Department of Biochemistry and Molecular Biology, Michigan State University, East Lansing, Michigan 48824.
MSU-Department of Energy, Plant Research Laboratory, East Lansing, Michigan 48824.
Plant Cell. 2018 May;30(5):1006-1022. doi: 10.1105/tpc.18.00250. Epub 2018 Apr 17.
Chloroplast membranes with their unique lipid composition are crucial for photosynthesis. Maintenance of the chloroplast membranes requires finely tuned lipid anabolic and catabolic reactions. Despite the presence of a large number of predicted lipid-degrading enzymes in the chloroplasts, their biological functions remain largely unknown. Recently, we described PLASTID LIPASE1 (PLIP1), a plastid phospholipase A that contributes to seed oil biosynthesis. The genome encodes two putative PLIP1 paralogs, which we designated PLIP2 and PLIP3. PLIP2 and PLIP3 are also present in the chloroplasts, but likely with different subplastid locations. In vitro analysis indicated that both are glycerolipid A lipases. In vivo, PLIP2 prefers monogalactosyldiacylglycerol as substrate and PLIP3 phosphatidylglycerol. Overexpression of or severely reduced plant growth and led to accumulation of the bioactive form of jasmonate and related oxylipins. Genetically blocking jasmonate perception restored the growth of the -overexpressing plants. The expression of and , but not , was induced by abscisic acid (ABA), and triple mutants exhibited compromised oxylipin biosynthesis in response to ABA. The triple mutants also showed hypersensitivity to ABA. We propose that PLIP2 and PLIP3 provide a mechanistic link between ABA-mediated abiotic stress responses and oxylipin signaling.
质体膜具有独特的脂质组成,对光合作用至关重要。质体膜的维持需要精细调节的脂质合成和分解反应。尽管质体中存在大量预测的脂质降解酶,但它们的生物学功能在很大程度上仍然未知。最近,我们描述了质体脂肪酶 1(PLIP1),一种参与种子油生物合成的质体磷脂酶 A。基因组编码两个假定的 PLIP1 旁系同源物,我们将其命名为 PLIP2 和 PLIP3。PLIP2 和 PLIP3 也存在于质体中,但可能具有不同的亚质体位置。体外分析表明,两者都是甘油酯 A 脂肪酶。在体内,PLIP2 优先作为底物使用单半乳糖二酰基甘油,而 PLIP3 使用磷脂酰甘油。或 的过表达严重降低了植物的生长,并导致生物活性形式的茉莉酸和相关氧化脂素的积累。遗传阻断茉莉酸感知恢复了过表达植物的生长。ABA 诱导 和 的表达,但不诱导 的表达,而 三重突变体在响应 ABA 时表现出氧化脂素生物合成受损。 三重突变体也对 ABA 表现出超敏性。我们提出 PLIP2 和 PLIP3 为 ABA 介导的非生物胁迫反应和氧化脂素信号之间提供了一种机制联系。