The Chromosomal Distribution of the Genetic Resistance of Rye to Wheat Pathogens

Wheat (Trit icuvz aes t im~m 272 = 6x = 42) is resistant to many of the fungal pathogens to which rye (Secale cererrle 212 = 14) is s~sceptible. T h e reciprocal condition of resistance in rye to wheat pathogens also applies. Yet many of the pathogenic forms that are specific to one or other host occur within the same fungal species. For example, specificity to both hosts is found in Pzlccilzirr ~ecolzditrr, P. striijormis, P. grrrmi71is and E ~ y s i p k e grmnilzis. This situation has bccn formally recognized by designing as fo7rnrre specirrles thosc forins confined absolutely to one or other host. Thus the powdery mildew of wheat is caused by E. gl-a??zi7?is f . sp. tritici while that of rye is caused by E. grrrmilzis f . sp. secrrlis. Trinomial designations are sometimes applied to some forms of species of Pz~cci~lirr usually confined to a single host species but occasio~~ally attacking a variety of a different species. For example isolates of Pz~cci~lia striifomnis tritlci usually attack only wheat varieties but they also attack the barley variety Fong Tien. l ' he biological meaning of genetic variation both in hosts and obligxte pathogens, in the capacity to give rise to disease symptoms, is not understood. In rclation to the pathogens there is some resemblance to the differentiation found between physiologic races of a single formzrr specirrle, where each is virulent on a distinctive and particular range of genotypes within a host species. T h e differences between the host species are analogous to those betwcen differential lines within a host specics, each of which is susceptible only to certain physiologic races of the pathogen. The full implication of this mutual adjustment within fol-mrre spccirrles and within host species only became apparent following the genetic analysis of both clements of the systcm (Flor, 1956; Pcrson, 1959). This showed that allelic variation determining resistance or susceptibility in the host was matchcd by complementary allelic variation determining virulence or avirulence in the pathogen. It may be that the contrast between formae specirrles of pathogens and between host specics has a similarly simple determination. Alternatively, the distinctions may be more c o m p l e ~ and subtle, the difference having arisen fortuitously during the greater evolutionary divergence of the host genotypes concerned. These possibilities can only be resolved by genetic analyses. However, the conduct of such analyses poses problems of a greater magnitude than the resolution of differences betwcen physiologic races and between differential lines within host species. Whereas fertile hybrids are readily made bctween physiologic races of some pathogens and between intraspecific host lines, difficulties are encountered in handling hybrids between fomzae specirrles and between wheat and rye. Apparently n6 study has been possible of the segregation in the F3 generation of crosses between fowzae ~peciales of cereal pathogens due to the difficulty of growing hybrids and to their low fertility (Staltman and Harrow, 1957). The barrier to the determination of the genetic basis of the