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首页> 外文期刊>Molecular and Cellular Biology >A Role for Dynein in the Inhibition of Germ Cell Proliferative Fate
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A Role for Dynein in the Inhibition of Germ Cell Proliferative Fate

机译：动力蛋白在抑制生殖细胞增殖命运中的作用

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During normal development as well as in diseased states such as cancer, extracellular “niches” often provide cues to proximal cells and activate intracellular pathways. Activation of such signaling pathways in turn instructs cellular proliferation and differentiation. In the Caenorhabditis elegans gonad, GLP-1/Notch signaling instructs germ line stem cells to self-renew through mitotic cell division. As germ cells progressively move out of the niche, they differentiate by entering meiosis and eventually form gametes. In this model system, we uncovered an unexpected role for the dynein motor complex in promoting normal differentiation of proliferating germ cells. We demonstrate that dynein light chain 1 (DLC-1) and its partner, dynein heavy chain 1, inhibit the proliferative cell fate, in part through regulation of METT-10, a conserved putative methyltransferase. We show that DLC-1 physically interacts with METT-10 and promotes both its overall levels and nuclear accumulation. Our results add a new dimension to the processes controlled by the dynein motor complex, demonstrating that dynein can act as an antiproliferative factor.
机译：在正常发育以及诸如癌症等疾病状态下，细胞外“利基”通常为近端细胞提供线索并激活细胞内途径。此类信号传导途径的激活又指示细胞增殖和分化。在秀丽隐杆线虫性腺中，GLP-1 / Notch信号指示种系干细胞通过有丝分裂细胞分裂自我更新。随着生殖细胞逐渐移出利基，它们通过进入减数分裂而分化并最终形成配子。在此模型系统中，我们发现了动力蛋白复合物在促进增殖性生殖细胞正常分化中的意外作用。我们证明，达因轻链1（DLC-1）及其伙伴达因重链1抑制增殖细胞的命运，部分是通过调节METT-10（一种保守的假定甲基转移酶）来进行的。我们表明，DLC-1与METT-10发生物理相互作用，并促进其总体水平和核积累。我们的结果为动力蛋白控制的过程增添了新的维度，证明动力蛋白可以作为抗增殖因子。

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