The toc132toc120 heterozygote mutant of Arabidopsis thaliana accumulates decreased levels of the major chloroplast lipids.

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.