Reference - Detail
|Author||Hamada-Kawaguchi N, Nore BF, Kuwada Y, Smith CI, Yamamoto D.|
|Title||Btk29A promotes Wnt4 signaling in the niche to terminate germ cell proliferation in Drosophila.|
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.
|MeSH||Animals Argonaute Proteins / biosynthesis* Cell Proliferation* DNA Breaks, Double-Stranded Drosophila Proteins / biosynthesis* Drosophila Proteins / genetics Drosophila Proteins / metabolism* Drosophila melanogaster / genetics Drosophila melanogaster / metabolism Drosophila melanogaster / physiology* Gene Knockdown Techniques Genomic Instability Germ Cells / cytology Germ Cells / metabolism Germ Cells / physiology* Glycoproteins / genetics Glycoproteins / metabolism* Phosphorylation Protein-Tyrosine Kinases / genetics Protein-Tyrosine Kinases / metabolism* RNA, Small Interfering / genetics RNA, Small Interfering / metabolism Signal Transduction Transcription, Genetic Tyrosine / genetics Tyrosine / metabolism Up-Regulation Wnt Proteins / genetics Wnt Proteins / metabolism* beta Catenin / genetics beta Catenin / metabolism*|
|WOS Category||CELL BIOLOGY|