Department of Biological Sciences, Western Illinois University, Waggoner Hall 311, 1 University Circle, Macomb, IL, 61455, USA.
Department of Biological Sciences, Western Illinois University, Waggoner Hall 311, 1 University Circle, Macomb, IL, 61455, USA.
Phytochemistry. 2021 Apr;184:112652. doi: 10.1016/j.phytochem.2020.112652. Epub 2021 Jan 31.
We used ESI-MS/MS to profile glycerolipids in a mutant of Arabidopsis thaliana that is null and heterozygous for the TOC132 and TOC120 genes, and is referred to as the toc132toc120± mutant. The goal was to assess the impact of a defective atToc132/120 receptor on the accumulation of chloroplast lipids. The mutant accumulated decreased amounts of monogalactosyldiacylglycerol (MGDG), digalactosyldiacylglycerol (DGDG) and phosphatidylglycerol (PG). In the cold-acclimated mutant, PG accumulated at the control levels. However, 34:4-PG (18:3/16:1Δ) was significantly decreased, which indicates that the mutant was impaired in synthesis of the chloroplast-derived PG. Major molecular species of MGDG and DGDG were significantly decreased, which was indicative of the decreased levels of triunsaturated fatty acids in galactolipids. The cold-acclimated mutant accumulated increased levels of phosphatidylcholine (PC), phosphatidylethanolamine (PE) and phosphatidylserine (PS), which indicate that defect in the atToc132/120 receptor did not impair the ER pathway of lipid synthesis. Both cold-acclimated wildtype and mutant plants accumulated increased levels of phosphatidic acid (PA). The increased levels of major molecular species of PA suggest that some pool of PA was derived from degradation of both the chloroplast and extra-chloroplast lipids. The cold-acclimated mutant had decreased double bond index (DBI) and increased acyl chain length (ACL), which was indicative of decreased membrane fluidity. However, a decrease in the ratio of MGDG to DGDG indicate that the mutant was capable of remodeling membrane lipids in response to low temperatures. We conclude that the defective Toc132/120 receptor resulted in decreased synthesis of chloroplast lipids and decreased membrane fluidity.
我们使用 ESI-MS/MS 分析了拟南芥 toc132toc120±突变体（TOC132 和 TOC120 基因缺失和杂合突变体）中的甘油脂。该突变体积累了较少的单半乳糖二酰甘油（MGDG）、双半乳糖二酰甘油（DGDG）和磷脂酰甘油（PG）。在冷驯化突变体中，PG 积累量与对照水平相当。然而，34:4-PG（18:3/16:1Δ）显著减少，这表明突变体在叶绿体衍生的 PG 合成中受到损伤。MGDG 和 DGDG 的主要分子种类显著减少，这表明半乳糖脂中的三不饱和脂肪酸水平降低。冷驯化突变体积累了增加的磷脂酰胆碱（PC）、磷脂乙醇胺（PE）和磷脂丝氨酸（PS），这表明 atToc132/120 受体的缺陷并没有损害 ER 途径的脂质合成。冷驯化的野生型和突变体植物都积累了增加的磷脂酸（PA）水平。PA 的主要分子种类增加表明，某些 PA 池可能来自叶绿体和质外体脂质的降解。冷驯化的突变体具有降低的双键指数（DBI）和增加的酰基链长（ACL），这表明膜流动性降低。然而，MGDG 与 DGDG 的比例降低表明，突变体能够响应低温重塑膜脂。我们得出结论，缺陷的Toc132/120 受体导致叶绿体脂质合成减少和膜流动性降低。
