PUBLICATION

Chemokine Signaling Controls Endodermal Migration During Zebrafish Gastrulation

Authors
Nair, S., and Schilling, T.F.
ID
ZDB-PUB-080826-45
Date
2008
Source
Science (New York, N.Y.)   322(5898): 89-92 (Journal)
Registered Authors
Nair, Sreelaja, Schilling, Tom
Keywords
none
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • Cell Adhesion
  • Cell Movement
  • Chemokine CXCL12/genetics
  • Chemokine CXCL12/metabolism*
  • Chemokines, CXC/genetics
  • Chemokines, CXC/metabolism*
  • Endoderm/cytology*
  • Endoderm/embryology
  • Endoderm/metabolism
  • Fibronectins/metabolism
  • Gastrula/cytology
  • Gastrula/embryology
  • Gastrula/metabolism*
  • Gastrulation*
  • Integrin beta Chains/metabolism
  • Integrins/metabolism
  • Mesoderm/cytology
  • Mesoderm/embryology
  • Mesoderm/metabolism
  • Morphogenesis
  • Receptors, CXCR4/genetics
  • Receptors, CXCR4/metabolism*
  • Signal Transduction
  • Zebrafish
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed
18719251 Full text @ Science
Abstract
Directed cell movements during gastrulation establish the germ layers of the vertebrate embryo and coordinate their contributions to different tissues and organs. Anterior migration of mesoderm and endoderm has largely been interpreted to result from epiboly and convergent-extension movements that drive body elongation. We show that the chemokine cxcl12b and its receptor Cxcr4A restrict anterior migration of endoderm during zebrafish gastrulation, thereby coordinating its movements with mesoderm. Depletion of either gene product causes the endoderm to separate from mesoderm and migrate farther anterior than normal, due to disruption of integrin-dependent cell adhesion. This results in bilateral duplications of endodermal organs, which may have relevance to human organ defects.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping