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首页> 外文期刊>Genes to cells : >Identification of CHD7S as a novel splicing variant of CHD7 with functions similar and antagonistic to those of the full-length CHD7L
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Identification of CHD7S as a novel splicing variant of CHD7 with functions similar and antagonistic to those of the full-length CHD7L

机译：将CHD7S鉴定为CHD7的新型剪接变异体，其功能与全长CHD7L相似且拮抗

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摘要

CHD7 is one of the nine members of the chromodomain helicase DNA-binding family of ATP-dependent chromatin remodeling enzymes. Mutations in CHD7 give rise to CHARGE syndrome, a human condition characterized by malformation of various organs. We have now identified a novel transcript of CHD7 that is generated by alternative splicing of exon 6. The protein encoded by this variant transcript (termed CHD7S) lacks one of the two chromodomains as well as the helicase/ATPase domain, DNA-binding domain and BRK domains of the full-length protein (CHD7L). CHD7S was found to localize specifically to the nucleolus in a manner dependent on a nucleolar localization signal. Over-expression of CHD7S, as well as that of CHD7L, resulted in an increase in 45S precursor rRNA production. Conversely, depletion of both CHD7S and CHD7L by RNA interference inhibited both 45S precursor rRNA production and cell proliferation to a greater extent than did depletion of CHD7L alone. Furthermore, we found that, like CHD7L, CHD7S binds to Sox2 in the nucleoplasm. Unexpectedly, however, whereas over-expression of CHD7L promoted Sox2-mediated transcriptional regulation, over-expression of CHD7S suppressed it. These results indicate that CHD7S functions cooperatively or antagonistically with CHD7L in the nucleolus and nucleoplasm, respectively.
机译：CHD7是ATP依赖的染色质重塑酶的染色体域解旋酶DNA结合家族的九个成员之一。 CHD7中的突变会引起CHARGE综合征，这是一种以各种器官畸形为特征的人类疾病。现在，我们已经确定了外显子6的可变剪接产生的CHD7的新转录本。该变异转录本（称为CHD7S）编码的蛋白质缺少两个染色体结构域之一，也缺少解旋酶/ ATPase结构域，DNA结合结构域和全长蛋白质的BRK结构域（CHD7L）。发现CHD7S以依赖于核仁定位信号的方式特异性地定位于核仁。 CHD7S和CHD7L的过度表达导致45S前体rRNA产量增加。相反，与单独消耗CHD7L相比，RNA干扰对CHD7S和CHD7L的消耗都在更大程度上抑制了45S前体rRNA的产生和细胞增殖。此外，我们发现，与CHD7L一样，CHD7S与核质中的Sox2结合。但是，出乎意料的是，尽管CHD7L的过表达促进了Sox2介导的转录调控，但CHD7S的过表达却抑制了它。这些结果表明CHD7S在核仁和核质中分别与CHD7L协同或拮抗。

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