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

    研究成果: Article査読

    38 被引用数 (Scopus)

    抄録

    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.

    本文言語English
    ページ(範囲)294-297
    ページ数4
    ジャーナルScience
    343
    6168
    DOI
    出版ステータスPublished - 2014

    ASJC Scopus subject areas

    • 一般

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