Peroxiredoxin Stabilization of DE-Cadherin Promotes Primordial Germ Cell Adhesion

SummaryRegulated 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.

Graphical AbstractFigure optionsDownload high-quality image (222 K)Download as PowerPoint slideHighlights
► The peroxiredoxin, Jafrac1, controls primordial germ cell adhesion during gastrulation
► H2O2 treatment of Drosophila embryos reduces DE-cadherin and β-catenin levels
► Increasing DE-cadherin levels is sufficient to rescue the Jafrac1 phenotype
► Jafrac1 stabilizes the level of adherens junction components in Drosophila embryos