Abstract
Exposure of photosynthetic organisms to strong light leads to photoinhibition of photosystem II (PSII). We isolated mutants of histidine kinases (Hiks) in which the extent of photoinhibition was higher than that in wild-type cells. In ΔHik2 cells, photoinhibition was apparently accelerated by hyperosmotic stress with 0.5 M sorbitol due to the inhibition of repair of damaged PSII. Inactivation of Hik16 and Hik33 also enhanced the photoinhibition. ΔHik16 cells were not able to uptake sorbitol under hyperosmotic conditions, whereas ΔHik33 degradated chlorophyll under strong light. Thus, effects of inactivation of Hik2, Hik16 and Hik33 on tolerance of PSII are different. These results suggest that Synechocystis assigns different function to Hik2, Hik16 and Hik33 to tolerate photoinhibition.