GENETICS OF RUST FUNGI 



rough wall of wild type. The mutant was observed in a greenhouse culture 

 because the spores appeared redder than wild type and remained clumped 

 together. The latter property would no doubt lead to its rapid elimination 

 in the field. 



MUTATION IN THE DIKARYON 



Genetic studies with Neurospora and other laboratory fungi are 

 greatly helped by the ready availability of haploid cells and mycelium. 

 Recessive mutants appear directly in homokaryons which survive treatment 

 with mutagens and a variety of procedures are available for screening 

 specific classes of mutants (Fincham and Day, 1965) . The difficulties of 

 screening for mutants in dikaryotic or diploid microorganisms are well 

 known (Snow, 1966) . In higher plants the screening procedure is carried 

 out on individuals which are raised following self-pollination of the 

 treated generation. Recessive mutants are recovered as homozygotes. In 

 the pathogen Phytophthora infestans , lack of success in obtaining auxo- 

 trophic or virulence mutants, which in other fungi are generally recessive, 

 has been used as evidence for diploidy (McKee , 1969; Clark and Robertson, 

 1966) . 



To date all induced mutation studies in rusts have been directed at 

 treating uredospores. These dikaryotic spores are of course functionally 

 equivalent to diploids. Two approaches have been made. The first is to 

 irradiate uredospores from cultures known to be heterozygous for certain 

 recessive virulence markers and to screen for mutants in which the 

 recessive virulence is revealed (Flor", 1956b; Schwinghamer , 1959; Rowell, 

 Loegering, and Powers, 1963). With X-rays or neutrons, the most frequent 

 class of mutants to be expected are chromosomal deletions which include 

 the dominant avirulence allele. An analysis of two such X-ray induced 

 mutants of M. lini by Flor (1960b) tends to confirm such an explanation 

 but raises many more questions about the nature of virulence than it 

 answers (Day, 1966) . 



The second method is to treat the uredospores of a clone of undeter- 

 mined genotype and screen for virulent mutants on one or several different 

 hosts resistant to the parent clone. A mutant recovered from P. ooronata 

 avenae by Griffiths and Carr (1961) following U.V. treatment of uredospores 

 was virulent on 6 oat varieties, all with different factors for resistance 

 to which the parent race was avirulent. The mutant was also avirulent to 

 a seventh variety to which the parent was virulent. It seems likely that 

 one result of U.V. irradiation was to induce genetic recombination to 

 generate the mutant. This is more plausible than the induction of 7 

 separate but simultaneous mutations. 



An approach which does not appear to have been tried is the treatment 

 of teleutospores either just prior to or during germination (meiosis) with 

 screening for mutants among the infections produced by the basidiospores 

 formed by the treated material. Green's (1964) search for pigment mutants 

 of P. graminis was essentially by this method but without mutagen treatment 

 The mutants Green recovered were probably present as heterozygotes since 

 their frequency was quite high in those teleutospore collections where 

 they occurred. Presumably this method could be used to isolate induced 

 mutants of C. ribioola on Pinus . An important advantage of screening 

 haploid spores is that recovery of recessive markers is much more effi- 

 cient. However, in most rusts it is difficult to obtain consistent 

 teleutospore formation, germination, and high rates of infection with 



