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

Peroxiredoxin stabilization of DE-cadherin promotes primordial germ cell adhesion.
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DOI:
10.1016/j.devcel.2010.12.007
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发表时间:
2011-02-15
期刊:
影响因子:
11.8
通讯作者:
Lehmann, Ruth
Lehmann, Ruth
中科院分区:
生物学1区
文献类型:
--
作者:
DeGennaro, Matthew;Hurd, Thomas Ryan;Siekhaus, Dania Elisabeth;Biteau, Benoit;Jasper, Heinrich;Lehmann, Ruth

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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.
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