PTBP1 and PTBP2 Repress Nonconserved Cryptic Exons.
PTBP1 and PTBP2 Repress Nonconserved Cryptic Exons.
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DOI：
10.1016/j.celrep.2016.08.071
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发表时间：
2016-09-27
期刊：
影响因子：
8.8
通讯作者：
Wong PC
中科院分区：
文献类型：
--
作者：
Ling JP;Chhabra R;Merran JD;Schaughency PM;Wheelan SJ;Corden JL;Wong PC
RNA剪接的保真度是由一系列因素维持的，但控制这一过程的分子机制尚未完全阐明。我们以前发现TDP-43，一种与神经退行性疾病有关的RNA结合蛋白，利用UG微卫星抑制非保守的隐蔽外显子，并阻止它们掺入mRNA。在这里，我们报告说，两个良好的特点剪接因子，多聚嘧啶道结合蛋白1（PTBP 1）和多聚嘧啶道结合蛋白2（PTBP 2），也是非保守的隐蔽外显子阻遏物。与TDP-43相反，PTBP 1和PTBP 2利用CU微卫星来抑制保守的组织特异性外显子以及非保守的隐蔽外显子。这些保守的剪接事件的分析表明，PTBP 1和PTBP 2的抑制滴定，以产生神经元分化所需的转录组多样性。总之，我们确定PTBP 1和PTBP 2是一个家庭的成员的隐蔽外显子阻遏物。
The fidelity of RNA splicing is maintained by a network of factors, but the molecular mechanisms that govern this process have yet to be fully elucidated. We previously found that TDP-43, an RNA-binding protein implicated in neurodegenerative disease, utilizes UG microsatellites to repress nonconserved cryptic exons and prevent their incorporation into mRNA. Here, we report that two well characterized splicing factors, polypyrimidine tract-binding protein 1 (PTBP1) and polypyrimidine tract-binding protein 2 (PTBP2), are also nonconserved cryptic exon repressors. In contrast to TDP-43, PTBP1 and PTBP2 utilize CU microsatellites to repress both conserved tissue-specific exons as well as nonconserved cryptic exons. Analysis of these conserved splicing events suggests that PTBP1 and PTBP2 repression is titrated to generate the transcriptome diversity required for neuronal differentiation. Together, we establish that PTBP1 and PTBP2 are members of a family of cryptic exon repressors.
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