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

Noriko Hamada-Kawaguchi, Beston F. Nore, Yusuke Kuwada, C. I.Edvard Smith, Daisuke Yamamoto

    Research output: Contribution to journalArticle

    33 Citations (Scopus)

    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.

    Original languageEnglish
    Pages (from-to)294-297
    Number of pages4
    JournalScience
    Volume343
    Issue number6168
    DOIs
    Publication statusPublished - 2014 Jan 1

    ASJC Scopus subject areas

    • General

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    Hamada-Kawaguchi, N., Nore, B. F., Kuwada, Y., Smith, C. I. E., & Yamamoto, D. (2014). Btk29A promotes Wnt4 signaling in the niche to terminate germ cell proliferation in Drosophila. Science, 343(6168), 294-297. https://doi.org/10.1126/science.1244512