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Mutants of Chlamydomonas reinhardtii affected in phosphatidylglycerol metabolism and thylakoid biogenesis



Mutants of Chlamydomonas reinhardtii affected in phosphatidylglycerol metabolism and thylakoid biogenesis



Plant Physiology & Biochemistry (paris). 36(8): 609-619,.



Four mutants of Chlamydomonas reinhardtii have been isolated. The mf1 and mf2 strains are not photosynthetically active because they lack PSII activity; they are also devoid of DELTA3-trans-hexadecanoic acid-containing phosphatidylglycerol, and are almost unable to form trimeric LHC2 or develop thylakoid appressions. Seventy-seven K fluorescence emission spectra have shown that mf1 and mf2 mutants are unable to perform significant state transition and are blocked in a permanent state II. The photosynthetic Pmf1 and Pmf2 strains were respectively selected from mf1 and mf2 mutants grown on a minimal medium. Compared to wild type cells, the Pmf1 mutant had about 5% of DELTA3-trans-hexadecanoic acid-containing phosphatidylglycerol, a weak oxygen evolution activity, the capacity to form low amounts of trimeric LHC2 and a significant level of membrane stacking. A similar partial restoration of the wild type phenotype was observed in the Pmf2 mutant, but to a larger extent: the recovery of about 50% of DELTA3-trans-hexadecanoic acid-containing phosphatidylglycerol is correlated with the recovery of about 50% of PSII activity, large amounts of trimeric LHC2 and stacking of photosynthetic membranes. These results demonstrate a clear correspondence between the level of DELTA3-trans-hexadecanoic acid-containing phosphatidylglycerol, the formation of the trimeric LHC2 and the development of grana stacks. The direct involvement of this lipid in these characteristics was demonstrated by the restoration of trimeric LHC2, appressed thylakoids and state I/state II transitions in mf1 and mf2 mutants after in vivo selective targeting of DELTA3-trans-hexadecanoic acid-containing phosphatidylglycerol in their photosynthetic membranes.

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Accession: 009066485

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DOI: 10.1016/s0981-9428(98)80009-0


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