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Global transcriptional repression in C-elegans germline precursors by regulated sequestration of TAF-4

机译:通过调节螯合TAF-4,对C-线虫种系前体的全局转录抑制

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摘要

In C. elegans, four asymmetric divisions, beginning with the zygote (P0), generate transcriptionally repressed germline blastomeres (P1-P4) and somatic sisters that become transcriptionally active. The protein PIE-1 represses transcription in the later germline blastomeres but not in the earlier germline blastomeres P0 and P1. We show here that OMA-1 and OMA-2, previously shown to regulate oocyte maturation, repress transcription in P0 and P1 by binding to and sequestering in the cytoplasm TAF-4, a component critical for assembly of TFIID and the pol II pre-initiation complex. OMA-1/2 binding to TAF-4 is developmentally regulated, requiring phosphorylation by the DYRK kinase MBK-2, which is activated at meiosis II after fertilization. OMA-1/2 are normally degraded after the first mitosis, but ectopic expression of wild-type OMA-1 is sufficient to repress transcription in both somatic and later germline blastomeres. We propose that phosphorylation by MBK-2 serves as a developmental switch, converting OMA-1/2 from oocyte to embryo regulators.
机译:在秀丽隐杆线虫中,从合子(P0)开始的四个不对称分裂产生转录受抑制的种系卵裂球(P1-P4)和具有转录活性的体细胞姐妹。蛋白PIE-1抑制后期种系卵裂球中的转录,但不抑制早期种系卵裂球P0和P1中的转录。我们在此处显示,先前显示可调节卵母细胞成熟的OMA-1和OMA-2通过结合并隔离在细胞质TAF-4中而抑制P0和P1的转录,TAF-4是组装TFIID和pol II前体的关键起始复合体。 OMA-1 / 2与TAF-4的结合受到发育调节,需要DYRK激酶MBK-2磷酸化,该分子在受精后的减数分裂II时被激活。 OMA-1 / 2通常在第一个有丝分裂后降解,但是野生型OMA-1的异位表达足以抑制体细胞和后来的种系卵裂球中的转录。我们建议由MBK-2的磷酸化作为一种​​发育的开关,将OMA-1 / 2从卵母细胞转化为胚胎调控因子。

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