A mutation designated , which was selected on the basis of the suppression of selflysis, produced a decrease in the density of protoperithecia and a deficiency in ascospore outgrowth at 26 °. Strains carrying the mutation were wild-type at 32°. Incubation of mutant ascospores revealed two abnormalities. First, the induction of ascospore outgrowth occurred only under a restricted range of conditions. Outgrowth of wild-type spores was normal down to 8 ° 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 two drugs or in a standard germination medium below 20 °. The second defect was the death of 80% of mutant ascospores when they were incubated in germination medium at 26 °. This killing was suppressed by β-phenylpyruvic acid, a protease inhibitor, and by a mutation () 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.


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