SummaryViruses are common in asexual Aspergilli but not in sexual Aspergilli. We found no viruses in 112 isolates of the sexual Aspergillus nidulans. We have investigated factors that could play a role in preventing the spread of mycoviruses through populations of A. nidulans. Experiments were performed with A. nidulans strains infected with viruses originating from A. niger. Horizontal virus transmission was restricted but not prevented by somatic incompatibility. Viruses were transmitted vertically via conidiospores but not via ascospores. Competition experiments revealed no effect of virus infection on host fitness. Outcrossing was found to limit the spread of viruses significantly more than selfing. It is concluded that the exclusion of viruses from sexual Aspergilli could be due to the formation of new somatic incompatibility groups by sexual recombination.
The imperfect ascomycetous yeasts Candida parapsilosis and Arxula adeninivorans degraded 3-hydroxybenzoic acid via gentisate which was the cleavage substrate. 4-Hydroxybenzoic acid was metabolized via protocatechuate. No cleavage enzyme for the latter was detected. In stead of this NADH- and NADPH-dependent monooxygenases were present. In cells grown at the expense of hydroquinone and 4-hydroxybenzoic acid, enzymes of the hydroxyhydroquinone variant of the 3-oxoadipate pathway were demonstrated, which also took part in the degradation of 2,4-dihydroxybenzoic acid by C. parapsilosis.
We have observed partial heterokaryon-incompatibility reactions in combinations of field isolates of A. nidulans. We have demonstrated that partial heterokaryon incompatibility is genetically controlled by genes (partial-het genes) operating in the same manner as the previously-described het genes. Our results also reveal that partial-het genes can act additively in causing heterokaryon incompatibility and that partial heterokaryon incompatibility is not a barrier to the horizontal transfer of a mitochondrial marker. These results add to the growing body of evidence that vegetative-incompatibility reactions are not an absolute barrier to horizontal gene flow.
Mitochondrial chloramphenicol and oligomycin resistance mutations were used to investigate mitochondrial inheritance in A. nidulans. Mitochondrial RFLPs could not be used to distinguish between paternal and maternal mitochondria because none were detected in the 54 isolates investigated. Several thousand ascospores from each of 111 hybrid cleistothecia from 21 different crosses between 7 heterokaryon incompatible isolates were tested for biparental inheritance. All mitochondrial inheritance was strictly uniparental. Not one instance of paternal inheritance of mitochondria was observed. The implications of our results for the theory that uniparental inheritance evolved to avoid cytoplasmic conflict are discussed. Possible explanations for the maintenance of strict uniparental inheritance of mitochondria in an inbreeding homothallic organism are suggested. The chloramphenicol resistance marker was inherited preferentially to the oligomycin resistance marker probably due to the inhibited energy production of mitochondria with the oligomycin resistance mutation. The maternal parent was determined for 93 hybrid cleistothecia from 17 crosses between 7 different strains. Contrary to previous reports A. nidulans strains functioned as both maternal and paternal parent in most crosses.
Successful intra- and interspecific mitochondrial transfers were performed by polyethylene glycol (PEG)-induced protoplast fusion among incompatible strains belonging to the Aspergillus niger species aggregate. The mitochondrial DNAs (mtDNAs) of the strains examined were of three main types based on their restriction fragment length polymorphism (RFLP) profiles. mtDNA types 1 and 2 correspond to A. niger and A. tubingensis species, respectively, while type 3 is represented by some Brazilian wild-type isolates (possibly a distinct species or subspecies). mtDNA types 1 and 2 could be further divided into several subgroups (1a-1e and 2a-2f). All these strains, representing different RFLP groups or subgroups, were fully incompatible with respect to nuclear complementation. The transfer experiments were carried out under selection pressure, using a mitochondrial oligomycin-resistant mutant of mtDNA type 1a as donor. Following fusion mitochondrial oligomycin-resistant progenies were recovered in the presence of oligomycin by selecting for the nuclear phenotypes of the oligomycin-sensitive recipient strains. All attempted transfers were successful, and resulted in different varieties of resistant recombinant mitochondrial progenies at various frequencies. Within the group of strains of mtDNA type 1, the transfer of oligomycin-resistant mitochondria resulted in the appearance of a single recombinant type of RFLP profile in each case. The recombination events were more complex when the transfer of oligomycin resistance occurred between strains representing different species (mtDNA groups 1a-->2 and 1a-->3). A great variety of recombinant mtDNA RFLP profiles appeared. Explanation for this phenomenon are discussed on the basis of preliminary physical mapping data.
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