Abstract
Respiration-defective pet mutants of Saccharomyces cerevisiae, assigned to complementation group G25, are grossly deficient in mitochondrial respiratory and ATPase complexes. This phenotype is usually found in strains impaired in mitochondrial protein synthesis. The G25 mutants, however, synthesize all of the proteins encoded by mitochondrial DNA. The mutants are also able to import and process cytoplasmically derived subunits of these enzymes. These results are most compatible with the idea that the gene defined by G25 mutants (RCA1) codes for a protein essential for the assembly of functional respiratory and ATPase complexes. The RCA1 gene has been cloned by complementation of an rca1 mutant with a yeast genomic library. The sequence of the encoded product shows Rca1 protein to be a new member of a recently described family of ATPases. The Rca1 protein is a mitochondrial membrane protein and is the third known member of this family implicated to function in the biogenesis of mitochondria. The primary structure of Rca1 protein indicates several distinct domains in addition to the common purine nucleotide binding region shared by all members of this protein family. One, located in the amino-terminal half, contains two hydrophobic stretches of sufficient length to span a membrane lipid bilayer.
Highlights
Is the third known member of this family implicated to Nor does the respiratory defect appear to be related to faulty function in the biogenesis of mitochondria
Structure of Rcal protein indicates several distinct do- the evidence is consistent with the idea that Rcal protein is mainsinadditiontothecommonpurinenucleotide requiredeither directlyor indirectly a t a later step during binding region shared by all members of this protein assembly of the subunits into thefunctional ATPase and resfamily
Mutations in RCAl Cause a Pleiotropic Deficiency of CytochromeOxidase,Coenzyme&Hz-cytochrome c Reductase, and ATPase-The rcal mutants reported here were previously assigned to complementationgroup G25 of our pet mutant collection [4]. This group consists of the mutant C30 and 16 other independent isolates, all derived from the respiration competent haploid strain S. cerevisiae D273-10B/A1
Summary
Mutations in RCAl Cause a Pleiotropic Deficiency of CytochromeOxidase,Coenzyme&Hz-cytochrome c Reductase, and ATPase-The rcal mutants reported here were previously assigned to complementationgroup G25 of our pet mutant collection [4] This group consists of the mutant C30 and 16 other independent isolates, all derived from the respiration competent haploid strain S. cerevisiae D273-10B/A1. Similar results have been reported in strainswith mutations that selectively block synthesis of the bc, complex [38, 39] These assays were extended to cytochrome oxidase, cu-ketoglutarate dehydrogenase, and ATPase subunits that are known to be stable even when the parent oligomeric complexes fail to be assembled [40,41,42].
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