Regulation of wee1(+) expression during meiosis in fission yeast.
Regulation of wee1(+) expression during meiosis in fission yeast.
复制标题
在裂变酵母中减数分裂过程中WEE1（+）表达的调节。
DOI：
10.4161/15384101.2014.946807
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发表时间：
2014
期刊：
影响因子：
--
通讯作者：
Murakami H
中科院分区：
文献类型：
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作者：
Murakami-Tonami Y;Ohtsuka H;Aiba H;Murakami H
在真核生物中，细胞周期蛋白依赖性激酶Cdk1p（Cdc2p）在有丝分裂和减数分裂期间进入核分裂并通过核分裂进展中起核心作用。cdk1p在减数分裂核分裂期间通过其酪氨酸-15残基的去磷酸化而被激活。该残基的磷酸化状态主要由Wee1p激酶和Cdc25p磷酸酶决定。在裂殖酵母中，叉头型转录因子Mei4p对于进入第一次减数分裂核分裂是必需的。我们最近发现cdc 25+是Mei 4p控制进入减数分裂I的重要靶点。在这里，我们表明wee1+是Mei4p控制进入减数分裂I的另一个重要靶标。Mei4p在体内和体外与wee1+的上游区域结合并抑制wee1+的表达，而Mei4p正调控邻近假基因的表达。Mei4p的过表达抑制wee1+的表达，并诱导假基因的表达。相反，Mei4p的缺失并没有降低wee1+的表达，但抑制了假基因的表达。此外，Mei4p结合区的缺失延迟了wee1+表达的抑制以及假基因表达的诱导。这些结果表明wee1+表达的抑制主要是由于Mei4p介导的转录干扰。
In eukaryotes, the cyclin-dependent kinase Cdk1p (Cdc2p) plays a central role in entry into and progression through nuclear division during mitosis and meiosis. Cdk1p is activated during meiotic nuclear divisions by dephosphorylation of its tyrosine-15 residue. The phosphorylation status of this residue is largely determined by the Wee1p kinase and the Cdc25p phosphatase. In fission yeast, the forkhead-type transcription factor Mei4p is essential for entry into the first meiotic nuclear division. We recently identified cdc25+ as an essential target of Mei4p in the control of entry into meiosis I. Here, we show that wee1+ is another important target of Mei4p in the control of entry into meiosis I. Mei4p bound to the upstream region of wee1+ in vivo and in vitro and inhibited expression of wee1+, whereas Mei4p positively regulated expression of the adjacent pseudogene. Overexpression of Mei4p inhibited expression of wee1+ and induced that of the pseudogene. Conversely, deletion of Mei4p did not decrease expression of wee1+ but inhibited that of the pseudogene. In addition, deletion of Mei4p-binding regions delayed repression of wee1+ expression as well as induction of expression of the pseudogene. These results suggest that repression of wee1+ expression is primarily owing to Mei4p-mediated transcriptional interference.