To promote breeding for Ascochyta blight in lentil, the genetics of resistance to lentil Ascochyta blight was investigated. In addition, some techniques needed to support the genetic research and breeding were developed in this study. An efficient procedure for producing genetically true-type plantlets was established based on stimulating elongation of the axilary buds. This technique was then used to multiply F₁ hybrid populations to make the population sizes of different generations large enough for careful genetic analyses.
Two regeneration systems, one based on multiple shoot induction from intact seedlings and the other based on cotyledonary node culture, were developed to facilitate the transfer of useful genes from wild lentils and/or other sources into cultivated lentil using tissue culture and genetic engineering techniques.
Ten major genes were identified for foliar resistance. The inheritance models for these genes were: one dominant gene for high resistance and one dominant gene for moderate resistance (ILL 5588); a single dominant gene (ILL 5684 and W6 3241), two complementary dominant genes (W3 3192 and Titore), two recessive genes with additive effect (Indian head); one recessive gene (Laird); and one partial dominant gene with large effect and one dominant gene with less effect (W3 3261). The gene in ILL 5684 is allelic to the one in ILL 5588 for high resistance.
The contributions of minor genes to Ascochyta blight resistance were established for the first time by creating recombinant inbreds with the same major genotypes but different minor genotypes from two crosses (ILL 5684 x Titore, W6 3241x Titore). A mixed model based analysis carried out for the cross ILL 5588 x Titore indicated that about 30% of the phenotypic variations in segregating populations were due to the minor genes.
The overall genetic effect and the partition of the genetic effect into additive, dominant and epistatic effects were done for four crosses using generation-mean analysis. The underlying genetic mechanisms for seed infection rate were more complicated than that for foliar disease severity. The six basic generations were sufficient to model foliar disease severity, whereas they were not sufficient for seed infection rate in two crosses. Dominance played an important role in all crosses for both seed and foliar resistance. Except for foliar resistance in the cross ILL 5684 x Titore, at least one type of inter-gene effect (epstastic) contributed to the increased/reduced resistance. Therefore, selection for resistance would be more efficient if the dominance and epistasis effects were reduced after a few generations of selfing.
The major gene for foliar resistance in ILL 5684 is linked to the genes for seed yield/plant or it has pleiotropic effect on seed yield/plant. The gene is independent of the genes for plant height and days to flowering. Within each set, there were significant differences among inbreds for all the three traits. The estimates of heritability based on inbred means were high for seed yield/plant and days to flowering, and moderate for plant height. For the set with major resistance gene, 1) disease severity was not correlated with seed yield/plant and plant height, but weakly and negatively correlated to days to flowering when measured under disease pressure. 2) Seed yield/plant was strongly and positively correlated with plant height, moderately and negatively correlated with days to flowering, and plant height was weakly and positively correlated with days to flowering under both testing conditions. 3) Inbred x environment interaction was not important and selection can be done with or without artificial inoculation. Thus, selection within the set of inbreds with the major resistance gene is required and is feasible for the improvements of yield and other traits and for the utilisation of resistance conferred by minor genes.
Based on the results from this study and previous studies, a breeding procedure suitable for the current situation was developed. This procedure is based on crossing resistant and high yielding cultivars and multi-location testing. Gene pyramiding, exploring slow blighting and partial resistance, and using genes contained in wild relatives will be the methods of the future. Identification of more sources of resistance genes, good characterisation of the host-pathogen system, and identification of molecular markers tightly linked to resistance genes are suggested to be the key areas for future study
