Wnt11 functions in gastrulation by controlling cell cohesion through Rab5c and E-Cadherin

Publikation: Beitrag in FachzeitschriftForschungsartikelBeigetragenBegutachtung

Beitragende

  • Florian Ulrich - , Max Planck Institute of Molecular Cell Biology and Genetics (Autor:in)
  • Michael Krieg - , Technische Universität Dresden (Autor:in)
  • Eva Maria Schötz - , Max Planck Institute of Molecular Cell Biology and Genetics (Autor:in)
  • Vinzenz Link - , Max Planck Institute of Molecular Cell Biology and Genetics (Autor:in)
  • Irinka Castanon - , Max Planck Institute of Molecular Cell Biology and Genetics (Autor:in)
  • Viktor Schnabel - , Max Planck Institute of Molecular Cell Biology and Genetics (Autor:in)
  • Anna Taubenberger - , Technische Universität Dresden (Autor:in)
  • Daniel Mueller - , Technische Universität Dresden (Autor:in)
  • Pierre Henri Puech - , Technische Universität Dresden (Autor:in)
  • Carl Philipp Heisenberg - , Max Planck Institute of Molecular Cell Biology and Genetics (Autor:in)

Abstract

Wnt11 plays a central role in tissue morphogenesis during vertebrate gastrulation, but the molecular and cellular mechanisms by which Wnt11 exerts its effects remain poorly understood. Here, we show that Wnt11 functions during zebrafish gastrulation by regulating the cohesion of mesodermal and endodermal (mesendodermal) progenitor cells. Importantly, we demonstrate that Wnt11 activity in this process is mediated by the GTPase Rab5, a key regulator of early endocytosis, as blocking Rab5c activity in wild-type embryos phenocopies slb/wnt11 mutants, and enhancing Rab5c activity in slb/wnt11 mutant embryos rescues the mutant phenotype. In addition, we find that Wnt11 and Rab5c control the endocytosis of E-cadherin and are required in mesendodermal cells for E-cadherin-mediated cell cohesion. Together, our results suggest that Wnt11 controls tissue morphogenesis by modulating E-cadherin-mediated cell cohesion through Rab5c, a novel mechanism of Wnt signaling in gastrulation.

Details

OriginalspracheEnglisch
Seiten (von - bis)555-564
Seitenumfang10
FachzeitschriftDevelopmental cell
Jahrgang9
Ausgabenummer4
PublikationsstatusVeröffentlicht - Okt. 2005
Peer-Review-StatusJa
Extern publiziertJa

Externe IDs

PubMed 16198297