Does Senescence in Podospora anserina Result from Instability of the Mitochondrial Genome?

Abstract

There has been remarkable progress over the last few years in the knowledge of the organization and functions of mitochondrial genomes in organisms ranging from yeast to human cells. In this paper we propose an additional function for mtDNA: a role in the control of life span, at least for obligate aerobes.

In the filamentous fungus Podospora anserina, genetic, physiological, and biochemical data gathered over the years have shown that the senescent state is correlated with modifications of the mitochondria. It has thus been suggested that senescence results from suppressive mitochondrial mutations (Belcour and Begel 1978). We present here new data on several mitochondrial mutations whose properties and effects on senescence and life span support this hypothesis.

MITOCHONDRIAL CHANGES IN SENESCENT CULTURES
In P. anserina, senescence and subsequent arrest of growth unavoidably occur when mycelia are maintained in continuous vegetative growth (Rizet 1953). Senescence is under cytoplasmic control and is infectious through anastomoses (Rizet 1957; Marcou 1961). Senescence is determined by the random appearance of a cytoplasmic factor but is expressed long after this event; during this incubation period the concentration of the cytoplasmic factor increases exponentially (Marcou 1961; Smith and Rubenstein 1973).

Physiological evidence indicates the involvement of mitochondria in senescence. The cytochrome-aa₃ content gradually decreases as the mycelium approaches arrest of growth (Belcour and Begel 1978; Cummings et al. 1979). Inhibitors of mitochondrial functions, such as chloramphenicol and ethidium bromide, prolong the life span of mycelia and furthermore can rejuvenate senescent mycelia (Tudzynski and Esser 1979; Belcour and...