Retinoic acid regulates Kit translation during spermatogonial differentiation in the mouse.
Retinoic acid regulates Kit translation during spermatogonial differentiation in the mouse.
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DOI：
10.1016/j.ydbio.2014.10.020
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发表时间：
2015-01-01
影响因子：
2.7
通讯作者：
Geyer, Christopher B.
中科院分区：
文献类型：
--
作者：
Busada, Jonathan T.;Chappell, Vesna A.;Niedenberger, Bryan A.;Kaye, Evelyn P.;Keiper, Brett D.;Hogarth, Cathryn A.;Geyer, Christopher B.
在睾丸中，一部分精原细胞保留了干细胞的潜能，而另一部分则分化为最终成为精子。这种微妙的平衡必须保持，因为缺陷会导致睾丸癌或不育。目前，人们对指导这些关键细胞命运决定的基因产物和信号通路知之甚少。视黄酸（RA）是精原细胞分化和进入减数分裂的必要驱动因子，但下游激活的机制尚不清楚。在这里，我们确定了RA在KIT表达中的要求，KIT是精原细胞分化所必需的酪氨酸激酶受体。我们发现RA信号通路利用PI3K/AKT/mTOR信号通路诱导Kit mrna的有效翻译，这些mrna在未分化的精原细胞中存在但未翻译。我们的研究结果提供了形态因子（RA）和KIT蛋白表达之间的重要分子联系，它们共同指导了整个男性生殖寿命中精原细胞的分化。
In the testis, a subset of spermatogonia retains stem cell potential, while others differentiate to eventually become spermatozoa. This delicate balance must be maintained, as defects can result in testicular cancer or infertility. Currently, little is known about the gene products and signaling pathways directing these critical cell fate decisions. Retinoic acid (RA) is a requisite driver of spermatogonial differentiation and entry into meiosis, yet the mechanisms activated downstream are undefined. Here, we determined a requirement for RA in the expression of KIT, a receptor tyrosine kinase essential for spermatogonial differentiation. We found that RA signaling utilized the PI3K/AKT/mTOR signaling pathway to induce the efficient translation of mRNAs for Kit, which are present but not translated in undifferentiated spermatogonia. Our findings provide an important molecular link between a morphogen (RA) and the expression of KIT protein, which together direct the differentiation of spermatogonia throughout the male reproductive lifespan.
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影响因子：
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通讯作者：
Pandolfi PP
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