A Database for Triticeae and Avena
*Agriculture and AgriFood Canada, Box 1000A, Brandon,
Manitoba, Canada, R7A 5Y3
*Agriculture and AgriFood Canada, 195 Dafoe Rd.,
Winnipeg, Manitoba, Canada, R3C 2M9
***Hoescht Canada, Product Development, 1503 55 S.W,
Calgary, Alberta, Canada, T3J OC4
Our original experiment consisted of at least two morphological markers for each of the seven linkage groups in barley crossed to CI 9973. We inoculated the F1 heads with loose smut to obtain infected F2 plants. In order to deal with the relatively large F2 population (circa 12,000 plants), we grew the F2 in the field. One of the first things we observed was that some of the markers simply did not survive, such as wst4 on chromosome 2 and lnt on chromosome 3, to name but a few. We also observed that, of those markers that did survive, some of these (y, f8, lb ) were greatly distorted from expected 3:1 ratios for the (recessive) marker (Group 2 in Table 1.). Obviously, environment, the pathogen, or both had preferentially eliminated those plants with the affected marker. Where the markers did segregate as expected, the ratios of "resistant" and "susceptible" did not fit any expected ratios for single or two gene systems. Further, one cross involving the wst2 marker showed complete resistance, even though the source wst2 parent tested as completely susceptible.
From our initial set of 28 markers, we were able to find only four (Group 1 in Table 1) that segregated predictably and had reasonable levels of infection. In looking at this very limited set of data, we could not make any firm conclusions. All we could determine was that 1) it appears (from the approx. 6/8:1 ratio for resistance) that we may have two dominant genes governing the resistance found in CI 9973 and 2) there is some evidence of linkage to gs3 (Chi-square of 4.062; significant at P=0.05) for one of the two genes. Given that gs3 is relatively close to Run1, the gene in question may actually be Run1, or allelic to it. This did not put us any further ahead, as we really wanted to identify the 'other' novel gene.
We attempted to repeat the experiment using the same and different markers, with similar results. We also tried using single seed descent (SSD), and obtained even poorer results. We concluded that using morphological markers as an aid in mapping novel loose smut genes was an exercise in futility and we do not recommend this technique.
Table 1. Segregation of phenotypes at the F2 for specific morphological markers and loose smut resistance in crosses involving the resistant genotype CI 9973.
_____________________________________________________________________ Segregation Morphological Phenotypes Ratios Marker +/+ +/smut marker marker/smut R:S¹ W:M² f 430 53 101 22 7:1 4:1 gp 258 45 65 9 6:1 3:1 mt2 188 27 68 6 8:1 3:1 Group 1 gs3 385 8 145 5 41:1 3:1 xno 335 5 99 13 24:1 3:1 wst2 129 0 76 0 1:0 2:1 y 487 52 82 8 10:1 6:1 Group 2 gs6 241 61 161 33 4:1 2:1 f8 463 18 81 2 27:1 6:1 lb 246 24 233 30 9:1 1:1 _____________________________________________________________________¹R=Resistant; S=Smut infected.