A mutation (modD) was selected in a gene involved in the control of protoplasmic incompatibility. Previous results (Labarere and Bernet 1979) showed that modD decreased the density of protoperithecia and caused a defect in ascospore germination. In addition, modD has a third defect: when modD stationary cells were isolated in order to obtain further development, renewal of growth rarely ensued. Instead, the modD cells lysed or produced microthalli from which normal growth never occurred. These defects were suppressed by β-phenyl pyruvic acid, a protease inhibitor, and by the presence of a mutation (modC) that suppresses the proteases associated with protoplasmic incompatibility. The stationary wild-type cells' regeneration was inhibited by β-phenyl pyruvic acid at levels that maintained modD cells' regeneration. These results suggest a biological role for the proteases associated with protoplasmic incompatibility.