Abstract
We have isolated, sequenced, mapped and disrupted a gene, CCC2, from Saccharomyces cerevisiae. This gene displays non-allelic complementation of the Ca(2+)-sensitive phenotype conferred by the csg1 mutation. Analysis of the CCC2p amino acid sequence reveals that it encodes a member of the P-type ATPase family and is most similar to a subfamily thought to consist of Cu2+ transporters, including the human genes that mutate to cause Wilson disease and Menkes disease. The ability of this gene, in two or more copies, to reverse the csg1 defect suggests that Ca(2+)-induced death of csg1 mutant cells is related to Cu2+ metabolism. Cells without CCC2 require increased Cu2+ concentrations for growth. Therefore CCC2p may function to provide Cu2+ to a cellular compartment rather than in removal of excess Cu2+.
Publication types
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adenosine Triphosphatases / classification
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Adenosine Triphosphatases / genetics*
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Adenosine Triphosphatases / metabolism
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Amino Acid Sequence
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Base Sequence
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Calcium / metabolism
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Cation Transport Proteins*
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Cloning, Molecular
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Copper / metabolism
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Copper Transport Proteins
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DNA, Fungal / genetics
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Fungal Proteins / genetics*
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Genes, Fungal*
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Genetic Complementation Test
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Molecular Sequence Data
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Mutation
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Phenotype
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Restriction Mapping
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Saccharomyces cerevisiae / enzymology*
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Saccharomyces cerevisiae / genetics*
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Saccharomyces cerevisiae / growth & development
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Saccharomyces cerevisiae Proteins*
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Sequence Homology, Amino Acid
Substances
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CCC2 protein, S cerevisiae
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Cation Transport Proteins
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Copper Transport Proteins
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DNA, Fungal
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Fungal Proteins
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Saccharomyces cerevisiae Proteins
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Copper
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Adenosine Triphosphatases
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Calcium