Asymmetrically dividing stem cells often show asymmetric behavior of the mother versus daughter centrosomes, whereby the self-renewing stem cell selectively inherits the mother or daughter centrosome. Although the asymmetric centrosome behavior is widely conserved, its biological significance remains largely unclear. Here, we show that Alms1a, a Drosophila homolog of the human ciliopathy gene Alstrom syndrome, is enriched on the mother centrosome in Drosophila male germline stem cells (GSCs). Depletion of alms1a in GSCs, but not in differentiating germ cells, results in rapid loss of centrosomes due to a failure in daughter centriole duplication, suggesting that Alms1a has a stem-cell-specific function in centrosome duplication. Alms1a interacts with Sak/Plk4, a critical regulator of centriole duplication, more strongly at the GSC mother centrosome, further supporting Alms1a’s unique role in GSCs. Our results begin to reveal the unique regulation of stem cell centrosomes that may contribute to asymmetric stem cell divisions.

中文翻译：

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Alstrom 综合征基因是果蝇睾丸中心粒复制的干细胞特异性调节因子

不对称分裂的干细胞通常表现出母体与子体中心体的不对称行为，从而自我更新的干细胞选择性地继承母体或子体中心体。尽管不对称中心体行为广泛保守，但其生物学意义仍不清楚。在这里，我们显示 Alms1a 是人类纤毛病基因 Alstrom 综合征的果蝇同源物，在果蝇雄性生殖干细胞 (GSC) 的母体中心体上富集。由于子中心粒复制失败，GSC 中 alms1a 的消耗，但在分化生殖细胞中没有消耗，导致中心体快速丢失，这表明 Alms1a 在中心体复制中具有干细胞特异性功能。Alms1a 与 Sak/Plk4 相互作用，Sak/Plk4 是中心粒复制的关键调节因子，在 GSC 母体中心体上更强烈，进一步支持 Alms1a 在 GSC 中的独特作用。我们的结果开始揭示可能导致不对称干细胞分裂的干细胞中心体的独特调节。