Stability of the Mitochondrial Genome of Podospora anserina and Its Genetic Control

Belcour, Léon; Sainsard-Chanet, Annie; Jamet‐Vierny, Còrinne; Picard, Marguerite

doi:10.1007/978-3-642-59884-5_16

Cited by 12 publications

(10 citation statements)

References 79 publications

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“…An analysis of the mtDNA content of the senescent revertant cultures revealed the presence of mtDNA rearrangements called senDNAs as in senescent wildtype cultures (Belcour et al 1999;Albert and Sellem 2002). However, in contrast to the wild-type strain in which senDNAa is systematically observed in a large amount, the senDNAs in the revertants originated mainly from the g region as previously shown in other mutants (Lorin et al 2001; Figure S3).…”

Section: Resultssupporting

confidence: 61%

Mutations in Two Zinc-Cluster Proteins Activate Alternative Respiratory and Gluconeogenic Pathways and Restore Senescence in Long-Lived Respiratory Mutants ofPodospora anserina

et al. 2009

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In Podospora anserina, inactivation of the respiratory chain results in a spectacular life-span extension. This inactivation is accompanied by the induction of the alternative oxidase. Although the functional value of this response is evident, the mechanism behind it is far from understood. By screening suppressors able to reduce the life-span extension of cytochrome-deficient mutants, we identified mutations in two zinc-cluster proteins, RSE2 and RSE3, which are conserved in other ascomycetes. These mutations led to the overexpression of the genes encoding the alternative oxidase and the gluconeogenic enzymes, fructose-1, 6 biphosphatase, and pyruvate carboxykinase. Both RSE2 and RSE3 are required for the expression of these genes. We also show that, even in the absence of a respiratory deficiency, the wild-type RSE2 and RSE3 transcription factors are involved in life-span control and their inactivation retards aging. These data are discussed with respect to aging, the regulation of the alternative oxidase, and carbon metabolism.

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Section: Resultssupporting

confidence: 61%

Mutations in Two Zinc-Cluster Proteins Activate Alternative Respiratory and Gluconeogenic Pathways and Restore Senescence in Long-Lived Respiratory Mutants ofPodospora anserina

et al. 2009

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“…Large amounts of senDNAa are systematically observed in senescent wild-type cultures (see Belcour et al 1999 for review). In marked contrast to this situation, in the dying PaAnt M106P rmp1-1 and PaAnt A121P rmp1-1 cultures ( Figure 2B), as in the dying PaAnt S296M rmp1-1 and rmp1-2 cultures (Figure 3), death is not associated with the accumulation of senDNAa.…”

Section: A121pmentioning

confidence: 99%

“…In this organism, life span is a reflection of mtDNA stability, and death is always associated with large mtDNA rearrangements. ''Natural death'' or aging is accompanied by large-scale reorganizations of the mtDNA whereas a nuclear-controlled premature death syndrome is accompanied by the accumulation of site-specific mtDNA deletions (Belcour et al 1999;Silar et al 2001 for reviews). P. anserina therefore occupies an interesting position among model systems for studying the cellular consequences of mutations in the ADP/ATP translocase gene.…”

mentioning

confidence: 99%

Suppression of Mitochondrial DNA Instability of Autosomal Dominant Forms of Progressive External Ophthalmoplegia-AssociatedANT1Mutations inPodospora anserina

