PMT1 deficiency extends the shortened replicative lifespan of TED1-deficient yeast in a Hac1p-dependent manner

PMT1 deficiency extends the shortened replicative lifespan of TED1-deficient yeast in a Hac1p-dependent manner
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PMT1 缺陷以 Hac1p 依赖性方式延长 TED1 缺陷酵母的复制寿命

DOI:
10.1093/femsle/fny234
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发表时间:
2018-09
影响因子:
2.1
通讯作者:
Xinguang Liu
Xinguang Liu
中科院分区:
生物学4区
文献类型:
--
作者:
Hongjing cui;Xingang Cui;Wei Zhao;Xin He;Tao Zhou;Zhiwen Jiang;Yuan Yuan;Kunpei Yuan;Xuerong Sun;Xinguang Liu

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蛋白O-甘露糖基转移酶-1(Pmt 1 p)缺陷延长了酿酒酵母的复制寿命(RLS),这与未折叠蛋白反应(UPR)的激活有关,UPR是缓解内质网(ER)应激的重要途径。Emp 24 p/Erv 25 p依赖性货物的运输被破坏1(Ted 1 p)已被报道为酵母Pmt 1 p的结合伴侣。我们探讨了Pmt 1 p和Ted 1 p在细胞寿命和内质网应激反应中的潜在关系。TED 1缺失的菌株(ted 1 Δ)具有较短的RLS而不增加UPR活性。然而,PMT 1缺陷以依赖于UPR途径上游转录因子Hac 1 p的方式延长了ted 1 Δ的短寿命。此外,PMT 1缺陷增强了ted 1 Δ菌株的UPR活性,降低了其内质网应激抗性。因此,假设增强的UPR活性可以解释pmt 1 Δ ted 1 Δ菌株的寿命,但是与短寿命ted 1 Δ菌株相比,长寿命的pmt 1 Δ ted 1 Δ菌株显示出降低的ER胁迫抗性。综上所述,我们的研究结果表明PMT 1和TED 1之间可能存在寿命调节和ER应激反应的关系。
Protein O-mannosyltransferase-1 (Pmt1p) deficiency extends the replicative lifespan (RLS) of Saccharomyces cerevisiae, which is related to the activation of the unfolded protein response (UPR), an important pathway for alleviating endoplasmic reticulum (ER) stress. Trafficking of Emp24p/Erv25p-dependent cargo disrupted 1 (Ted1p) has been reported as a binding partner of yeast Pmt1p. We explored the potential relationship between Pmt1p and Ted1p in the cell lifespan and ER stress responses. The TED1-deleted strain (ted1Δ) had a shorter RLS with no increase in UPR activity. However, PMT1 deficiency prolonged the short lifespan of ted1Δ in a manner dependent on Hac1p, an upstream transcription factor of the UPR pathway. In addition, PMT1 deficiency enhanced the UPR activity and alleviated the ER stress resistance of the ted1Δ strain. Thus, the enhanced UPR activity was hypothesized to explain the longevity of the pmt1Δted1Δ strain, but this long-lived pmt1Δted1Δ strain showed decreased ER stress resistance compared with the short-lived ted1Δ strain. Taken together, our results suggest a possible relationship between PMT1 and TED1 regarding lifespan regulation and the ER stress response.
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