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The wheat MAP kinase phosphatase 1 confers higher lithium tolerance in yeast

机译:小麦MAP激酶磷酸酶1赋予酵母更高的锂耐受性

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The durum wheat TMKP1 gene encodes a MAP kinase phosphatase. When overexpressed in Saccharomyces cerevisiae, TMKP1 leads to salt stress tolerance (especially LiCl), which is dependent on the phosphatase activity of the protein. The TMKP1-associated Li + resistance is restricted to a galactose-containing medium. Interestingly, this salt tolerance is abolished in the absence of one member of the yeast type 2C Ser/Thr protein phosphatase family (Ptc1) but not when other members such as Ptc2 or Ptc3 are lacking. Increased Li + tolerance is not mediated by regulation of the P-type ATPase Ena1, a major determinant for salt tolerance. In contrast, the effect of TMKP1 depends on Hal3 (a negative regulator of Ppz phosphatases) and on the presence of the high-afnity potassium transporters Trk1/Trk2. Tolerance to Li + is also abolished in cells lacking the aldose reductase Gre3, previously shown to be involved in the resistance to this cation. This study provides evidence that the wheat TMKP1 phosphatase is contributing to reduce the exacerbated lithium toxicity in galactose-grown cells, in a way that depends on the presence of the potassium Trk transporters.
机译:硬质小麦TMKP1基因编码一个MAP激酶磷酸酶。当在酿酒酵母中过表达时,TMKP1会导致盐胁迫耐受性(尤其是LiCl),这取决于蛋白质的磷酸酶活性。与TMKP1相关的Li +耐药性仅限于含半乳糖的培养基。有趣的是,在不存在酵母2C型Ser / Thr蛋白磷酸酶家族(Ptc1)的一个成员的情况下,该耐盐性得以消除,但在缺少其他成员(例如,Ptc2或Ptc3)的情况下,则不存在。 Li +耐受性的提高不是由P型ATPase Ena1(盐耐受性的主要决定因素)的调节介导的。相反,TMKP1的作用取决于Hal3(Ppz磷酸酶的负调节剂)和高亲和力钾转运蛋白Trk1 / Trk2的存在。在缺乏醛糖还原酶Gre3的细胞中,对Li +的耐受性也被取消,先前证明与该阳离子的抗性有关。这项研究提供了证据,证明小麦TMKP1磷酸酶以依赖于Trk钾转运蛋白的方式,有助于减轻半乳糖生长的细胞中加剧的锂毒性。

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