Citations: 1-3
<1>
Authors
Jamet-Vierny C. Rossignol M. Haedens V. Silar P.
Institution
Institut de Genetique et Microbiologie, URA 2225, Universite de Paris Sud,
Orsay cedex, 91405, France.
Title
What triggers senescence in Podospora
anserina?.
Source
Fungal Genetics & Biology. 27(1):26-35, 1999 Jun.
Abstract
Senescence of Podospora anserina is
triggered by a cytoplasmic and infectious factor (the determinant of
senescence) and is always correlated with mitochondrial DNA modifications,
especially with the accumulation of small circular subgenomic DNA molecules,
the senDNAs. Several observations have suggested that the senDNAs could be
the cytoplasmic and infectious determinant. However, we show here (1) that
senDNA molecules can be transferred to a young culture without the
cotransmission of the determinant of senescence and (2) that the determinant
of senescence does not segregate as a mitochondrial DNA mutation. Overall,
our data strongly argue that amplification of senDNA molecules in the
mitochondria is not an intrinsic property of these small DNA molecules. They
question the nature of the actual determinant of senescence. Copyright 1999
Academic Press.
<2>
Authors
Esser K. Tudzynski P.
Title
Prevention of senescence in the ascomycete Podospora
anserina by the antibiotic tiamulin.
Source
Nature. 265(5593):454-6, 1977 Feb 3.
<3>
Authors
Esser K. Keller W.
Title
Genes inhibiting senescence in the ascomycete Podospora
anserina.
Source
Molecular & General Genetics. 144(1):107-10, 1976 Feb 27.
Abstract
Senescence occurs in all wild strains of Podospora
anserina after continued growth. This syndrome can be
inhibited by a synergistic interaction of two linked genes, incoloris and
vivax. Whereas the wild strain starts to become senescent after 26 d and the
mutants incoloris and vivax after 42 and 66 d respectively, the double mutant
shows no signs of aging after culture for more than one year.
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