Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C1832526 (
PCC
)
5,967
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
We investigated the functions of a membrane-associated manganese superoxide dismutase (MnSOD) of the heterocystous cyanobacterium Anabaena sp.
PCC
7120. The gene sodA encoding MnSOD was inactivated by interposon mutagenesis and it was confirmed by Southern hybridization and immunoblotting. The strain
A17
, lacking sodA, grew more slowly than the wild type, and the difference in growth rates between the two strains became larger with an increase in growth light intensity. More severe inhibition of growth of
A17
was observed when the cells were grown in the absence of combined nitrogen. Complementation of
A17
with a full copy of the sodA gene restored the wild-type phenotypes. Strain
A17
produced more malondialdehyde than did the wild type, especially under high light intensity, indicating more lipid peroxidation in the absence of MnSOD.
A17
was also more susceptible to photoinhibition by a high light, and it was shown that both PSII and PSI were more severely damaged by the photoinhibitory light in
A17
, suggesting that the MnSOD plays important roles in protection of both photosystems. Immunoblotting revealed that the MnSOD was present in vegetative cells and heterocysts. Light greatly stimulated nitrogenase activity in the wild type under both aerobic and anaerobic conditions, but stimulated nitrogenase activity in
A17
only slightly in air. The results suggest that reactive oxygen species produced in heterocysts under aerobic conditions cause the inactivation of nitrogenase in the absence of MnSOD.
...
PMID:A membrane-associated Mn-superoxide dismutase protects the photosynthetic apparatus and nitrogenase from oxidative damage in the Cyanobacterium Anabaena sp. PCC 7120. 1730 50