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Mutagenesis and Repair in Yeast Mitochondrial DNA

  • Chapter
Molecular and Cellular Mechanisms of Mutagenesis

Summary

The mitochondrial DNA (mtDNA) is a dispensable genome in the facultative aerobe Saccharomyces cerevisiae, Since cell viability is maintained even if mtDNA is nonfunctional, mitochondrial mutagenesis can be studied. Marked dissimilarities exist between nuclear and mtDNA with respect to base composition, structure, multiplicity, and heterogeneity of molecules; differences in mutagenic processes are consequently expected. Mitochondrial mutants belong to two classes that both exhibit non-Mendelian inheritance; the rho − (or “petite” mutation) results from massive deletions with a preferential loss of a specific segment, accompanied by repetitions of retained sequences; the other type is due to point mutations or small deletions and includes antibiotic resistant mutants and mutants defective in the synthesis of one or more components of the mitochondrial membrane complex (mit−) or in the mitochondrial protein machinery (syn−). The rho− mutation is extremely frequent even spontaneously (from 1 to a few percent), whereas mitochondrial point mutations are relatively rare even with induced mutagenesis. Nuclear mutations due to molecular modifications similar to those seen in rho− are rather infrequent. The genetic control of mitochondrial mutagenesis requires gene products involved either (1) in both nuclear and mitochondrial mutagenesis, the genes being located in the nucleus; or (2) specifically in mitochondrial mutagenic processes, the genes being located either in the nuclear or in the mitochondrial genomes.

Since the frequency of rho − mutants and the loss of mitochondrial genetic markers by ultraviolet light can be modulated according to growth phases, the genetic background (rad, uvsρ, gam genes, etc.), dark holding in presence or absence of protein synthesis inhibitors, etc., it was hypothesized that mtDNA-induced lesions could be repaired in certain conditions. Indeed, pyrimidine dimers in mtDNA can be photoreactivated but not removed in a controlled process, as in the nucleus, by excision repair. When growing cells are UV-treated, a degradation of the mtDNA is observed and this is accompanied by a reduction in size of mtDNA parental molecules. However, this is followed upon transfer in growth medium by restitution of high molecular weight mtDNA molecules. Consequently, it is proposed that the recovery of the rho + phenotype is due to a nonexcision dark repair process possibly depending upon replication and/or recombination acting on damaged mtDNA.

The comparative susceptibility of the nuclear and mitochondrial genomes to different families of chemicals will be presented.

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Authors and Affiliations

  1. Institut Curie-Biologie, Centre Universitaire, Bâtiment 110, 91405, Orsay, France

    E. Moustacchi & M. Heude

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  1. E. Moustacchi
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  2. M. Heude
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  1. Oak Ridge National Laboratory, Oak Ridge, Tennessee, USA

    J. F. Lemontt  & W. M. Generoso  & 

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© 1982 Plenum Press, New York

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Moustacchi, E., Heude, M. (1982). Mutagenesis and Repair in Yeast Mitochondrial DNA. In: Lemontt, J.F., Generoso, W.M. (eds) Molecular and Cellular Mechanisms of Mutagenesis. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-3476-7_19

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  • DOI: https://doi.org/10.1007/978-1-4613-3476-7_19

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