聚（ADP-核糖）控制着 DE-钙粘蛋白依赖性干细胞的维持和卵母细胞的定位。
Poly(ADP-ribose) controls DE-cadherin-dependent stem cell maintenance and oocyte localization.
机构信息
Cancer Biology Program, Epigenetics and Progenitor Cell Program, Fox Chase Cancer Center, Philadephia 19111, USA.
出版信息
Nat Commun. 2012 Mar 27;3:760. doi: 10.1038/ncomms1759.
Abstract
Within the short span of the cell cycle, poly(ADP-ribose) (pADPr) can be rapidly produced by poly(ADP-ribose) polymerases and degraded by poly(ADP-ribose) glycohydrolases. Here we show that changes in association between pADPr and heterogeneous nuclear ribonucleoproteins (hnRNPs) regulate germline stem cell (GSC) maintenance and egg chamber polarity during oogenesis in Drosophila. The association of pADPr and Hrp38, an orthologue of human hnRNPA1, disrupts the interaction of Hrp38 with the 5'-untranslated region of DE-cadherin messenger RNA, thereby diminishing DE-cadherin translation in progenitor cells. Following the reduction of DE-cadherin level, GSCs leave the stem cell niche and differentiate. Defects in either pADPr catabolism or Hrp38 function cause a decrease in DE-cadherin translation, leading to a loss of GSCs and mislocalization of oocytes in the ovary. Taken together, our findings suggest that Hrp38 and its association with pADPr control GSC self-renewal and oocyte localization by regulating DE-cadherin translation.
摘要
在细胞周期的短暂时间内，多聚（ADP-核糖）（pADPr）可以由多聚（ADP-核糖）聚合酶迅速产生，并由多聚（ADP-核糖）糖基水解酶降解。在这里，我们表明 pADPr 与异质核核糖核蛋白（hnRNPs）之间的关联变化调节果蝇生殖干细胞（GSC）的维持和卵子发生过程中的卵室极性。pADPr 与 Hrp38（人类 hnRNPA1 的同源物）的结合破坏了 Hrp38 与 DE-cadherin 信使 RNA 的 5'-非翻译区的相互作用，从而减少了祖细胞中的 DE-cadherin 翻译。在 DE-cadherin 水平降低后，GSCs 离开干细胞龛并分化。pADPr 代谢或 Hrp38 功能的缺陷导致 DE-cadherin 翻译减少，导致 GSCs 丧失和卵母细胞在卵巢中的定位错误。总之，我们的发现表明 Hrp38 及其与 pADPr 的关联通过调节 DE-cadherin 翻译来控制 GSC 的自我更新和卵母细胞的定位。
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