PARENT SESSION
Posters P1B Photo-oxidative stress, photoinhibition. Abstracts (394-443)

The FtsH protease is involved in the repair of Photosystem II after damage by UV-B radiation in Synechocystis 6803. Cosmin Sicora^{*,1, 2}, Otilia Cheregi², Peter Kos², Peter Nixon³, Imre Vass², ¹ Department of Biology, Mount Allison University, Sackville, NB, Canada² Institute of Plant Biology, Biological Research Center, Szeged, Hungary³

ABSTRACT- We have investigated the role of the FtsH protease in the repair of UV-damaged PSII in Synechocystis 6803 cells. UV-B radiation induces a 3-4 fold increase in the transcript level of the sll0028 gene, that encodes an FtsH homologue. The UV-B induced loss of oxygen evolving activity was accelerated in the FtsH mutant as compared to the WT cells. In the presence of the protein synthesis inhibitor lincomycin the rate of UV-B induced inhibition of oxygen evolution was significantly accelerated in the WT, but not in the FtsH mutant. In addition, the mutation almost completely abolished the restoration of oxygen evolution in visible light following the UV-B treatment. Decay of flash-induced fluorescence when measured in the presence of DCMU has a fast phase, which arises from the Tyr-Z^.Q_A^- recombination in UV-illuminated cells showing that UV light disrupts the electron transfer between the Mn cluster and Tyr-Z. The fast phase is more pronounced in the FtsH than in the WT cells, and restored completely under visible light in the WT, but only to a small extent in the FtsH strain. These data show that PSII repair is almost completely blocked in the absence of the FtsH protease both under UV illumination and in visible light following the UV-B exposure. The loss of the D1 protein during UV-B illumination is also slowed down in the FtsH mutant as compared to the WT cells both in the presence and absence of lincomycin, showing that D1 degradation is retarded in the FtsH mutant. From these data we conclude that the FtsH protease is involved in the degradation of the UV-damaged D1 protein, which is required for PSII repair via de novo synthesis and incorporation of new D1copies into the PSII reaction centers.

KEY WORDS: UV-B, Synechocystis , protease, PSII