Maintenance of functional Photosystem II by D1 protein turnover

摘要

Water splitting in PS II involves a series of dangerous reactions potentially harmful for both the functional and structural properties of the complex. Despite a number of protection mechanisms there is, however, always an inherent inhibition occurring in PS II with a very low quantum yield (Tyystjarvi and Aro, 1996; Anderson et al., 1997). Thus, even at low light irradiances oxidative damages are occurring in PS II and lead to an irreversible damage of the PS II complex (Keren et al., 1997). Withincreasing irradiances such damages occur more and more frequently. Visible light induced oxidative damage is directed mainly towards only one specific target protein, the D1 protein in the reaction center of PS II (Mattoo et al., 1989), whereas the other protein components of PS II remain largely unaffected. As long as plants can cope with the light-induced damage to the D1 protein by constant D1 synthesis and repair of PS II, no visible or measurable symptoms of photoinhibition of photosynthesis can be recorded in vivo. Indeed, such constant turnover of the D1 protein in PS II cannot be detected by monitoring chlorophyll fluorescence parameters or by measurements of steady state oxygen evolution. However, as soon as the capacity for repair of damagedPS II centers is exceeded at increasing irradiances by the more frequently occurring damaging reactions, an irreversible inhibition of PS II can be recorded in vivo (Aro et al., 1993). A mere light-induced irreversible inhibition of PS II is not commonin vivo but occurs more often when high irradiances prevail in combination with other stress factors like drought, low or high temperatures, CO_2 limitation or nutrient deprivation, which generally hamper the repair of damaged PSII. Here we provide someinsights into the mechanisms involved in the maintenance of functional PSII via rapid D1 protein turnover.