S, Xue H-W. Casein kinase 1 regulates ethylene synthesis by phosphorylating
and promoting the turnover of ACS5. Cell Reports. 2014;9(5):1692-1702.
doi:10.1016/j.celrep.2014.10.047
apa: Tan, S., & Xue, H.-W. (2014). Casein kinase 1 regulates ethylene synthesis
by phosphorylating and promoting the turnover of ACS5. Cell Reports. Elsevier.
https://doi.org/10.1016/j.celrep.2014.10.047
chicago: Tan, Shutang, and Hong-Wei Xue. “Casein Kinase 1 Regulates Ethylene Synthesis
by Phosphorylating and Promoting the Turnover of ACS5.” Cell Reports. Elsevier,
2014. https://doi.org/10.1016/j.celrep.2014.10.047.
ieee: S. Tan and H.-W. Xue, “Casein kinase 1 regulates ethylene synthesis by phosphorylating
and promoting the turnover of ACS5,” Cell Reports, vol. 9, no. 5. Elsevier,
pp. 1692–1702, 2014.
ista: Tan S, Xue H-W. 2014. Casein kinase 1 regulates ethylene synthesis by phosphorylating
and promoting the turnover of ACS5. Cell Reports. 9(5), 1692–1702.
mla: Tan, Shutang, and Hong-Wei Xue. “Casein Kinase 1 Regulates Ethylene Synthesis
by Phosphorylating and Promoting the Turnover of ACS5.” Cell Reports, vol.
9, no. 5, Elsevier, 2014, pp. 1692–702, doi:10.1016/j.celrep.2014.10.047.
short: S. Tan, H.-W. Xue, Cell Reports 9 (2014) 1692–1702.
date_created: 2020-03-21T16:08:18Z
date_published: 2014-12-11T00:00:00Z
date_updated: 2021-01-12T08:14:24Z
day: '11'
ddc:
- '580'
doi: 10.1016/j.celrep.2014.10.047
extern: '1'
file:
- access_level: open_access
checksum: 23c30de4ac98ce9879fc054121517626
content_type: application/pdf
creator: dernst
date_created: 2020-03-23T12:23:40Z
date_updated: 2020-07-14T12:48:01Z
file_id: '7613'
file_name: 2014_CellPress_Tan.pdf
file_size: 2755808
relation: main_file
file_date_updated: 2020-07-14T12:48:01Z
has_accepted_license: '1'
intvolume: ' 9'
issue: '5'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
page: 1692-1702
publication: Cell Reports
publication_identifier:
issn:
- 2211-1247
publication_status: published
publisher: Elsevier
quality_controlled: '1'
status: public
title: Casein kinase 1 regulates ethylene synthesis by phosphorylating and promoting
the turnover of ACS5
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 9
year: '2014'
...