Excision sequences in the mitochondrial genome of yeast

Zamaroczy, Miklos de; Faugeron-Fonty, Godeleine; Bernardi, Giorgio

doi:10.1016/0378-1119(83)90002-1

Cited by 86 publications

(42 citation statements)

References 28 publications

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“…Subgenomic recombinations also take place at short and direct sequence repeats, a pattern consistent with the involvement of a recombination-excision mechanism. These events underlie the frequent generation of respiration-deficient petite mutants in S. cerevisiae, which stably transmits the extensively deleted Ϫ genomes (41)(42)(43). Similar repeat-mediated recombination events were seen in Neurospora crassa, which are manifested by the generation of plasmid-like supercoiled subgenomic circles in mitochondria (44).…”

Section: Mtdna Recombination In Yeastmentioning

confidence: 86%

Mechanism of Homologous Recombination and Implications for Aging-Related Deletions in Mitochondrial DNA

Chen

2013

Microbiol Mol Biol Rev

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SUMMARY Homologous recombination is a universal process, conserved from bacteriophage to human, which is important for the repair of double-strand DNA breaks. Recombination in mitochondrial DNA (mtDNA) was documented more than 4 decades ago, but the underlying molecular mechanism has remained elusive. Recent studies have revealed the presence of a Rad52-type recombination system of bacteriophage origin in mitochondria, which operates by a single-strand annealing mechanism independent of the canonical RecA/Rad51-type recombinases. Increasing evidence supports the notion that, like in bacteriophages, mtDNA inheritance is a coordinated interplay between recombination, repair, and replication. These findings could have profound implications for understanding the mechanism of mtDNA inheritance and the generation of mtDNA deletions in aging cells.

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Section: Mtdna Recombination In Yeastmentioning

confidence: 86%

Mechanism of Homologous Recombination and Implications for Aging-Related Deletions in Mitochondrial DNA

Chen

2013

Microbiol Mol Biol Rev

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“…3). Direct repeats are also found at the sites of deletions in mtDNA in different situations, as petite mutations in yeast (36) or deletions associated with human diseases (3,4,37). However, in the case of the premature death syndrome in Podospora, the sequence similarity observed between the direct repeats (11- (41,42).…”

Section: Discussionmentioning

confidence: 99%

A site-specific deletion in mitochondrial DNA of Podospora is under the control of nuclear genes.

Belcour

Begel

Picard

1991

Proc. Natl. Acad. Sci. U.S.A.

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In the filamentous fungus Podospora anserina, the association of two nuclear genes inevitably leads to a "premature death" phenotype consisting of an early end of vegetative growth a few days after ascospore germination. Mycelia showing this phenotype contain a mitochondrial chromosome that always bears the same deletion. One of the break points is exactly at the 5' splice site of a particular mitochondrial intron, suggesting that the deletion event could result from molecular mechanisms also involved in intron mobility.One of the nuclear genes involved in triggering this site-specific event belongs to the mating-type minus haplotype; the other is a mutant allele of a gene encoding a cytosolic ribosomal protein.In obligate aerobes, rearrangements of mitochondrial DNA (mtDNA) are responsible for various deleterious symptoms, such as maternally inherited male sterility in plants (1), several mycelial degenerative phenomena in fungi (2), and, as described more recently in humans, numerous neuromuscular (3) or hematological (4) diseases. In some cases, nuclear genes have been shown to control the mtDNA rearrangements (5, 6). The molecular mechanisms producing these rearrangements and the role played by nuclear-encoded proteins remain unclear in all cases.In the filamentous fungus Podospora anserina, vegetative growth is limited by a maternally inherited syndrome, called senescence, ending in cessation of mycelial elongation and apical cell death (7,8). In this species, senescence is clearly associated with mtDNA rearrangements and most probably is caused by them. More precisely, it has been shown that short mtDNA sequences are amplified as circular multimeric DNA molecules in senescent cultures (9)(10)(11)(12)(13)(14). It was shown that the most frequently amplified sequence corresponds exactly to a mitochondrial intron (15), intron a, and that most of the mutations allowing mycelia to escape senescence are rearrangements in intron a (12,(16)(17)(18). It has been known for a long time (19) that the nuclear genome controls the life-span of the fungus. For instance, the life-span of our reference strains differs according to their mating type: the process of senescence is delayed in mat+ strains compared with matones. However the differences, although significant, are not striking (see Table 1). Moreover the functions encoded by these genes are still unknown.The work presented here follows the observation that, in Podospora, mutations in several genes involved in the control of translational accuracy have an effect on the life-span (A. Raynal, personal communication; Table 1). As a first step, we focused our attention on the AS1-4 mutation. This particular allele confers a very long life-span to mat+ mycelia, while, when associated with mat-, it leads systematically to the premature death phenotype, consisting of an early end of mycelial growth a few days after ascospore germination.We showed that mycelia presenting this phenotype were in all cases heteroplasmic and that they systematically contained the same ...

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“…5). Excisions from the p+ genome often occur in such short 100% A+T regions (17). The position of the S4 and S5 sequences within the 963 bp of HS3324 DNA and the regions essential for ARS activity in an E. coli-yeast plasmid are shown in Fig.…”

Section: Methodsmentioning

confidence: 99%

Yeast mitochondrial genomes consisting of only A.T base pairs replicate and exhibit suppressiveness.

Fangman¹,

Dujon²

1984

Proc. Natl. Acad. Sci. U.S.A.

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Mutants, called p-, that result from extensive deletions of the 75-kilobase Saccharomyces cerevisiae mitochondrial genome arise at high frequency. The remaining mitochondrial DNA is amplified in the p-cells, often as headto-tail multimers, producing a cell with the normal amount of mitochondrial DNA. In matings, some of these p-mutants exhibit zygotic hypersuppressiveness, excluding the wild-type mitochondrial genome (p+) from all the diploids that are produced. From a hypersuppressive p-strain, we isolated two mutants with reduced suppressiveness. These mutants, one moderately suppressive and one nonsuppressive, retain only 89 and 70 base pairs, respectively, of the wild-type mitochondrial genome. Their sequences consist of 100% A-T base pairs. Replication of DNA in the mitochondrion, formation and amplification of new deletion genomes, and exhibition of suppressiveness do not require a single G C base pair.

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Excision sequences in the mitochondrial genome of yeast

Cited by 86 publications

References 28 publications

Mechanism of Homologous Recombination and Implications for Aging-Related Deletions in Mitochondrial DNA

Mechanism of Homologous Recombination and Implications for Aging-Related Deletions in Mitochondrial DNA

A site-specific deletion in mitochondrial DNA of Podospora is under the control of nuclear genes.

Yeast mitochondrial genomes consisting of only A.T base pairs replicate and exhibit suppressiveness.

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