Abstract

Biometric analyses of variability in the disease incidence phenotype were performed using three F2 dikaryotic populations of the smut fungus Ustilago hordei (Pers.) Lagerh. on barley cultivars 'Trebi' (partially resistant) and 'Odessa' (universal suscept). The variance component involving interactions between segregating genes of U. hordei and environmental factors made the largest contribution towards the disease incidence on both cultivars. Additive and nonadditive (dominant and epistatic) gene effects contributed significantly to total disease incidence variation on both 'Trebi' and 'Odessa'. Heritability (additive genetic variance) was 2.5 times higher on 'Trebi' than on 'Odessa', and nonadditive variance effects were higher on 'Odessa' than on 'Trebi' by a factor of 1.5. Five effective factors were estimated to be segregating in the F2 populations; the virulence gene and four agressiveness factors. It is hypothesized that certain aggressiveness polygenes interact either with at least one other aggressiveness polygene or with the virulence gene. Analysis of variance–covariance provided supporting evidence for the epistatic activity of some genes and weak evidence for possible previous selection for intermediate optimal rather than maximal expression of the disease incidence phenotype. Key words: Ustilago hordei, aggressiveness, polygenes, disease incidence, smut.

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