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首页> 外文期刊>Biology Open >Ole1, fatty acid desaturase, is required for Atg9 delivery and isolation membrane expansion during autophagy in?Saccharomyces cerevisiae
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Ole1, fatty acid desaturase, is required for Atg9 delivery and isolation membrane expansion during autophagy in?Saccharomyces cerevisiae

机译：酿酒酵母自噬过程中Atg9的传递和分离膜的扩张需要脂肪酸去饱和酶Ole1

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摘要

Macroautophagy, a major degradation pathway of cytoplasmic components, is carried out through formation of a double-membrane structure, the autophagosome. Although the involvement of specific lipid species in the formation process remains largely obscure, we recently showed that mono-unsaturated fatty acids (MUFA) generated by stearoyl-CoA desaturase 1 (SCD1) are required for autophagosome formation in mammalian cells. To obtain further insight into the role of MUFA in autophagy, in this study we analyzed the autophagic phenotypes of the yeast mutant of?OLE1, an orthologue of SCD1.?Δole1?cells were defective in nitrogen starvation-induced autophagy, and the Cvt pathway, when oleic acid was not supplied. Defects in elongation of the isolation membrane led to a defect in autophagosome formation. In the absence of Ole1, the transmembrane protein Atg9 was not able to reach the pre-autophagosomal structure (PAS), the site of autophagosome formation. Thus, autophagosome formation requires Ole1 during the delivery of Atg9 to the PAS/autophagosome from its cellular reservoir.
机译：巨自噬是细胞质成分的主要降解途径，是通过形成双膜结构即自噬小体来进行的。尽管特定脂质物种在形成过程中的参与仍然不清楚，但我们最近表明，在哺乳动物细胞中自噬体形成需要硬脂酰辅酶A去饱和酶1（SCD1）产生的单不饱和脂肪酸（MUFA）。为了进一步了解MUFA在自噬中的作用，在这项研究中，我们分析了OLE1酵母突变体（SCD1的直系同源物）的酵母突变体的自噬表型.Δole1？细胞在氮饥饿诱导的自噬和Cvt途径中存在缺陷。 ，当不提供油酸时。隔离膜伸长的缺陷导致自噬体形成的缺陷。在没有Ole1的情况下，跨膜蛋白Atg9无法到达自噬体前结构（PAS），即自噬体形成的位点。因此，自吞噬体的形成在将Atg9从其细胞贮库传递至PAS /自噬体的过程中需要Ole1。

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