Role of Swi4 in cell cycle regulation of CLN2 expression.
Role of Swi4 in cell cycle regulation of CLN2 expression.
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Swi4 在 CLN2 表达的细胞周期调节中的作用。
DOI：
10.1128/mcb.14.7.4779-4787.1994
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发表时间：
1994
影响因子：
5.3
通讯作者：
Tinkelenberg,AH
中科院分区：
文献类型：
--
作者：
Cross,FR;Hoek,M;McKinney,JD;Tinkelenberg,AH
酿酒酵母CLN1和CLN2基因的表达受细胞周期调控，可能受正反馈调控。已有研究认为，正反馈是通过CLN/CDC28激活Swi4/Swi6转录因子来实现的，由于Swi4与CLN1和CLN2启动子中的特定位点(SCB)结合，从而导致CLN1和CLN2转录。为了测试这一建议，我们检查了CLN2启动子中潜在的SCB的缺失或SWI4基因对CLN2转录控制的影响。从启动子中删除含有已鉴定的SCB的限制性片段并不能阻止对CLN2表达的细胞周期调节，尽管CLN2在所有细胞周期位置的表达都降低了。在含有SCB的限制性片段的缺失点包含5.5kb的质粒插入或独立的2.5kb的插入的启动子也表现出细胞周期调节，因此不太可能涉及未知的上游SCB。整合型CLN2启动子的细胞周期调控不需要Swi4或相关的MBPL转录因子。相反，Swi4(而不是MBPL)是正确调节缺少SCB位点的插入/缺失启动子的细胞周期所必需的。我们扩展了之前的遗传证据，证明Swi4参与了CLN2功能的某些方面：对CLN2阳性调控因子的突变搜索只产生了饱和时的SW4突变。Swi4可能与CLN2启动子中的非共同序列结合(可能与共同位点结合)，也可能间接调节CLN2的表达。
Expression of theSaccharomyces cerevisiae CLN1andCLN2genes is cell cycle regulated, and the genes may be controlled by positive feedback. It has been proposed that positive feedback operates via Cln/Cdc28 activation of the Swi4/Swi6 transcription factor, leading toCLN1andCLN2transcription due to Swi4 binding to specific sites (SCBs) in theCLN1andCLN2promoters. To test this proposal, we have examined the effects of deletion either of the potential SCBs in theCLN2promoter or of theSWI4gene onCLN2transcriptional control. Deletion of a restriction fragment containing the identified SCBs from the promoter does not prevent cell cycle regulation ofCLN2expression, although expression is lowered at all cell cycle positions. A promoter containing a 5.5-kb plasmid insertion or an independent 2.5-kb insertion at the point of deletion of the SCB-containing restriction fragment also exhibits cell cycle regulation, so involvement of unidentified upstream SCBs is unlikely. Neither Swi4 nor the related Mbpl transcription factor is required for cell cycle regulation of the intactCLN2promoter. In contrast, Swi4 (but not Mbpl) is required for correct cell cycle regulation of the insertion/deletion promoter lacking SCB sites. We have extended previous genetic evidence for involvement of Swi4 in some aspect ofCLN2function: a mutant hunt forCLN2positive regulatory factors yielded onlyswi4mutations at saturation. Swi4 may bind to nonconsensus sequences in theCLN2promoter (possibly in addition to consensus sites), or it may act indirectly to regulateCLN2expression.