3.4.14
INHERITANCE OF LOOSE SMUT (USTILAGO TRITICI) RESISTANCE IN WHEAT (TRITICUM AESTIVUM )

RE KNOX1, MR FERNANDEZ1, AL BRŰLÉ-BABEL2 and RM DE PAUW1

1SPARC, AAFC, Box 1030, Swift Current, SK S9H 3X2, Canada; 2Department of Plant Science, University of Manitoba, Winnipeg, MB R3T 2N2, Canada

Background and objectives
The inheritance of resistance in wheat (Triticum aestivum) to loose smut caused by Ustilago tritici (Pers.) Rostr. is not well understood. Previously F2 and F3 generations have been studied to determine the inheritance of resistance to loose smut [1]. Large populations and continuing segregation make genetic analysis difficult. In our study anther-culture-derived doubled-haploid populations and random inbred populations were used to study inheritance of loose smut resistance. Our objective was to determine if loose smut resistance in the experimental line HY377 was controlled by one or more than one major gene and to determine if the resistance was the same as the resistance in the line SC8021V2. A further objective of the study was to determine whether or not the pattern of segregation for loose smut resistance within random inbred line populations was similar to the segregation within anther-culture-derived doubled-haploid populations.

Materials and methods
The experimental wheat lines HY377 and SC8021V2 possess resistance to loose smut whereas, the line L8474-D1 is susceptible to loose smut. Anther-culture-derived doubled-haploid and F4-derived random inbred line populations were produced from each of the crosses HY377/L8474-D1 and HY377/SC8021V2. The lines were grown in the growth room and inoculated with a combination of individual U. tritici races T2, T10, T15, T19, T39 or a mixture of races T2, T10 and T39 [2]. The incidence of loose smut in the lines was determined, and observed segregation ratios were tested against expected segregation ratios for one and two gene control with the aid of the Chi square test.

Results and conclusions
The resistance from HY377 to loose smut races T2, T10, T19 and T39 in both doubled-haploid and random inbred line populations, derived from the cross HY377/L8474-D1, segregated clearly into resistant and susceptible lines. Lines resistant to one race were resistant to the other three and lines susceptible to one race were susceptible to the other three. The observed ratio of lines fit the expected ratio for a single major gene. The ratios showed a poor fit with an expected two gene segregation ratio. The doubled-haploid population, when inoculated to race T15, produced a group of lines with intermediate disease reactions. When intermediate and completely resistant genotypes were considered as seperate phenotypic classes, the segregation fit a two gene expected ratio. The lines resistant to race T19 expressed complete resistance and were the same lines which, when inoculated to race T15, expressed complete and intermediate resistance. Lines susceptible to race T19 were the same lines moderately susceptible to susceptible to race T15. The results indicated at least one major gene was segregating for resistance to all races studied but that an additional minor gene was segregating for resistance to race T15. Both the doubled-haploid and random inbred line populations from the HY377/SC8021V2 cross showed transgressive segregation for resistance to race T19. The occurrence of susceptible lines from this cross indicated HY377 and SC8021V2 differed in genes for resistance to race T19. The interpretations of inheritance drawn from random inbred line populations and doubled-haploid populations were the same. Under the conditions of this study HY377 appears to possess two genes for resistance to loose smut and this resistance differs from that present in SC8021V2. The use of both doubled-haploid and random inbred line populations simplified the genetic study compared to genetic analysis of an F2 and F3 population by reducing the population size required and by avoiding segregating genotypes, particularly in the doubled-haploid population.

References
1. Do Valle Ribeiro MAM, 1963. Trans. Brit. mycol. Soc. 46, 179-192.
2. Nielsen J, 1987. Can. J. Plant Pathol. 9, 91-105.