Disease relevance of sod2

• However, initial attempts to express sod2 in Escherichia coli using the T7 promoter failed [1].

High impact information on sod2

• The sod2 gene amplification could be selected stepwise and the degree of such amplification correlated with the level of Na+ or Li+ tolerance [2].
• The proton flux mediated by sod2 was also found to be unaffected by perturbation of membrane potential or the plasma membrane proton gradient [3].
• This bidirectional activity was also detected in S. cerevisiae strains expressing sod2 and expression of this gene complemented the sodium and lithium sensitivity resulting from inactivation of the ENA1/PMR2 encoded Na+-exporting ATPases [3].
• The Schizosaccharomyces pombe sod2 gene provides a useful model system to analyze this process. sod2 is near the telomere of chromosome I and encodes a plasma membrane Na(+)(Li(+))/H(+) antiporter [4].
• To determine whether proximity to a telomere is necessary for sod2 amplification, a strain was constructed in which the gene was moved to the middle of the same chromosomal arm [5].

Biological context of sod2

• Relative to wild-type cells, mutants with defects in the DNA damage aspect of the rad checkpoint control pathway had an increased frequency of sod2 amplification, whereas mutants defective in the S-phase completion checkpoint did not [5].
• Effects of genome position and the DNA damage checkpoint on the structure and frequency of sod2 gene amplification in fission yeast [5].
• However, they showed a Na(+)-sensitive phenotype which was greatly intensified by deletion of the sod2+ gene (which encodes the major determinant for efflux of Na+ ions), and clearly ameliorated by deletion of the pzh1 phosphatase, as well as by moderate concentrations of KCl in the medium [6].
• The effect of sod2 expression on E. coli varied depending on the E. coli genotype [1].
• The effect of mutagenesis of conserved polar amino acids of sod2 was examined by expressing 10 different mutant forms of sod2 in sod2 deficient S. pombe and characterizing salt tolerance [7].

Associations of sod2 with chemical compounds

• Conservative mutations (Asp to Glu) of Asp266 and 267 failed to restore sod2 function [7].

Other interactions of sod2

• Na+ efflux and Na+ tolerance depend on a putative P-type ATPase encoded by the gene ENA1(PMR2) in Saccharomyces cerevisiae and on a putative Na+/H+ antiporter encoded by the gene sod2 in Schizosaccharomyces pombe [8].

References