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.

The lipid composition of thylakoid membranes inside chloroplasts is conserved from leaves to developing embryos. A finely tuned lipid assembly machinery is required to build these membranes during development. Contrary to thylakoid lipid biosynthetic enzymes, the functions of most predicted chloroplast lipid-degrading enzymes remain to be elucidated. Here, we explore the biochemistry and physiological function of an Arabidopsis thylakoid membrane-associated lipase, PLASTID LIPASE1 (PLIP1). PLIP1 is a phospholipase A In vivo, PLIP1 hydrolyzes polyunsaturated acyl groups from a unique chloroplast-specific phosphatidylglycerol that contains 16:1 as its second acyl group. Thus far, a specific function of this 16:1 -containing phosphatidylglycerol in chloroplasts has remained elusive. The gene is highly expressed in seeds, and mutant seeds contain less oil and exhibit delayed germination compared with the wild type. Acyl groups released by PLIP1 are exported from the chloroplast, reincorporated into phosphatidylcholine, and ultimately enter seed triacylglycerol. Thus, 16:1 uniquely labels a small but biochemically active plastid phosphatidylglycerol pool in developing Arabidopsis embryos, which is subject to PLIP1 activity, thereby contributing a small fraction of the polyunsaturated fatty acids present in seed oil. We propose that acyl exchange involving thylakoid lipids functions in acyl export from plastids and seed oil biosynthesis.

SENSITIVE TO FREEZING2 (SFR2) is crucial for protecting chloroplast membranes following freezing in Arabidopsis (Arabidopsis thaliana). It has been shown that SFR2 homologs are present in all land plants, including freezing-sensitive species, raising the question of SFR2 function beyond freezing tolerance. Similar to freezing, salt and drought can cause dehydration. Thus, it is hypothesized that in freezing-sensitive plants SFR2 may play roles in their resilience to salt or drought. To test this hypothesis, SlSFR2 RNAi lines were generated in the cold/freezing-sensitive species tomato (Solanum lycopersicum [M82 cv]). Hypersensitivity to salt and drought of SlSFR2-RNAi lines was observed. Higher tolerance of wild-type tomatoes was correlated with the production of trigalactosyldiacylglycerol, a product of SFR2 activity. Tomato SFR2 in vitro activity is Mg 2+ -dependent and its optimal pH is 7.5, similar to that of Arabidopsis SFR2, but the specific activity of tomato SFR2 in vitro is almost double that of Arabidopsis SFR2. When salt and drought stress were applied to Arabidopsis, no conditions could be identified at which SFR2 was induced prior to irreversibly impacting plant growth, suggesting that SFR2 protects Arabidopsis primarily against freezing. Discovery of tomato SFR2 function in drought and salt resilience provides further insights into general membrane lipid remodeling-based stress tolerance mechanisms and together with protection against freezing in freezing-resistant plants such as Arabidopsis, it adds lipid remodeling as a possible target for the engineering of abiotic stress-resilient crops.

In the Methods section of the above publication, the SALK T-DNA insertion line identifiers were stated incorrectly. We also omitted important details describing the construction of triple mutant lines, and the germination assay. Under "Plant Material and Growth Conditions," we mistakenly defined "SALK_1234548 (plip2-1)" and "SALK_134525 (plip2-2)". The correct numbers should be SALK_123548 (plip2-1) and SALK_134251 (plip2-2), respectively.