ATP is a driving force in the repair of photosystem II during photoinhibition

Abstract

Repair of photosystem II (PSII) during photoinhibition involves replacement of photodamaged D1 protein by newly synthesized D1 protein. In this review, we summarize evidence for the indispensability of ATP in the degradation and synthesis of D1 during the repair of PSII. Synthesis of one molecule of the D1 protein consumes more than 1,300 molecules of ATP equivalents. The degradation of photodamaged D1 by FtsH protease also consumes approximately 240 molecules of ATP. In addition, ATP is required for several other aspects of the repair of PSII, such as transcription of psbA genes. These requirements for ATP during the repair of PSII have been demonstrated by experiments showing that the synthesis of D1 and the repair of PSII are interrupted by inhibitors of ATP synthase and uncouplers of ATP synthesis, as well as by mutation of components of ATP synthase. We discuss the contribution of cyclic electron transport around photosystem I to the repair of PSII. Furthermore, we introduce new terms relevant to the regulation of the PSII repair, namely, “ATP-dependent regulation” and “redox-dependent regulation,” and we discuss the possible contribution of the ATP-dependent regulation of PSII repair under environmental stress.