| The objective of this project has been to study molecular mechanisms that plants use to avoid damage caused by excess light. Light that exceeds the photosynthetic capacity of a plant can impair the ability of photosystem II to evolve oxygen and can ultimately lead to degradation of proteins within the reaction center. Photoinhibitory reactions caused by ultraviolet B radiation (280-320 nm) are of particular concern since decreased stratospheric ozone is predicted to enhance levels of this radiation incident on the earth's surface. Photoinhibition can be initiated by inopportune events that create damaging redox states within the photosystem II complex. One mechanism for protection against high light involves thermal deactivation of energy within pigment beds. In addition, there is increasing evidence that secondary electron transport pathways within photosystem II can protect against potentially damaging redox states. Experiments using photosynthetic membranes poised at different ambient redox potentials demonstrate that light-induced damage to photosystem II is controlled by a redox component within the reaction center with a pH-independent midpoint potential of +20 mV in thylakoid membranes and +100 mV in photosystem II-enriched membranes. The rate of photoinhibition is slow when the redox component is oxidized, but increases up to 30-fold when the component is reduced. Here, evidence is provided that the redox component is cytochrome b559, an intrinsic heme protein of the photosystem II reaction center, and that the photoprotective pathway involves electron transfer to the cytochrome from the reduced form of pheophytin. The results of this dissertation support a model in which the low potential (LP) form of cytochrome b559 protects photosystem II against photoinhibition by deactivating a rarely formed, but unfavorable redox state of photosystem II, namely, P680/Pheo... |
