1. Mitochondria of Saccharomyces cerevisiae contain two tRNA's that are acylated with threonine. The two isoaccepting species (tRNA1Thr and tRNA2Thr) can be separated by reversed-phase chromatography on RPC-5. 2. A cytoplasmic mutant has been isolated which lacks tRNA1Thr but has normal levels of tR
Assembly of the mitochondrial membrane system XVIII
β Scribed by Tzagoloff, Alexander ;Foury, Francoise ;Akai, Anna
- Publisher
- Springer
- Year
- 1976
- Tongue
- English
- Weight
- 943 KB
- Volume
- 149
- Category
- Article
- ISSN
- 0026-8925
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β¦ Synopsis
- Fourteen cytoplasmic mutants of Saccharomyces cerevisiae with a specific deficiency of cytochrome b have been studied. The mutations have been shown to occur in two separate genetic loci, COB 1 and COB 2. These loci can be distinguished by mit- X mit- crosses. Pairwise crosses of cytochrome b mutants belonging to different loci yield 4-6% wild type recombinants corresponding to recombinational frequencies of 8-12%. In intra-locus crosses, the recombinational frequencies range from 1% to less than 0.01%. The two loci can also be distinguished by mit- X rho- crosses. Twenty rho- testers have been isolated of which ten preferentially restore mutations in COB 1 and ten others in COB 2. 2. The COB 1 and COB 2 loci have been localized on mitochondrial DNA between the two antibiotic resistance loci OLI 1 and OLI 2 in the order OLI 2-COB 2-COB 1-OLI 1. The results of mit- X mit- and mit- X rho- crosses have also been used to map the cytochrome b mutations relative to each other. The maps obtained by the two independent methods are in good agreement. 3. Mutations in COB 1 have been found to be linked to the OLI1 locus in some but not in other strains of S. cervisiae. This evidence suggests that there may be a spacer region between the two loci whose length varies from strain to strain. 4. Two mutations in COB 2 have been found to cause a loss of a mitochondrial translation product corresponding to the cytochrome b apoprotein. Instead of the wild type protein the mutants have a new low-molecular weight product which is probably a fragment of cytochrome b. The fact that the mutations revert suggests that they are nonsense mutations in the structural gene of cytochrome b.
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