Alastair McEwan - Academia.edu (original) (raw)

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Papers by Alastair McEwan

Research paper thumbnail of Phenotypic and genetic characterization of cytochrome c2-deficient mutants of Rhodobacter sphaeroides

Biochemistry, 1988

Rhodobacter sphaeroides mutants lacking cytochrome c2 (cyt c2) have been constructed by site-spec... more Rhodobacter sphaeroides mutants lacking cytochrome c2 (cyt c2) have been constructed by site-specific recombination between the wild-type genomic cyt c2 structural gene (cycA) and a suicide plasmid containing a defective cyc operon where deletion of cycA sequences was accompanied by insertion of a KnR gene. Southern blot analysis confirmed that the wild-type cyc operon was exchanged for the inactivated cycA gene, presumably by double-reciprocal recombination. Spectroscopic and immunochemical measurements, together with genetic complementation, established that the inability of these mutants to grow under photosynthetic conditions was due to the lack of cyt c2. The cyt c2 deficient strains reduced photooxidized reaction center complexes approximately 4 orders of magnitude more slowly than the parent strain.

Research paper thumbnail of Phenotypic and genetic characterization of cytochrome c2-deficient mutants of Rhodobacter sphaeroides

Biochemistry, 1988

Rhodobacter sphaeroides mutants lacking cytochrome c2 (cyt c2) have been constructed by site-spec... more Rhodobacter sphaeroides mutants lacking cytochrome c2 (cyt c2) have been constructed by site-specific recombination between the wild-type genomic cyt c2 structural gene (cycA) and a suicide plasmid containing a defective cyc operon where deletion of cycA sequences was accompanied by insertion of a KnR gene. Southern blot analysis confirmed that the wild-type cyc operon was exchanged for the inactivated cycA gene, presumably by double-reciprocal recombination. Spectroscopic and immunochemical measurements, together with genetic complementation, established that the inability of these mutants to grow under photosynthetic conditions was due to the lack of cyt c2. The cyt c2 deficient strains reduced photooxidized reaction center complexes approximately 4 orders of magnitude more slowly than the parent strain.

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