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Activation of CLN1 and CLN2 G1 cyclin gene expression by BCK2.

机译:BCK2激活CLN1和CLN2 G1细胞周期蛋白基因表达的激活。

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The Saccharomyces cerevisiae CLN3 protein, a G1 cyclin, positively regulates the expression of CLN1 and CLN2, two additional G1 cyclins whose expression during late G1 is activated, in part, by the transcription factors SWI4 and SWI6. We isolated 12 complementation groups of mutants that require CLN3. The members of one of these complementation groups have mutations in the BCK2 gene. In a wild-type CLN3 genetic background, bck2 mutants have a normal growth rate but have a larger cell size, are more sensitive to alpha-factor, and have a modest defect in the accumulation of CLN1 and CLN2 RNA. In the absence of CLN3, bck2 mutations cause an extremely slow growth rate: the cells accumulate in late G1 with very low levels of CLN1 and CLN2 RNA. The slow growth rate and long G1 delay of bck2 cln3 mutants are cured by heterologous expression of CLN2. Moreover, overexpression of BCK2 induces very high levels of CLN1, CLN2, and HCS26 RNAs. The results suggest that BCK2 and CLN3 provide parallel activation pathways for the expression of CLN1 and CLN2 during late G1.
机译:酿酒酵母CLN3蛋白(一种G1细胞周期蛋白)正调控CLN1和CLN2的表达,这两种另外的G1细胞周期蛋白在G1晚期的表达部分被转录因子SWI4和SWI6激活。我们分离了需要CLN3的突变体的12个互补组。这些互补基团之一的成员在BCK2基因中具有突变。在野生型CLN3遗传背景下,bck2突变体具有正常的生长速率,但具有较大的细胞大小,对α因子更敏感,并且在CLN1和CLN2 RNA的积累中存在适度的缺陷。在没有CLN3的情况下,bck2突变会导致极慢的生长速度:细胞在G1晚期以非常低的CLN1和CLN2 RNA水平积聚。 bck2 cln3突变体的缓慢生长速度和长的G1延迟可以通过CLN2的异源表达来治愈。此外,BCK2的过表达诱导非常高水平的CLN1,CLN2和HCS26 RNA。结果表明,BCK2和CLN3为晚期G1期间CLN1和CLN2的表达提供了平行的激活途径。

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