The transcription factor Swi5 regulates expression of the cyclin kinase inhibitor p40SIC1.
The transcription factor Swi5 regulates expression of the cyclin kinase inhibitor p40SIC1.
复制标题
转录因子 Swi5 调节细胞周期蛋白激酶抑制剂 p40SIC1 的表达。
DOI：
10.1128/mcb.16.10.5701
复制
发表时间：
1996
影响因子：
5.3
通讯作者：
Nasmyth,K
中科院分区：
文献类型：
--
作者：
Knapp,D;Bhoite,L;Stillman,DJ;Nasmyth,K
DNA replication in budding yeast cells depends on the activation of the Cdc28 kinase (Cdkl ofSaccharomyces cerevisiae) associated with B-type cyclins Clb1 to Clb6. Activation of the kinase depends on proteolysis of the Cdk inhibitor p40SIC1in late G1, which is mediated by the ubiquitin-conjugating enzyme Cdc34 and two other proteins, Cdc4 and Cdc53. Inactivation of any one of these three proteins prevents p40SIC1degradation and causes cells to arrest in G1, with active Cln kinases but no Clb-associated Cdc28 kinase activity. Deletion ofSIC1allows these mutants to replicate. p40SIC1disappears at the G1/S transition and reappears only after nuclear division. Cell cycle-regulated proteolysis seems largely responsible for this pattern, but transcriptional control could also contribute;SIC1RNA accumulates to high levels as cells exit M phase. To identify additional factors necessary for the inhibition of the Cdk1/Cdc28 kinase in G1, we isolated mutants that can replicate DNA in the absence of Cdc4 function. Mutations in three loci (SIC1, SWI5, andRIC3) were identified. We have shown that highSIC1transcript levels at late M phase depend on Swi5. Swi5 accumulates in the cytoplasm during S, G2, and M phases of the cell cycle but enters the nuclei at late anaphase. Our data suggest that cell cycle-regulated nuclear accumulation of Swi5 is responsible for the burst ofSIC1transcription at the end of anaphase. This transcriptional control may be important for inactivation of the Clb/Cdkl kinase in G2/M transition and during the subsequent G1period.
