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Sam68 Regulates a Set of Alternatively Spliced Exons during Neurogenesis

机译：Sam68调节神经发生过程中的一组剪接的外显子。

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Sam68 (Src-associated in mitosis, 68 kDa) is a KH domain RNA binding protein implicated in a variety of cellular processes, including alternative pre-mRNA splicing, but its functions are not well understood. Using RNA interference knockdown of Sam68 expression and splicing-sensitive microarrays, we identified a set of alternative exons whose splicing depends on Sam68. Detailed analysis of one newly identified target exon in epsilon sarcoglycan (Sgce) showed that both RNA elements distributed across the adjacent introns and the RNA binding activity of Sam68 are necessary to repress the Sgce exon. Sam68 protein is upregulated upon neuronal differentiation of P19 cells, and many Sam68 RNA targets change in expression and splicing during this process. When Sam68 is knocked down by short hairpin RNAs, many Sam68-dependent splicing changes do not occur and P19 cells fail to differentiate. We also found that the differentiation of primary neuronal progenitor cells from embryonic mouse neocortex is suppressed by Sam68 depletion and promoted by Sam68 overexpression. Thus, Sam68 controls neurogenesis through its effects on a specific set of RNA targets.
机译：Sam68（与有丝分裂相关的Src，68 kDa）是一种KH域RNA结合蛋白，涉及多种细胞过程，包括替代性的pre-mRNA剪接，但其功能尚不清楚。使用RNA干扰敲除Sam68表达和剪接敏感的微阵列，我们确定了一组替代外显子，其剪接取决于Sam68。对ε糖聚糖（ Sgce ）中一个新发现的目标外显子的详细分析表明，分布在相邻内含子中的两个RNA元件以及Sam68的RNA结合活性都是抑制 Sgce 外显子。在P19细胞的神经元分化后，Sam68蛋白被上调，在此过程中，许多Sam68 RNA靶标的表达和剪接发生变化。当通过短发夹RNA敲除Sam68时，不会发生许多依赖Sam68的剪接变化，并且P19细胞无法分化。我们还发现Sam68耗竭抑制了胚胎小鼠新皮层对原代神经元祖细胞的分化，而Sam68的过表达促进了它们的分化。因此，Sam68通过其对一组特定的RNA靶标的作用来控制神经发生。

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