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Mutations relieving hypersensitivity to paromomycin caused by ribosomal suppressors in Podospora anserina

Published online by Cambridge University Press:  14 April 2009

Evelyne Coppin-Raynal
Affiliation:
Laboratoire de Génétique de l'Université de Paris-Sud, Bât. 400 (Laboratoire associé au CNRS no. 86) 91405 ORSAY Cedex, France
Denise Le Coze
Affiliation:
Laboratoire de Génétique de l'Université de Paris-Sud, Bât. 400 (Laboratoire associé au CNRS no. 86) 91405 ORSAY Cedex, France

Summary

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In the fungus Podospora 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, AS7 was uncovered. The AS7–1 mutant displays a pleiotropic phenotype and particularly a sporulation defect. On the other hand, a new su1 mutant was obtained which acts as a suppressor and also as an antisuppressor: it can specifically reduce the suppressor effect of certain su2 mutations. This property of some su1 and su2 mutations 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 the Pm1 and Pm2 loci previously identified, the two others define a new gene which controls paromomycin and neomycin resistance, Pm3. Strains carrying the Pm3–1 allele 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 the su1 background. They are closely linked to the su2 locus.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1982

References

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