For over two billion years, most life on earth has depended on oxygenic photosynthesis for fuel and sustenance. In plants, the descendants of ancient cyanobacteria operate as subcellular photosynthetic organelles, the chloroplasts, where an extensive membrane infrastructure converts light into high-energy chemical bonds. Chloroplast membranes are distinctive in that their lipid components primarily rely on sugars as head groups, as opposed to phosphate-based moieties. Plant membrane metabolism is therefore highly geared towards the conversion of de novo-synthesized phospholipids into chloroplast galactolipids, and in Arabidopsis thaliana, portions of these pathways operate in parallel at the chloroplast and the endoplasmic reticulum (ER). Here, I present novel insights into the roles of chloroplast-associated lipid phosphate phosphatases LPPγ, LPPε1, and LPPε2, which dephosphorylate phosphatidic acid (PA) to make diacylglycerol (DAG), the substrate for galactosylation reactions. LPPγ and LPPε1 were determined to act on ER-assembled PA, with their catalytic activity at the chloroplast outer envelope membrane. All three chloroplast LPPs appeared uninvolved in the dephosphorylation of chloroplast-derived PA, despite localization of LPPε2 to the interior chloroplast membranes. Growth inhibition in lppγ lppε1 double mutant plants implicated PA pools at the outer envelope membrane as affecting developmental regulation, thus linking LPPγ or LPPε1 to plant growth and development.The connection between chloroplast lipid metabolism and plant growth regulation was also exploited in a suppressor screen using a transgenic Arabidopsis line, in which overexpression of the plastid lipase-encoding gene PLIP3 leads to accumulation of the defense hormone jasmonic acid (JA). These PLIP3-OX lines exhibit unique JA-induced morphological phenotypes, and suppression of these phenotypes was targeted in the screen. One mutant, sup72, had a point mutation in KEEP ON GOING (KEG) which co-segregated with the suppression phenotype. KEG is known to have a repressive role in abscisic acid (ABA) signaling, and its apparent effects on JA signaling in sup72 indicate it may also facilitate coordination of the ABA and JA pathways. In another mutant, sup11, PLIP3-OX suppression was caused by a nonsense mutation in CDK8, linking the gene product to activation of JA-responsive transcription. Overall, these Arabidopsis lines with distorted chloroplast lipid pathways provide greater insight into the nuances of metabolism and lipid trafficking, as well as connections to broader elements of plant growth and development.
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