Abstract
A mutation designated modD, which was selected on the basis of the suppression of self-lysis, produced a decrease in the density of protoperithecia and a deficiency in ascospore outgrowth at 26.degree. C. Strains carrying the mutation were wild-type at 32.degree. C. Incubation of mutant ascospores revealed 2 abnormalities. The induction of ascospore outgrowth occurred only under a restricted range of conditions. Outgrowth of wild-type spores was normal down to 8.degree. C in a standard germination medium and could also be initiated in a non-germinating medium by the addition of actinomycin D or 5-fluorouracil. Mutant ascospores did not exhibit outgrowth in the presence of these 2 drugs or in a standard germination medium below 20.degree. C. The 2nd defect was the death of 80% of mutant ascospores when they were incubated in germination medium at 26.degree. C. This killing was suppressed by .beta.-phenylpyruvic acid, a protease inhibitor and by a mutation (modC) which suppresses the lytic proteases associated with protoplasmic incompatibility and self-lysis. The killing of mutant spores was also suppressed by cycloheximide but was unaffected by actinomycin D and 5-fluorouracil.