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Dev Cell. 2011 Feb 15;20(2):233-43. doi: 10.1016/j.devcel.2010.12.007.

Peroxiredoxin stabilization of DE-cadherin promotes primordial germ cell adhesion.

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  • 1Department of Cell Biology, HHMI and Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, NY 10016, USA.

Abstract

Regulated adhesion between cells and their environment is critical for normal cell migration. We have identified mutations in a gene encoding the Drosophila hydrogen peroxide (H₂O₂)-degrading enzyme Jafrac1, which lead to germ cell adhesion defects. During gastrulation, primordial germ cells (PGCs) associate tightly with the invaginating midgut primordium as it enters the embryo; however, in embryos from jafrac1 mutant mothers this association is disrupted, leaving some PGCs trailing on the outside of the embryo. We observed similar phenotypes in embryos from DE-cadherin/shotgun (shg) mutant mothers and were able to rescue the jafrac1 phenotype by increasing DE-cadherin levels. This and our biochemical evidence strongly suggest that Jafrac1-mediated reduction of H₂O₂ is required to maintain DE-cadherin protein levels in the early embryo. Our results present in vivo evidence of a peroxiredoxin regulating DE-cadherin-mediated adhesion.

Copyright © 2011 Elsevier Inc. All rights reserved.

PMID:
21316590
[PubMed - indexed for MEDLINE]
PMCID:
PMC3712085
Free PMC Article
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