El-Khoury

Sainsard-Chanet

2009

Genetics

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Maintenance and expression of mitochondrial DNA (mtDNA) are essential for the cell and the organism. In humans, several mutations in the adenine nucleotide translocase gene ANT1 are associated with multiple mtDNA deletions and autosomal dominant forms of progressive external ophthalmoplegia (adPEO). The mechanisms underlying the mtDNA instability are still obscure. A current hypothesis proposes that these pathogenic mutations primarily uncouple the mitochondrial inner membrane, which secondarily causes mtDNA instability. Here we show that the three adPEO-associated mutations equivalent to A114P, L98P, and V289M introduced into the Podospora anserina ANT1 ortholog dominantly cause severe growth defects, decreased reactive oxygen species production (ROS), decreased mitochondrial inner membrane potential (Dc), and accumulation of large-scale mtDNA deletions leading to premature death. Interestingly, we show that, at least for the adPEO-type M106P and A121P mutant alleles, the associated mtDNA instability cannot be attributed only to a reduced membrane potential or to an increased ROS level since it can be suppressed without restoration of the Dc or modification of the ROS production. Suppression of mtDNA instability due to the M106P and A121P mutations was obtained by an allele of the rmp1 gene involved in nucleo-mitochondrial cross-talk and also by an allele of the AS1 gene encoding a cytosolic ribosomal protein.In contrast, the mtDNA instability caused by the S296M mutation was not suppressed by these alleles.

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“…A number of distinct deletions with different 3Ј ends can accumulate in AS1-4 strains (41). It is the case for C (lane pair 7), in which the HaeIII fragment 2 is still present and hybridization reveals a 980-bp junction fragment as in ⌬5 (41) ectopic copy of mthmg1 (long life) and screened for phleomycin-resistant transformants which have recovered a premature death phenotype (life span of about 2 cm). Eight transformants were finally recovered, displaying the expected phenotype and DNA structure.…”

Section: Downloaded Frommentioning

confidence: 99%

Two Copies of mthmg1 , Encoding a Novel Mitochondrial HMG-Like Protein, Delay Accumulation of Mitochondrial DNA Deletions in Podospora anserina

Dequard-Chablat

Alland

2002

Eukaryot Cell

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In the filamentous fungus Podospora anserina, two degenerative processes which result in growth arrest are associated with mitochondrial genome (mitochondrial DNA [mtDNA]) instability. Senescence is correlated with mtDNA rearrangements and amplification of specific regions (senDNAs). Premature death syndrome is characterized by the accumulation of specific mtDNA deletions. This accumulation is due to indirect effects of the AS1-4 mutation, which alters a cytosolic ribosomal protein gene. The mthmg1 gene has been identified as a double-copy suppressor of premature death. It greatly delays premature death and the accumulation of deletions when it is present in two copies in an AS1-4 context. The duplication of mthmg1 has no significant effect on the wild-type life span or on senDNA patterns. In an AS1؉ context, deletion of the mthmg1 gene alters germination, growth, and fertility and reduces the life span. The ⌬mthmg1 senescent strains display a particular senDNA pattern. This deletion is lethal in an AS1-4 context. According to its physical properties (very basic protein with putative mitochondrial targeting sequence and HMG-type DNA-binding domains) and the cellular localization of an mtHMG1-green fluorescent protein fusion, mtHMG1 appears to be a mitochondrial protein possibly associated with mtDNA. It is noteworthy that it is the first example of a protein combining the two DNA-binding domains, AT-hook motif and HMG-1 boxes. It may be involved in the stability and/or transmission of the mitochondrial genome. To date, no structural homologues have been found in other organisms. However, mtHMG1 displays functional similarities with the Saccharomyces cerevisiae mitochondrial HMG-box protein Abf2.

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Stability of the Mitochondrial Genome of Podospora anserina and Its Genetic Control

Cited by 12 publications

References 79 publications

Mutations in Two Zinc-Cluster Proteins Activate Alternative Respiratory and Gluconeogenic Pathways and Restore Senescence in Long-Lived Respiratory Mutants ofPodospora anserina

Mutations in Two Zinc-Cluster Proteins Activate Alternative Respiratory and Gluconeogenic Pathways and Restore Senescence in Long-Lived Respiratory Mutants ofPodospora anserina

Suppression of Mitochondrial DNA Instability of Autosomal Dominant Forms of Progressive External Ophthalmoplegia-AssociatedANT1Mutations inPodospora anserina

Two Copies of mthmg1 , Encoding a Novel Mitochondrial HMG-Like Protein, Delay Accumulation of Mitochondrial DNA Deletions in Podospora anserina

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