Long-Term Artificial Selection Reveals a Role of TCTP in Autophagy in Mammalian Cells

Long-Term Artificial Selection Reveals a Role of TCTP in Autophagy in Mammalian Cells
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长期人工选择揭示了 TCTP 在哺乳动物细胞自噬中的作用

DOI:
10.1093/molbev/msu181
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发表时间:
2014-08-01
影响因子:
10.7
通讯作者:
Zhou, Rongjia
Zhou, Rongjia
中科院分区:
生物学1区
文献类型:
--
作者:
Chen, Ke;Huang, Chunhua;Zhou, Rongjia

文献摘要

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理解基因组变异和检测选择下的基因组中的选择标记已经是世纪的巨大挑战。哺乳动物卵巢中原始卵泡的激活、发育/耗竭决定生殖成功、绝经/雌性生殖生命的结束。然而,卵子发生的分子机制,特别是在人工选择下,在很大程度上是未知的。我们报告说,在9,000多年的卵巢人工压力下,对基因组中的选择特征进行了蛋白质组范围的扫描,揭示了基因组中选择特征的一般情况,特别是在启动子和内含子区域检测到了通过人工选择产生的基因组变异。国内和野生物种之间的杂交育种结果超过一半的蛋白质点表现出杂种优势。翻译控制肿瘤蛋白(TCTP)通过人工选择上调,并通过AMP激活的蛋白激酶途径正向调节自噬。值得注意的是,TCTP与ATG 16复合物相互作用。除细胞质自噬外,卵巢颗粒细胞和卵丘细胞的细胞核也发生了噬核作用,表明细胞核物质在噬核作用下降解的重要性。我们的研究结果提供了对改善卵巢功能相关的细胞和分子机制的深入了解,并确定了长期人工选择压力下卵巢功能基因组中的选择特征。
Understanding genomic variation and detecting selection signatures in a genome under selection have been great challenges for a century. Activation, development/exhaustion of primordial follicles in mammalian ovary determines reproductive success, menopause/end of female reproductive life. However, molecular mechanisms underlying oogenesis, particularly under artificial selection, are largely unknown. We report that a proteome-wide scan for selection signatures in the genome over 9,000 years of artificial pressure on the ovary revealed a general picture of selection signatures in the genome, especially genomic variations through artificial selection were detected in promoter and intron regions. Crossbreeding between domestic and wild species results in more than half of the protein spots exhibiting heterosis. Translationally controlled tumor protein (TCTP) is upregulated by artificial selection and positively regulates autophagy through the AMP-activated protein kinase pathway. Notably, TCTP interacts with ATG16 complex. In addition to cytoplasmic autophagy, nucleophagy occurs in the nuclei of granulosa and cumulus cells in ovaries, indicating an importance of the nuclear material for degradation by nucleophagy. Our findings provide insight into cellular and molecular mechanisms relevant for improvement of ovary functions, and identify selection signatures in the genome for ovary function over long-term artificial selection pressure.