The highly effective resistance to crown rust (caused by Puccinia coronata Cda.f. sp. avenae Eriks.), identified in an accession of a diploid oat, Schreb, was introgressed into the hexaploid cultivar Sun II (T. Aung, J. Chong, and M. Leggett, see previous article). Genetic analysis indicated that the resistance was inherited as a single near-complete dominant gene, designated Pc94. This gene conditions an immune reaction to crown rust in the field. However, to be able to combine this gene with other resistance genes for use in oat breeding programs, it is important to characterize this gene with respect to other resistance genes, since linkages and allelism are common in oat.
 

To determine linkage relationship, a Sun II backcross line with Pc94 was crossed to five single gene lines, each carrying one of the resistance genes, Pc38, Pc39, Pc45, Pc48, or Pc68. When tested with isolates virulent to these Pc genes and avirulent to Pc94, all F₁ seedlings derived from the crosses were resistant, typically producing a ; to ;1 infection type. This indicated that Pc94 mainly behaved as a dominant gene in these backgrounds. However, with the Pc38/Pc94 cross, gene Pc94 behaved like a recessive gene, as all 15 F₁ hybrids were susceptible to a crown rust isolate avirulent to Pc94 and virulent to Pc38. F₂ populations of all the crosses, however, segregated to give a good fit to an expected 15 resistant :1 susceptible ratio, when tested with an avirulent isolate (Table 1). This indicated that Pc94 is independent of these genes, including Pc38.
 

The results of segregation of F₃ families to several crown rust isolates in crosses between Pc94 and Pc38, Pc48, and Pc68 are shown in Table 1. F₃ families of the Pc48/Pc94 cross segregated to fit an expected 1:2:1 single gene ratio for Pc94 when tested with CR13, an isolate avirulent to Pc94 and virulent to Pc48. F₃ families of this cross also segregated to fit a 1:2:1 single gene ratio for Pc48 when tested with CR223, an isolate avirulent to Pc48 and virulent to Pc94. Similarly, F₃ families of the Pc68/Pc94 cross segregated to fit a 1:2:1 ratio for Pc94 when tested with CR225 (virulent to Pc68 and avirulent to Pc94), and segregated to fit an expected 1:2:1 ratio for Pc68 when tested with CR223.
 

The reversal of Pc94 expression from dominance to recessiveness was also evident in all F₁ plants derived from crosses involving nine other cultivars with Pc38. This phenomenon was investigated further in the Pc38/Pc94 cross. Segregation of the F₃ families gave a good fit to a single gene 1:2:1 ratio for gene Pc38, when tested with CR223 (Table 1). However, when tested with CR36, an isolate virulent to Pc38 and avirulent to Pc94, F₃ families did not segregate to fit a single gene 1:2:1 ratio expected for Pc94 (Table 1). The number of homozygous resistant families observed was far fewer than the expected number, whereas the number of homozygous susceptible families observed was far in excess of the number expected. While these deviations could be explained by the differential transmission of the resistance in the gametes, the observed numbers of homozygous resistant, segregating, and susceptable families gave a good fit to a two-gene 1:8:7 ratio (Table 1), which can be best explained by the presence of a suppressor interacting with Pc94. Our results from tests with CR223 (which detects Pc38) and CR36 (which detects Pc94) indicated that Pc38 could well be the suppressor. This would explain why Pc94 resistance was not expressed in any the 27 families homozygous resistant to CR223, because these families were homozygous for the presence of the suppressor, Pc38. That Pc38 is a suppressor would also explain why Pc94 homozygosity was only detected in families that were homozygous susceptible to CR223, because these were the only families homozygous for the absence of the suppressor.
 

It has been shown previously that several Pc genes (e.g. Pc1, Pc3) were inhibited by inhibitor genes (Simons set al. 1978). More recently, Pc38 was reported to be a suppressor of Pc62 (Wilson and McMullen 1997). Our present study indicated that Pc38 also is a suppressor of Pc94, although we have not excluded the possibility that the suppressor actually is not Pc38 but a gene tightly linked to it. We are currently working on other crosses involving different cultivars with Pc38 to determine if suppression of Pc94 also occurred in these backgrounds.
 

Wilson, W.A., and M.S. McMullen. 1997. Dosage dependent genetic suppression of oat crown rust resistance gene Pc62. Crop Sci. 37:1699-1705.
 

Simons, M.D., J.W. Martens, R.I.H. McKenzie, I. Nishiyama, K. Sadanaga, J. Sebesta, and H. Thomas. 1978. Oats: a standardized system of nomenclature for genes and chromosomes and catalog of genes governing characters. U.S. Government Printing Office, Washington, DC. USDA Agric. Handb. 408.
 

Table 1. Segregation for resistance to Puccinia coronata isolates in F₂ and F₃ populations of crosses between Pc94 and several Pc genes
 

^¶ CR13 - virulent to Pc48, avirulent to Pc94
CR36 - virulent to Pc38, avirulent to Pc94
CR152 - avirulent to the Pc genes
CR223 - virulent to Pc94, avirulent to Pc38
CR225 - virulent to Pc68, avirulent to Pc94
* not applicable

Table 2. Segregation for resistance to Puccinia coronata isolates* CR36 and CR223 in F₃ families of the Pc38/P94 cross
 

 *CR36 - virulent to Pc38, avirulent to Pc94
CR223 - virulent to Pc94, avirulent to Pc38
^¶Hom. res = homozygous resistant, Seg = segregating, and Hom. susc = homozygous susceptible