Restoration of thylakoid appression by Δ 3- trans-hexadecenoic acid-containing phosphatidylglycerol in a mutant of Chlamydomonas reinhardtii. Relationships with the regulation of excitation energy distribution

Abstract

The mf 2 mutant of Chlamydomonas reinhardtii lacks both Photosystem II reaction centers (RC II) and Δ3-trans-hexadecenoic fatty acid (C16:1-trans). Previous studies have shown that, by comparison with a simple mutant lacking only RC II, the additional deficiency in C16:1-trans results in: (1) a very low fluorescence yield; (2) a predominant and persistent energy transfer from the main light-harvesting antenna towards Photosystem I, which cannot be reversed by state II-state I transition; (3) absence of the oligomeric form of the chlorophyll a + b-protein complex CP II. These defects can be reversed by incorporating this fatty acid in vivo into the photosynthetic membranes of the mf 2 mutant with C16:1-trans-containing phosphatidylglycerol (PG-C16:1-trans) liposomes. In this paper, subsequent ultrastructural analyses show that: (1) by comparison with the simple RC-II-lacking mutant, the additional C16:1-trans deficiency in the mf 2 mutant results in extensive thylakoid destacking; (2) supplementation of the mf 2 mutant with PG-C16:1-trans liposomes during growth induces a significant re-appression of thylakoid membranes; (3) such restacking was not observed in the presence of cycloheximide or using PG-C16:0 (PG-palmitate) liposomes. A strong correlation therefore appears between the presence of C16:1-trans in the thylakoid membranes of C. reinhardtii and the ability of these membranes to stack, to present the oligomeric organization of CP II and to restore state II-state I transitions in excitation energy distribution between the two photosystems. The possible involvement of PG-C16:1-trans in the synthesis and/or in the stabilization of the CP II apoproteins during the biogenesis of thylakoids is considered.