P. R. DAY 



physiologic races. The gene-for-gene hypothesis developed bv Flor (1956a), 

 and discussed by Loegering (these proceedings) provides a rational genetic 

 scheme for explaining this interrelationship. The practical importance 

 of rust resistance and the problems created by physiologic specialization 

 explains why so much attention has been paid to genetic studies of 

 virulence. The nature of host resistance and hence the nature of pathogen 

 avirulence and virulence are of course relevant to this discussion and 

 are briefly considered later. 



The availability of virulence markers depends on the availability of 

 differentially resistant strains of the economic host. Unless physiologic 

 specialization has been detected virulence markers will not normally be 

 available. But this does not mean that they cannot be induced. Many 

 studies with rusts have shown that virulent mutants may be isolated 

 spontaneously or following treatment with a mutagen (Table 1) . Presumably, 

 if treated spores were applied to a susceptible host, mutants with reduced 

 virulence could be detected and, if their fitness were not too greatly 

 impaired, could be propagated and used as markers. Indeed such forms were 

 observed in crosses between certain races of M. lini (Flor, 1950) and as 

 a result of inbreeding P. graminis tritici (Johnson and Newton, 1938). 

 Both examples illustrate how selection works against such mutants arising 

 in nature. 



In the heteroecious rusts, one would expect to find resistance in both 

 hosts and indeed this is so. Race 15B of P. graminis is unable to infect 

 barberry by basidiospores (Green and Johnson, 1958). D'Oliveira (1940) 

 has shown variation in susceptibility to basidiospore infection by P. 

 triticina among species of Thaliotrum , by P. anomala among species of 

 Omithogalum and by P. coronata among species of Rhamnus . We may also 

 note the resistance of Ribes ussuriense , and the variety Consort derived 

 from it by hybridization with R. nigrum (Hunter and Davis, 1943), to 

 infection by aeciospores and uredospores of C. ribioola. 



In autoecious rusts like M. lini where all the spore forms occur on 

 flax, the virulence markers which determine the host range of the dikaryon 

 also function in the haploid infection. Avirulence in M. lini is dominant 

 in the dikaryon (Flor, 1965) . Haploid pycnia on a resistant host neces- 

 sarily carry the appropriate allele(s) for virulence. If their receptive 

 hyphae are fertilized with spermatia carrying a dominant allele for 

 avirulence, produced on a susceptible host, we may ask whether aecia and 

 aeciospores will form on the resistant host. In fact, aeciospores are 

 formed even though they are unable to infect the host genotype which bore 

 them (Flor, 1959). A comparable experiment with pigment mutants of P. 

 graminis on barberry is noted below. 



While in some circumstances the gene-for-gene relationship largely 

 determines the outcome of rust-host interactions we must not lose sight of 

 the fact that pathogen fitness and adaptability is subject to many other 

 controls which may not be so susceptible to genetic analysis. We call 

 this variation in aggressiveness and assume that it is determined, like 

 non-race specific or "field" resistance in the host, by polygenes. 



The two aspects of pathogenicity, virulence and aggressiveness, have 

 been considered in some detail by van der Plank (1968) in relation to the 

 problem of disease resistance and are also dealt with by Zadoks (these 

 proceedings) in his paper. 



