Effects of Inactivating psbM and psbT on Photodamage and Assembly of Photosystem II in Synechocystis sp. PCC 6803

• Published in: Biochemistry (Easton) 2008-11, Vol.47 (44), p.11637-11646
• Main Authors: Bentley, Fiona K, Luo, Hao, Dilbeck, Preston, Burnap, Robert L, Eaton-Rye, Julian J
• Format: Article
• Language: English
• Subjects: Bacterial Proteins - antagonists & inhibitors; Bacterial Proteins - chemistry; Bacterial Proteins - genetics; Bacterial Proteins - metabolism; Base Sequence; DNA Primers - genetics; DNA, Bacterial - genetics; Gene Deletion; Genes, Bacterial; Kinetics; Multiprotein Complexes; Mutation; Oxygen - metabolism; Photochemistry; Photosystem II Protein Complex - antagonists & inhibitors; Photosystem II Protein Complex - chemistry; Photosystem II Protein Complex - genetics; Photosystem II Protein Complex - metabolism; Recombinant Proteins - chemistry; Recombinant Proteins - genetics; Recombinant Proteins - metabolism; Synechocystis - genetics; Synechocystis - metabolism
• ISSN: 0006-2960; 1520-4995
• DOI: 10.1021/bi800804h

PsbM and PsbT have been assigned to electron densities on both photosystem II (PSII) monomers at the PSII dimer interface in X-ray crystallographic structures from Thermosynechoccocus elongatus and T. vulcanus. Our results show that removal of either or both proteins from Synechocystis sp. PCC 6803 resulted in photoautotrophic strains but the ΔPsbM:ΔPsbT mutant did not form stable dimers. A CP43-less PSII monomer accumulated in both single mutants, although absence of PsbT destabilized PSII to a greater extent than removing PsbM. Additionally, ΔPsbT cells exhibited slowed electron transfer between the plastoquinone electron acceptors, QA and QB; however, S-state cycling in both mutants was similar to wild type. Oxygen evolution in these mutants rapidly inactivated following exposure to high light where recovery required protein synthesis and could proceed in the dark in ΔPsbM cells but required light in ΔPsbT cells. Interestingly, the extent of recovery of oxygen-evolving activity was greatest in the ΔPsbM:ΔPsbT strain. We also found recovery required Psb27 in ΔPsbT cells although, under our conditions, the ΔPsb27 strain remained similar to wild type. In contrast, the ΔPsbM:ΔPsb27 mutant could not assemble PSII beyond a CP43-minus intermediate. Our results suggest essential roles for Psb27 in biogenesis in the ΔPsbM strain and for repair from photodamage in cells lacking PsbT.