PuSH - Publikationsserver des Helmholtz Zentrums München

Export: TXT Text RIS Endnote (RIS) BIB BibTeX
Bakhti, M. ; Bastidas-Ponce, A. ; Tritschler, S. ; Czarnecki, O. ; Tarquis Medina, M. ; Nedvedova, E.* ; Jaki, J. ; Willmann, S. ; Scheibner, K. ; Cota, P. ; Salinno, C. ; Boldt, K.* ; Horn, N.* ; Ueffing, M.* ; Burtscher, I. ; Theis, F.J. ; Coskun, Ü. ; Lickert, H.

Synaptotagmin-13 orchestrates pancreatic endocrine cell egression and islet morphogenesis.

Nat. Commun. 13:4540 (2022)
Verlagsversion Forschungsdaten Forschungsdaten Forschungsdaten DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
During pancreas development endocrine cells leave the ductal epithelium to form the islets of Langerhans, but the morphogenetic mechanisms are incompletely understood. Here, we identify the Ca2+-independent atypical Synaptotagmin-13 (Syt13) as a key regulator of endocrine cell egression and islet formation. We detect specific upregulation of the Syt13 gene and encoded protein in endocrine precursors and the respective lineage during islet formation. The Syt13 protein is localized to the apical membrane of endocrine precursors and to the front domain of egressing endocrine cells, marking a previously unidentified apical-basal to front-rear repolarization during endocrine precursor cell egression. Knockout of Syt13 impairs endocrine cell egression and skews the α-to-β-cell ratio. Mechanistically, Syt13 is a vesicle trafficking protein, transported via the microtubule cytoskeleton, and interacts with phosphatidylinositol phospholipids for polarized localization. By internalizing a subset of plasma membrane proteins at the front domain, including α6β4 integrins, Syt13 modulates cell-matrix adhesion and allows efficient endocrine cell egression. Altogether, these findings uncover an unexpected role for Syt13 as a morphogenetic driver of endocrinogenesis and islet formation.
Impact Factor
Scopus SNIP
Scopus
Cited By
Altmetric
17.694
3.341
1
Tags
Anmerkungen
Besondere Publikation
Auf Hompepage verbergern

Zusatzinfos bearbeiten
Eigene Tags bearbeiten
Privat
Eigene Anmerkung bearbeiten
Privat
Auf Publikationslisten für
Homepage nicht anzeigen
Als besondere Publikation
markieren
Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Sprache englisch
Veröffentlichungsjahr 2022
HGF-Berichtsjahr 2022
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Zeitschrift Nature Communications
Quellenangaben Band: 13, Heft: 1, Seiten: , Artikelnummer: 4540 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Regeneration Research (IDR)
Institute of Computational Biology (ICB)
Institute of Pancreatic Islet Research (IPI)
POF Topic(s) 30201 - Metabolic Health
90000 - German Center for Diabetes Research
30205 - Bioengineering and Digital Health
Forschungsfeld(er) Helmholtz Diabetes Center
Enabling and Novel Technologies
PSP-Element(e) G-502300-001
G-501900-231
G-503800-001
G-501900-234
G-502600-002
Förderungen Tistou & Charlotte Kerstan Stiftung
DZD, DZD-Next funding
Helmholtz Association-Initiative and Networking Fund (IVF)
German Center for Diabetes Research (DZD e.V.)
German Research Foundation (DFG)
Helmholtz Portfolio Theme'Metabolic Dysfunction and Common Disease
Helmholtz Association
DOI 10.1038/s41467-022-31862-8
WOS ID WOS:000836424200020
Scopus ID 85135398893
PubMed ID 35927244
Erfassungsdatum 2022-08-29
[➜Korrektur melden]