Btk29A promotes Wnt4 signaling in the niche to terminate germ cell proliferation in Drosophila

  • Hamada-Kawaguchi N
  • Nore B
  • Kuwada Y
 et al. 
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Abstract

Btk29A is the Drosophila ortholog of the mammalian Bruton's tyrosine kinase (Btk), mutations of which in humans cause a heritable immunodeficiency disease. Btk29A mutations stabilized the proliferating cystoblast fate, leading to an ovarian tumor. This phenotype was rescued by overexpression of wild-type Btk29A and phenocopied by the interference of Wnt4-β-catenin signaling or its putative downstream nuclear protein Piwi in somatic escort cells. Btk29A and mammalian Btk directly phosphorylated tyrosine residues of β-catenin, leading to the up-regulation of its transcriptional activity. Thus, we identify a transcriptional switch involving the kinase Btk29A/Btk and its phosphorylation target, β-catenin, which functions downstream of Wnt4 in escort cells to terminate Drosophila germ cell proliferation through up-regulation of piwi expression. This signaling mechanism likely represents a versatile developmental switch.

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Authors

  • Noriko Hamada-Kawaguchi

  • Beston F. Nore

  • Yusuke Kuwada

  • C. I.Edvard Smith

  • Daisuke Yamamoto

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