Subject(s)
Pneumococcal Infections/microbiology , Shock, Septic/microbiology , Splenectomy , Streptococcus pneumoniae/isolation & purification , Streptococcus pneumoniae/pathogenicity , Humans , Male , Middle Aged , Pneumococcal Infections/pathology , Shock, Septic/pathology , Streptococcus pneumoniae/growth & developmentABSTRACT
We have studied the reversion of 8 nonsense alleles located in 7 different genes of Schizosaccharomyces pombe using 4-nitroquinoline-1-oxide (NQO) as a mutagenic agent. The nonsense mutants of S. pombe have been classified according to their suppressibility by defined opal and ochre suppressors into a class of efficiently suppressed opal and a class of inefficiency suppressed ochre mutants. The UGA alleles tested all revert consistently with NQO, in agreement with the high specificity of this mutagen for G-residues reported for bacteria and yeast. The UAA alleles show a lack or a low level of reversion with NQO. This low level of reversion is due to the low level of non-G-specific transversions at A sites of the UAA triplet. Within each class of nonsense mutants the extent of induction is site-dependent. We conclude that NQO acts predominantly on G-residues in S. pombe.
Subject(s)
4-Nitroquinoline-1-oxide/pharmacology , Ascomycota/genetics , Mutation/drug effects , Nitroquinolines/pharmacology , Schizosaccharomyces/genetics , Alleles , DNA, Fungal/metabolism , Guanine/metabolism , Mutagens , Schizosaccharomyces/classificationABSTRACT
Meiotic and mitotic fine-structure maps of two efficient UGA suppressors of Schizosaccharomyces pombe which are known (sup3-e) or inferred (sup9-e) to code for two serine tRNAs carrying the mutant anticodon U*CA (Kohli et al. 1979a, b, Rafalski et al. 1979) are presented. Maps based on spontaneous meiotic, spontaneous mitotic and MMS induced mitotic recombination between the primary site of the anticodon mutation and a number of inactivating second-site mutations are similar. Specific marker effects, which drastically increase the frequency of spontaneous meiotic and mitotic recombination in crosses involving one or the other of four exceptional sites (including the anticodon sites of both sup3-e and sup9-e), disappear when mapping is based on MMS induced mitotic recombination. The meiotic marker effect characterizing the anticodon site of one of the two efficient UGA suppressors (sup3-e) also disappears upon further mutation to an inefficient UAA suppressor allele (sup3-i), as shown by its absence in a fine-structure map based on meiotic recombination between the anticodon mutation of this ochre suppressor allele and a new set of inactivating second-site mutations derived from it.
