SUMMARYIn the fungusPodospora anserina, mutations were selected which relieved the hypersensitivity to paromomycin caused by four suppressors assumed to be ribosomal ambiguity mutations (su1–31,su1–49,su1–60,su2–5). Our first purpose was to isolate new antisuppressor mutations and in fact a new antisuppressor gene,AS7was uncovered. TheAS7–1mutant displays a pleiotropic phenotype and particularly a sporulation defect. On the other hand, a newsu1mutant was obtained which acts as a suppressor and also as an antisuppressor: it can specifically reduce the suppressor effect of certainsu2mutations. This property of somesu1andsu2mutations was already known. Apart from these mutations probably involved in the control of translational fidelity, six mutations conferring cross-resistance to paromomycin and neomycin were isolated. While four of them are localized in thePm1andPm2loci previously identified, the two others define a new gene which controls paromomycin and neomycin resistance,Pm3. Strains carrying thePm3–1allele are sensitive to temperature at the level of growth and sporulation. The three last mutations which were obtained confer no mutant phenotype when separated from thesu1background. They are closely linked to thesu2locus.
Different alterations of the ribosomal protein S7 lead to opposite effects on translational fidelity in the fungus Podospora anserina.
