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首页> 外文期刊>Molecular and Cellular Biology >Oxidative Stress-Induced Destruction of the Yeast C-Type Cyclin Ume3p Requires Phosphatidylinositol-Specific Phospholipase C and the 26S Proteasome
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Oxidative Stress-Induced Destruction of the Yeast C-Type Cyclin Ume3p Requires Phosphatidylinositol-Specific Phospholipase C and the 26S Proteasome

机译：氧化应激诱导的酵母C型细胞周期蛋白Ume3p的破坏需要磷脂酰肌醇特定的磷脂酶C和26S蛋白酶体。

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The yeast UME3 (SRB11/SSN3) gene encodes a C-type cyclin that represses the transcription of the HSP70family member SSA1. To relieve this repression, Ume3p is rapidly destroyed in cells exposed to elevated temperatures. This report demonstrates that Ume3p levels are also reduced in cultures subjected to ethanol shock, oxidative stress, or carbon starvation or during growth on nonfermentable carbons. Of the three elements (RXXL, PEST, and cyclin box) previously shown to be required for heat-induced Ume3p destruction, only the cyclin box regulates Ume3p degradation in response to these stressors. The one exception observed was growth on nonfermentable carbons, which requires the PEST region. These findings indicate that yeast cells contain multiple, independent pathways that mediate stress-induced Ume3p degradation. Ume3p destruction in response to oxidative stress, but not to ethanol treatment, requires DOA4 and UMP1, two factors required for 26S proteasome activity. This result for the first time implicates ubiquitin-mediated proteolysis in C-type cyclin regulation. Similarly, the presence of a membrane stabilizer (sorbitol) or the loss of phosphatidylinositol-specific phospholipase C (PLC1) protects Ume3p from oxidative-stress-induced degradation. Finally, a ume3 null allele suppresses the growth defect of plc1 mutants in response to either elevated temperature or the presence of hydrogen peroxide. These results indicate that the growth defects observed in plc1mutants are due to the failure to downregulate Ume3p. Taken together, these findings support a model in which Plc1p mediates an oxidative-stress signal from the plasma membrane that triggers Ume3p destruction through a Doa4p-dependent mechanism.
机译：酵母 UME3 （ SRB11 / SSN3 ）基因编码一个C型细胞周期蛋白，可抑制 HSP70 家族成员 SSA1 < / em>。为了缓解这种抑制，Ume3p在暴露于高温的细胞中会被迅速破坏。该报告表明，在遭受乙醇冲击，氧化应激或碳饥饿或在不可发酵碳上生长的培养物中，Ume3p水平也降低。先前显示出热诱导的Ume3p破坏需要三个元素（RXXL，PEST和cyclin框），只有cyclin框响应这些压力源调节Ume3p的降解。观察到的一个例外是在不可发酵碳上的生长，这需要PEST区域。这些发现表明，酵母细胞包含多个独立的途径来介导应激诱导的Ume3p降解。响应氧化应激而不是乙醇处理的Ume3p破坏需要 DOA4 和 UMP1 ，这是26S蛋白酶体活性所需的两个因素。该结果首次将泛素介导的蛋白水解牵连到C型细胞周期蛋白调节中。同样，膜稳定剂（山梨糖醇）的存在或磷脂酰肌醇特异性磷脂酶C（ PLC1 ）的丢失可保护Ume3p免受氧化应激诱导的降解。最后， ume3 无效等位基因可抑制 plc1 突变体的生长缺陷，以应对温度升高或过氧化氢的存在。这些结果表明在 plc1 突变体中观察到的生长缺陷是由于未能下调Ume3p。综上所述，这些发现支持了一个模型，其中Plc1p介导质膜的氧化应激信号，该信号通过Doa4p依赖性机制触发Ume3p破坏。

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