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脂滴介导. 盐胁迫耐受

Lipid Droplets Mediate Salt Stress Tolerance in .

机构信息

State Key Laboratory of Microbial Metabolism, School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai 200240, China.

Joint International Research Laboratory of Metabolic and Developmental Sciences, Shanghai Jiao Tong University, Shanghai 200240, China.

出版信息

Plant Physiol. 2019 Oct;181(2):510-526. doi: 10.1104/pp.19.00666. Epub 2019 Jul 24.

Abstract

Microalgae are known to respond to salinity stress via mechanisms that include accumulation of compatible solutes and synthesis of antioxidants. Here, we describe a salinity-tolerance mechanism mediated by lipid droplets (LDs). In the alga grown under salt-stress conditions, we observed significant increases in cell size and LD content. LDs that were closely grouped along the plasma membrane shrank as the plasma membrane expanded, and some LDs were engulfed by vacuoles. Transcriptome analysis showed that genes encoding lysophospholipid acyltransferases (LPLATs) and phospholipase A2 were significantly up-regulated following salt stress. Diacylglycerol kinase and LPLAT were identified in the proteome of salt-induced LDs, alongside vesicle trafficking and plastidial proteins and histone H2B. Analysis of fatty acid composition revealed an enrichment of C18:1 and C18:2 at the expense of C18:3 in response to salt stress. Pulse-chase experiments further suggested that variations of fatty acid composition were associated with LDs. Acetate stimulation research further confirmed a positive role of LDs in cell growth under salt stress. These results suggest that LDs play important roles in salt-stress tolerance, through harboring proteins, participating in cytoplasmic component recycling, and providing materials and enzymes for membrane modification and expansion.

摘要

微藻被认为通过包括积累相容性溶质和合成抗氧化剂在内的机制来响应盐胁迫。在这里,我们描述了一种由脂滴(LDs)介导的耐盐机制。在盐胁迫条件下生长的藻类中,我们观察到细胞大小和 LD 含量显著增加。与质膜紧密聚集的 LD 随着质膜的扩张而缩小,一些 LD 被液泡吞噬。转录组分析表明,编码溶血磷脂酰基转移酶(LPLAT)和磷脂酶 A2 的基因在盐胁迫后显著上调。二酰甘油激酶和 LPLAT 在盐诱导的 LD 蛋白质组中被鉴定出来,同时还有囊泡运输和质体蛋白以及组蛋白 H2B。脂肪酸组成分析表明,C18:1 和 C18:2 的丰度增加,而 C18:3 的丰度减少,以响应盐胁迫。脉冲追踪实验进一步表明,脂肪酸组成的变化与 LD 有关。乙酸刺激研究进一步证实了 LD 在盐胁迫下细胞生长中的积极作用。这些结果表明,LD 通过容纳蛋白质、参与细胞质成分的回收以及为膜修饰和扩张提供物质和酶,在耐盐性中发挥重要作用。

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