Mitochondrial genes inPodospora anserina: Recombination and linkage

Belcour, Léon; Begel, Odile

doi:10.1007/bf01035991

Cited by 51 publications

(19 citation statements)

References 20 publications

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“…All of the cytoplasmic mutants observed, whether resistant to erythromycin or to CAP, have a longer generation time than that of the wild type and show a decreased amount of cytochrome oxidase, increased levels of cyanide-insensitive respiration, and a lowered P/O ratio. These results are similar to those obtained with Neurospora (6,10,21) and with a CAPresistant mutant of Podospora (2).…”

supporting

confidence: 81%

Effects of Chloramphenicol on the Mitochondrial Respiratory Chain in the Wild Strain and in a Cytoplasmic Chloramphenicol-Resistant Mutant ofTetrahymena pyriformis

Perasso¹,

Curgy²,

Stelly³

et al. 1982

Mol. Cell. Biol.

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The effects of chloramphenicol (CAP) on mitochondrial respiratory activity in the wild strain (ST) and in a cytoplasmic CAP-resistant mutant (STR1) of Tetrahymena pyriformis were studied by determining oxygen consumption, by spectrophotometry, and by cytochemistry. In the absence of CAP both strains had the same respiration capacity, and the low-temperature spectra of their isolated mitochondria were similar. Furthermore, the mitochondria of both strains showed a positive reaction with diaminobenzidine, denoting a similar cytochrome oxidase activity. However, when cells were grown in CAP for 24 or 48 h, the peaks of cytochrome oxidase and cytochrome b were almost absent in the wild type. In this type the oxygen consumption was greatly decreased, and the mitochondria were no longer stained by diaminobenzidine. In the mutant, the peaks of cytochrome oxidase and cytochrome b were decreased only; respiration was less affected than in the wild type, and cytochrome oxidase activity was still disclosed by the diaminobenzidine reaction. These results show that CAP inhibits the synthesis of two cytochromes (b and oxidase) which are partially translated into the mitochrondria of T. pyriformis. In the mutant, CAP reduces only the mitochondrial translation, resulting in reduced mitochondrial activity and reduced growth rate of the cell. These results are compared with the nucleo-mitochondrial regulation mechanisms discussed in our previous works.The respiratory chain of Tetrahymena pyriformis ST is well known (9,11,22). This chain differs from those of yeasts and higher organisms in many respects (see reference 9 for a review), one of which is the presence of abundant cytochrome a2, which absorbs at 617 nm. A

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supporting

confidence: 81%

Effects of Chloramphenicol on the Mitochondrial Respiratory Chain in the Wild Strain and in a Cytoplasmic Chloramphenicol-Resistant Mutant ofTetrahymena pyriformis

Perasso¹,

Curgy²,

Stelly³

et al. 1982

Mol. Cell. Biol.

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“…This has been shown by experiments carried out in Podospora anserina (214). Mitochondria in this filamentous ascomycete are inherited in a strictly uniparental manner (215,216). However, heteroplasmons may be formed in the contact zone of heterokaryon incompatible strains, in which leakage of paternal mitochondria into the maternal mycelium occurs after transient hyphal fusion.…”

Section: Mtdna Recombination In Agingmentioning

confidence: 88%

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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“…Reverse transcription-PCR (RT-PCR) assays were performed to define the position of the introns and localize the polyadenylation site. Thirty micrograms of total RNA and 50 pM V(T) 34 oligonucleotide (V ϭ G, C, or A) were denatured and annealed. Reverse transcription was performed with 5 units of avian myeloblastosis virus (AMV) reverse transcriptase, 10 mol of each dNTP in 1ϫ AMV buffer at 42°C for 1 h. PCR amplification was carried out in 25 l containing 1% of the cDNA obtained, 50 pM COX5-specific and V(T) 34 primers, 250 M each dNTP, and one unit of Pfu DNA polymerase (Stratagene) for 30 cycles.…”

Section: Methodsmentioning

confidence: 99%

A causal link between respiration and senescence in Podospora anserina

Dufour

Boulay

Rincheval

et al. 2000

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

160

139

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Senescence, a progressive degenerative process leading to agerelated increase in mortality, is found in most eukaryotes. However, the molecular events underlying aging remain largely unknown. Understanding how longevity is regulated is a fundamental problem. Here we demonstrate that the respiratory function is a key factor that contributes to shortening lifespan of the filamentous fungus Podospora anserina. In this organism, senescence is systematically associated with mitochondrial DNA instabilities. We show that inactivation of the nuclear COX5 gene encoding subunit V of the cytochrome c oxidase complex leads to the exclusive use of the alternative respiratory pathway and to a decrease in production of reactive oxygen species. This inactivation results in a striking increase of longevity associated with stabilization of the mitochondrial chromosome. Moreover, accumulation of several senescence-specific mitochondrial DNA molecules is prevented in this nuclear mutant. These findings provide direct evidence of a causal link between mitochondrial metabolism and longevity in Podospora anserina.

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Mitochondrial genes inPodospora anserina: Recombination and linkage

Cited by 51 publications

References 20 publications

Effects of Chloramphenicol on the Mitochondrial Respiratory Chain in the Wild Strain and in a Cytoplasmic Chloramphenicol-Resistant Mutant ofTetrahymena pyriformis

Effects of Chloramphenicol on the Mitochondrial Respiratory Chain in the Wild Strain and in a Cytoplasmic Chloramphenicol-Resistant Mutant ofTetrahymena pyriformis

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

A causal link between respiration and senescence in Podospora anserina

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