The mitochondrial plasmid of Podospora anserina: A mobile intron of a mitochondrial gene

Osiewacz, Heinz D.; Esser, Karl

doi:10.1007/bf00419728

Cited by 200 publications

(64 citation statements)

References 23 publications

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“…These findings strongly suggest that genetic exchange be-tween mitochondria and nuclei has occurred continuously during evolution. The exciting possibility of transfer of mitochondrial DNA sequences into the nuclear genome during the life-cycle of the fungus, Podospora anserina, and its possible role in senescence [78,79] are presently not proven [80].…”

Section: Hypothesismentioning

confidence: 99%

Do mitochondrial DNA fragments promote cancer and aging?

Richter

1988

FEBS Letters

211

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Reactive oxygen species are important in carcinogenesis, diseases, and aging, probably through oxidative damage of DNA. Our understanding of this relationship at the molecular level is very sketchy. It has recently been found that in mitochondria oxidative DNA damage is particularly high and may not be repaired efficiently. I propose that oxidatively generated DNA fragments escape from mitochondria and become integrated into the nuclear genome. This may transform cells to a cancerous state. Time‐dependent nuclear accumulation of mitochondrial DNA fragments may progressively change the nuclear information content and thereby cause aging. This proposal can be tested experimentally.

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Section: Hypothesismentioning

confidence: 99%

Do mitochondrial DNA fragments promote cancer and aging?

Richter

1988

FEBS Letters

211

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“…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.…”

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 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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“…First, ablation of mitochondrial fission in two fungal systems led to a considerable increase in lifespan and not, as one might have expected, to a reduction in lifespan [65]. Second, clonal expansion of mtDNA alterations in fungi and humans during aging or during the pathogenesis of certain mitochondriopathies is a widely observed phenomenon that is not well understood [3,[66][67][68][69][70][71][72][73][74][75][76][77]. Mitochondrial content mixing might well promote clonal expansion of mutated mtDNA molecules and thus has potentially rather harmful consequences.…”

Section: Mitochondrial Hyperfusion Helps To Ensure Mitochondrial Qualmentioning

confidence: 99%

Quality control of mitochondria during aging: Is there a good and a bad side of mitochondrial dynamics?

2013

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Maintenance of functional mitochondria is essential in order to prevent degenerative processes leading to disease and aging. Mitochondrial dynamics plays a crucial role in ensuring mitochondrial quality but may also generate and spread molecular damage through a population of mitochondria. Computational simulations suggest that this dynamics is advantageous when mitochondria are not or only marginally damaged. In contrast, at a higher degree of damage, mitochondrial dynamics may be disadvantageous. Deceleration of fusion‐fission cycles could be one way to adapt to this situation and to delay a further decline in mitochondrial quality. However, this adaptive response makes the mitochondrial network more vulnerable to additional molecular damage. The “mitochondrial infectious damage adaptation” (MIDA) model explains a number of inconsistent and counterintuitive data such as the “clonal expansion” of mutant mitochondrial DNA. We propose that mitochondrial dynamics is a double‐edged sword and suggest ways to test this experimentally.

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The mitochondrial plasmid of Podospora anserina: A mobile intron of a mitochondrial gene

Cited by 200 publications

References 23 publications

Do mitochondrial DNA fragments promote cancer and aging?

Do mitochondrial DNA fragments promote cancer and aging?

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

Quality control of mitochondria during aging: Is there a good and a bad side of mitochondrial dynamics?

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