TY - JOUR
T1 - A physiological role for Saccharomyces cerevisiae copper/zinc superoxide dismutase in copper buffering
AU - Culotta, Valeria Cizewski
AU - Joh, Hung Dong
AU - Lin, Su Ju
AU - Slekar, Kimberly Hudak
AU - Strain, Jeffrey
PY - 1995/12/15
Y1 - 1995/12/15
N2 - The copper toxicity of yeast lacking the CUP1 metallothionein is suppressed by overexpression of the CRS4 gene. We now demonstrate that CRS4 is equivalent to SOD1, encoding copper/zinc superoxide dismutase (SOD). While overexpression of SOD1 enhanced copper resistance, a deletion of SOD1, but not SOD2 (encoding manganese SOD), conferred an increased sensitivity toward copper. This role of SOD1 in copper buffering appears unrelated to its superoxide scavenging activity, since the enzyme protected against copper toxicity in anaerobic as well as aerobic conditions. The distinct roles of SOD1 in copper and oxygen radical homeostasis could also be separated genetically: the pmr1, bsd2, and ATX1 genes that suppress oxygen toxicity in sod1 mutants failed to suppress the copper sensitivity of these cells. The Saccharomyces cerevisiae SOD1 gene is transcriptionally induced by copper and the ACE1 transactivator, and we demonstrate here that this induction of SOD1 promotes protection against copper toxicity but is not needed for the SOD1- protection against oxygen free radicals. Collectively, these findings indicate that copper/zinc SOD functions in the homeostasis of copper via mechanisms distinct from superoxide scavenging.
AB - The copper toxicity of yeast lacking the CUP1 metallothionein is suppressed by overexpression of the CRS4 gene. We now demonstrate that CRS4 is equivalent to SOD1, encoding copper/zinc superoxide dismutase (SOD). While overexpression of SOD1 enhanced copper resistance, a deletion of SOD1, but not SOD2 (encoding manganese SOD), conferred an increased sensitivity toward copper. This role of SOD1 in copper buffering appears unrelated to its superoxide scavenging activity, since the enzyme protected against copper toxicity in anaerobic as well as aerobic conditions. The distinct roles of SOD1 in copper and oxygen radical homeostasis could also be separated genetically: the pmr1, bsd2, and ATX1 genes that suppress oxygen toxicity in sod1 mutants failed to suppress the copper sensitivity of these cells. The Saccharomyces cerevisiae SOD1 gene is transcriptionally induced by copper and the ACE1 transactivator, and we demonstrate here that this induction of SOD1 promotes protection against copper toxicity but is not needed for the SOD1- protection against oxygen free radicals. Collectively, these findings indicate that copper/zinc SOD functions in the homeostasis of copper via mechanisms distinct from superoxide scavenging.
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U2 - 10.1074/jbc.270.50.29991
DO - 10.1074/jbc.270.50.29991
M3 - Article
C2 - 8530401
AN - SCOPUS:0038153078
SN - 0021-9258
VL - 270
SP - 29991
EP - 29997
JO - Journal of Biological Chemistry
JF - Journal of Biological Chemistry
IS - 50
ER -