A role for polycystin-1 and polycystin-2 in neural progenitor cell differentiation

摘要: Polycystin-1 (PC1) and polycystin-2 (PC2) are transmembrane proteins encoded by the Pkd1 Pkd2 genes, respectively. Mutations in these genes causative for development of autosomal-dominant polycystic kidney disease. A prominent feature this disease is an unbalanced cell proliferation. PC1 PC2 physically interact to form a complex, which localizes primary cilia renal epithelial cells. Recently, have also been described be present radial glial cells (RGCs) contribute planar polarity late RGCs E1 ependymal As neural progenitor (NPCs), early balance proliferation expansion, or self-renewal differentiation generate neurons. It not known whether polycystins play role process. Here, we show that expressed developing mouse cerebral cortex during neurogenesis. Loss-of-function analysis cell-based assays reveal reduction expression leads increased NPC proliferation, while neurons becomes impaired. The preceded enhanced Notch signaling accompanied rise number symmetric divisions. transcription factor STAT3 seems mechanistically important polycystin NPCs as either knockdown inhibition function abrogates driven reduced expression. Our findings indicate critical maintaining between NPCs.