What Triggers Senescence in Podospora anserina?

senescent: A New Neurospora crassa Nuclear Gene Mutant Derived from Nature Exhibits Mitochondrial Abnormalities and a “Death” Phenotype

“…In P. anserina, senescence is inherited maternally (Rizet, 1953;Marcou, 1961) and is associated with the excision of an intron in the mitochondrial gene coding for a subunit of cytochrome oxidase and its accumulation as circular DNA molecules referred to as the senDNA (Jamet-Vierny et al, 1980). Though senescence is always associated with the appearance of senDNA, there is disagreement whether senDNAs are the actual determinants of senescence (Silar et al, 1997;Jamet-Vierny et al, 1999). In the kalilo and the maranhar strains of Neurospora, senescence phenotype is also transmitted maternally.…”

Mitochondrial plasmid-like elements in some hypovirulent strains of Cryphonectria parasitica

“…The role of the senDNAs in the aging process of this fungus is still being debated, but it is accepted now that their appearance and accumulation is a stress response induced by the loss of function in the cytochrome pathway of respiration (Lorin et al, 2006), as deemed to be true also for the plMEs that appear sporadically in respiration defective mitochondrial and nuclear mutants of Neurospora (Hausner et al, 2006a,b). That the plMEs are a consequence rather than a cause of the fungal degenerative mitochondrial syndromes, such as senescence and hypovirulence, is evident from at least three observations: (1) circularized, amplified segments of mtDNAs also occur in non-senescent cultures of Podospora (Jamet-Vierny et al, 1999;Silar et al, 1997;Silliker and Cummings, 1990;Turker et al, 1987a), (2) senescence also occurs in strains that do not produce plMEs (Lorin et al, 2006), and (3) some nuclear mutations affecting cytosolic ribosome functions can abolish the accumulation of senDNAs without preventing senescence (Silar et al, 1997). Similarly, in Ophiostoma, where a cytoplasmically transmissible disease is caused by mitochondrial mycoviruses, transmission of the disease appears to result in the generation and amplification of circular, plasmid-like molecules derived from mtDNA (Charter et al, 1993).…”

“…Sci in the strain designation indicates that the culture was started from a single conidium. synthesis of DNA by reverse transcription of intronic RNAs have been implicated in the generation of such elements in Ophiostoma, Podospora and Neurospora; whereas the amplification of plMEs by reverse transcription of RNAs or the presence of an origin of replication have been invoked to explain their autonomous mode of replication (Abu-Amero et al, 1995;Almasan and Mishra, 1990;Cummings et al, 1985;Gross et al, 1989a,b;Hausner et al, 2006a;Jamet-Vierny et al, 1999;Sethuraman et al, 2008;Turker et al, 1987b).…”

Informational suppressor alleles of the eEF1A gene, fertility and cell degeneration in Podospora anserina

“…The ®lamentous fungus Podospora anserina is a model organisms that is extensively used in ageing studies (Jamet-Vierny et al 1999;Osiewacz and Kimple 1999). We have shown that mutations in AS4, the sole gene that encodes eEF1A in P. anserina drastically increase life span, diminish fertility and permit the propagation of a non-conventional infectious element responsible for a growth alteration called Crippled Growth (Silar and Picard 1994;Silar et al 1999).…”