Mitochondrial DNA from Podospora anserina

Cummings, Donald J.; Belcour, Léon; Grandchamp, Claude

doi:10.1007/bf00267578

Cited by 149 publications

(23 citation statements)

References 27 publications

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“…Preparation, purification, cloning, restriction analyses, and DNADNA hybridization of mtDNA were done by standard methods as described (9,16,18 …”

Section: Methodsmentioning

confidence: 99%

“…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).…”

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confidence: 99%

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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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“…Preparation, purification, cloning, restriction analyses, and DNADNA hybridization of mtDNA were done by standard methods as described (9,16,18 …”

Section: Methodsmentioning

confidence: 99%

mentioning

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 all cases, the activity of mobile genetic elements of circular or linear structure were found to be relevant. More specifically, in P. anserina, it appears that the mobility of a circular plasmid, termed plasmid-like DNA (plDNA) or ␣senDNA (19,20), which is a derivative of the first intron of the cytochrome oxidase gene subunit I (COI), is responsible for the prominent age-related mtDNA rearrangements (21-23).Because of experimental difficulties in the cloning of relevant nuclear genes, very little is known about the role these nuclear traits play in the control of senescence. In particular, the molecular interactions between age-related nuclear genes and mitochondrial genetic traits are unclear.…”

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confidence: 99%

Mitochondrial DNA rearrangements of Podospora anserina are under the control of the nuclear gene grisea

Borghouts

Kimpel²,

Osiewacz³

1997

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

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Podospora anserina is a filamentous fungus with a limited life span. Life span is controlled by nuclear and extranuclear genetic traits. Herein we report the nature of four alterations in the nuclear gene grisea that lead to an altered morphology, a defect in the formation of female gametangia, and an increased life span. Three sequence changes are located in the 5 upstream region of the grisea ORF. One mutation is a G 3 A transition at the 5 splice site of the single intron of the gene, leading to a RNA splicing defect. This loss-of-function affects the amplification of the first intron of the mitochondrial cytochrome c oxidase subunit I gene (COI) and the specific mitochondrial DNA rearrangements that occur during senescence of wild-type strains. Our results indicate that the nuclear gene grisea is part of a molecular machinery involved in the control of mitochondrial DNA reorganizations. These DNA instabilities accelerate but are not a prerequisite for the aging of P. anserina cultures.Aging of biological systems, as the progressive functional impairment of living beings leading to an increase in agerelated mortality, is a complex process that is dependent on both environmental and genetic factors. With regard to the genetic basis, instabilities of the mitochondrial DNA (mtDNA) were reported in various organisms to be involved in aging leading to mitochondrial dysfunction and degeneration (for reviews, see refs. 1 and 2). Moreover, increased instabilities of the mtDNA were found to lead to premature degeneration processes. Examples of this type are premature death syndromes in fungi and various neuromuscular diseases in humans (for reviews, see refs. 3-5). Interestingly, in some cases, these syndromes are due to the mutation of a nuclear gene that demonstrate that the integrity of the mtDNA is under the control of nuclear factors (6-10). Unfortunately, until now, the molecular mechanisms involved in this maintenance function have not been elucidated in any case.In the filamentous fungus Podospora anserina, all wildstrains are characterized by a limited life span. After prolonged vegetative growth, they display various symptoms of senescence. Since the first description of this syndrome (11), it has become clear that nuclear-mitochondrial interactions are crucially involved in its control (for reviews, see refs. 12-15). Detailed molecular investigations revealed that gross reorganizations of the mtDNA occur during senescence. These reorganizations are almost quantitative and lead to impairment of the energy-generating system located in mitochondria. Similar processes were subsequently reported to occur in senescing strains of Neurospora (16)(17)(18). In all cases, the activity of mobile genetic elements of circular or linear structure were found to be relevant. More specifically, in P. anserina, it appears that the mobility of a circular plasmid, termed plasmid-like DNA (plDNA) or ␣senDNA (19,20), which is a derivative of the first intron of the cytochrome oxidase gene subunit I (COI), is responsible f...

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“…The P. anserina strains used in this study were routinely grown in corn meal agar race tubes at 27°C as described previously (3). To induce senescence, mycelial plugs were placed in new race tubes and then incubated at 34°C.…”

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confidence: 99%

“…Restriction enzyme analysis was performed as described previously (5). DNA-DNA hybridization was done by the method of Southern (18) as modified by Wright et al (28).…”

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confidence: 99%

A Podospora anserina longevity mutant with a temperature-sensitive phenotype for senescence.

Turker¹,

Nelson²,

Cummings³

1987

Mol. Cell. Biol.

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A Podospora anserina longevity mutant was identified with a temperature-sensitive phenotype for senescence. This mutant, termed TS1, grew for over 3 m at 27°C, but when shifted to 34°C, it underwent senescence between 10 and 18 cm. A previously described senescence-associated plasmid, a senDNA, derived from the mitochondrial genome, was not detected in TS1 at 27°C but was present in senescent cultures at 34°C. A similar result was observed in progeny strains obtained by crossing the TS1 mutant with a wild-type strain. Other mitochondrial excision-amplification DNAs in addition to a senDNA were also observed in the senescent cultures. Most were derived from a specific region of the mitochondrial genome. These results provide evidence that asenDNA is involved in TS1 senescence and suggest that this plasmid may play a role in the formation of other mitochondrial excision-amplification plasmids.

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Mitochondrial DNA from Podospora anserina

Cited by 149 publications

References 27 publications

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

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

Mitochondrial DNA rearrangements of Podospora anserina are under the control of the nuclear gene grisea

A Podospora anserina longevity mutant with a temperature-sensitive phenotype for senescence.

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