Characterization of the effects of chloride depletion on oxygen evolving activity in the R305D and R305K mutants of the CP43 protein of photosystem II / by Brandon Douglas Burch.

Author/creator Burch, Brandon Douglas author.
Other author Putnam-Evans, Cindy, degree supervisor.
Other author East Carolina University. Department of Biology.
Format Theses and dissertations
Production2003.
Descriptionv, 117 leaves : illustrations ; 28 cm
Supplemental ContentAccess via ScholarShip
Subjects

Summary The CP43 protein, encoded by the psbC gene, is a component of Photosystem II (PSII) in higher plants, algae, and cyanobacteria. Previously, alteration of arginine 305 in the large extrinsic loop (LEE) of CP43 to a serine residue was shown to result in a mutant exhibiting decreased rates of oxygen evolving activity and enhanced sensitivity to photoinactivation. These effects were greatly exacerbated when the mutant was grown in chloride-deficient media. In the present study, two additional CP 43 mutants, R305K and R305D, were characterized to determine the effect on PSII activity of altering the charge distribution at this site under both complete and chloride-deficient growth conditions. In complete media, the R305K and R305D strains exhibited near normal growth and evolved oxygen at high rates (80% and 60-65% of control rates, respectively). Both showed small increases in susceptibility to photoinactivation. Under conditions of chloride depletion, the R305K strain exhibited slightly reduced growth, evolved oxygen at 35-40% of the wild type rate, and produced PSII centers that were more sensitive to photoinactivation by a factor of two. The R305D mutant lost the capacity for photoautotrophic growth in low chloride media and evolved oxygen to only 5% of control rates. In addition, this mutant photoinactivated at a rate 6 times faster than the control. Isolated PSII particles from both R305K and R305D lacked spectrophotometrically-detectable levels of cytochrome c₅₅₀, regardless of media type. Collectively, these results indicate that both the R305K and R305D strains are defective in their ability to utilize chloride to carry out efficient oxygen evolution, with the R305D mutant being more severely affected, and that these defects may arise due to an interruption in the interaction between the LEL of CP43 and another component of PSII, possibly cytochrome c₅₅₀.
General notePresented to the faculty of the Department of Biology.
General noteAdvisor: Cindy L. Putnam-Evans
Dissertation noteM.S. East Carolina University 2003
Bibliography noteIncludes bibliographical references (leaves 102-117).
Genre/formAcademic theses.
Genre/formAcademic theses.
Genre/formThèses et écrits académiques.

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