The intraspecific variability of mitochondrial genes of Agaricus bisporus reveals an extensive group I intron mobility combined with low nucleotide substitution rates.

Intraspecific mitochondrial variability was studied in ten strains of A. bisporus var. bisporus, in a strain representative of A. bisporus var. eurotetrasporus and in a strain of the closely related species Agaricus devoniensis. In A. bisporus, the cox1 gene is the richest in group I introns harboring homing endonuclease genes (heg). This study led to identify group I introns as the main source of cox1 gene polymorphism. Among the studied introns, two groups were distinguished according to the heg they contained. One group harbored heg maintained putatively functional. The other group was composed of eroded heg sequences that appeared to evolve toward their elimination. Low nucleotide substitution rates were found in both types of intronic sequences. This feature was also shared by all types of studied mitochondrial sequences, not only intronic but also genic and intergenic ones, when compared with nuclear sequences. Hence, the intraspecific evolution of A. bisporus mitochondrial genome appears characterized by both an important mobility (presence/absence) of large group I introns and by low nt substitution rates. This stringent conservation of mitochondrial sequences, when compared with their nuclear counterparts, appears irrespective of their apparent functionality and contrasts to what is widely accepted in fungal sequence evolution. This strengthens the usefulness of mtDNA sequences to get clues on intraspecific evolution.

The life cycle of the smut fungus Moesziomyces penicillariae is adapted to the short-cycle of the host, Pennisetum glaucum.

Moesziomyces penicillariae (Brefield) Vànky is a basidiomycete fungus responsible for smut disease on pearl millet, an important staple food in the sub-Sahelian zone. We revisited the life cycle of this fungus. Unlike other Ustilaginales, mating of sporidia was never observed and monoclonal cultures of monokaryotic sporidia were infectious in the absence of mating with compatible partner. These data argued for an atypical monokaryotic diploid cell cycle of M. penicillariae, where teliospores only form solopathogenic sporidia. After inoculation of monoclonal solopathogenic strains on spikelets, the fungus infects the ovaries and induces the folding of the micropilar lips, as observed during early pollination steps. The infected embryo then becomes disorganized and the fungus invades peripheral ovary tissues before sporulating. We evaluated the systemic growth abilities of the fungus. After root inoculation, mycelium was observed around and inside the roots. As argued by transmission electron microscopy (TEM) observations and polymerase chain reaction (PCR) detection using specific primers for M. penicillariae, the fungus can grow from roots to the caulinar meristems. In spite of this systemic growth, no sori were formed on the varieties of pearl millet tested after root inoculation. All together, these data suggest that the reduced life cycle of M. penicillariae--i.e. dispersal of 'ready to infect' solopathogenic sporidia, floral infection--is an adaptation to the aetiology of this disease to short-cycle pearl millet varieties from the sub-Sahel.