Lack of phosphatidylglycerol inhibits chlorophyll biosynthesis at multiple sites and limits chlorophyllide reutilization in the cyanobacterium Synechocystis 6803.

The negatively charged lipid phosphatidylglycerol (PG) constitutes up to 10% of total lipids in photosynthetic membranes and its deprivation in cyanobacteria is accompanied by chlorophyll (Chl) depletion. Indeed, radioactive labeling of the PG depleted DeltapgsA mutant of Synechocystis 6803, which is not able to synthesize PG, proved inhibition of Chl biosynthesis due to restriction on the formation of 5-aminolevulinic acid and protochlorophyllide. Although the mutant accumulated chlorophyllide, the last Chl precursor, we demonstrated that it originated from dephytylation of existing Chl and not from the block in the Chl biosynthesis. The lack of de novo produced Chl under PG depletion was accompanied by a significantly weakened biosynthesis of both monomeric and trimeric photosystem I (PSI) complexes, though the decrease in cellular content was manifested only for the trimeric form. However, our analysis of DeltapgsA mutant, which lacked trimeric PSI due to the absence of the PsaL subunit, suggested that the virtually stability of monomeric PSI is a result of disintegration of PSI trimers. Interestingly, the loss of trimeric PSI was accompanied by accumulation of monomeric PSI associated with the newly synthesized CP43 subunit of Photosystem II. We conclude that the absence of PG results in the inhibition of Chl biosynthetic pathway, which impairs synthesis of PSI despite the accumulation of chlorophyllide released from the degraded Chl-proteins. Based on the knowledge about the role of PG in prokaryotes we hypothesize that the synthesis of Chl and PSI complexes are co-located in a membrane microdomain requiring PG for integrity