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首页> 外文期刊>Molecular and Cellular Biology >The Yeast Ser/Thr Phosphatases Sit4 and Ppz1 Play Opposite Roles in Regulation of the Cell Cycle
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The Yeast Ser/Thr Phosphatases Sit4 and Ppz1 Play Opposite Roles in Regulation of the Cell Cycle

机译:酵母Ser / Thr磷酸酶Sit4和Ppz1在细胞周期调控中发挥相反的作用

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Yeast cells overexpressing the Ser/Thr protein phosphatase Ppz1 display a slow-growth phenotype. These cells recover slowly from α-factor or nutrient depletion-induced G1 arrest, showing a considerable delay in bud emergence as well as in the expression of the G1 cyclins Cln2 and Clb5. Therefore, an excess of the Ppz1 phosphatase interferes with the normal transition from G1 to S phase. The growth defect is rescued by overexpression of the HAL3/SIS2 gene, encoding a negative regulator of Ppz1. High-copy-number expression of HAL3/SIS2has been reported to improve cell growth and to increase expression of G1 cyclins in sit4 phosphatase mutants. We show here that the described effects of HAL3/SIS2 onsit4 mutants are fully mediated by the Ppz1 phosphatase. The growth defect caused by overexpression ofPPZ1 is intensified in strains with low G1cyclin levels (such as bck2Δ or cln3Δ mutants), whereas mutation of PPZ1 rescues the synthetic lethal phenotype of sit4 cln3 mutants. These results reveal a role for Ppz1 as a regulatory component of the yeast cell cycle, reinforce the notion that Hal3/Sis2 serves as a negative modulator of the biological functions of Ppz1, and indicate that the Sit4 and Ppz1 Ser/Thr phosphatases play opposite roles in control of the G1/S transition.
机译:过量表达Ser / Thr蛋白磷酸酶Ppz1的酵母细胞表现出缓慢生长的表型。这些细胞从α因子或营养耗竭诱导的G 1 停滞中缓慢恢复,显示出芽萌发以及G 1 细胞周期蛋白Cln2表达的显着延迟。和Clb5。因此,过量的Ppz1磷酸酶会干扰从G 1 到S相的正常转变。通过过表达 HAL3 / SIS2 基因(编码Ppz1的负调控子)可以挽救生长缺陷。据报道, HAL3 / SIS2 的高拷贝数表达可改善 sit4 磷酸酶突变体中的细胞生长并增加G 1 细胞周期蛋白的表达。 。我们在这里显示, HAL3 / SIS2 sit4 突变体的描述作用完全由Ppz1磷酸酶介导。 G 1 细胞周期蛋白水平较低的菌株(例如 bck2 Δ或 cln3 < / em>Δ突变体),而 PPZ1 的突变可以挽救 sit4 cln3 突变体的合成致死表型。这些结果揭示了Ppz1作为酵母细胞周期调控成分的作用,强化了Hal3 / Sis2充当Ppz1生物学功能的负调节剂的观念,并表明Sit4和Ppz1 Ser / Thr磷酸酶起相反的作用。来控制G 1 / S过渡。

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