Genetic effects on controlling resistance to stripe rust (Puccinia striiformis f. sp. tritici Eriksson)were determined in two wheat crosses, Bakhtawar-92 (B-92) x Frontana and Inqilab-91 x Fakhre Sarhad using area under the disease progress curve (AUDPC) as a measure of stripe rust resistance. The resistant and susceptible parents involved in developing genetic populations were identified by initial assessment of 45 wheat accessions for stripe rust reaction. Mixed inheritance model was applied to the data analysis of six basic populations (P(1), F(1), P(2), B(1), B(2), and F(2)) in the crosses. The results indicated that AUDPC in cross 1 was controlled by two major genes with additive-dominance epistatic effect plus polygenes with additive-dominance-epistatic effects (model E) whereas, in the case of cross 2, it was under the control of two major genes with additive-dominance epistatic effect plus additive-dominant polygenes (model E-1). Additive effect was predominant over all other types of genetic effects, suggesting that the delay in selection for resistance until maximum favorable genes are accumulated in the individuals is desired. The tendency of backcrosses toward their respective pollen donor parents indicated the control of resistance through nuclear genes rather than the cytoplasmic factors. Occurrence of resistant as well as susceptible transgressive segregates (though very few in F(2) for each cross) indicated the presence of favorable as well as some adverse genes for resistance to stripe rust in the parents. The major gene heritability was higher than that of the polygene in B(1), B(2), and F(2) for the crosses. The major gene as well as the polygene heritability was 48.99 to 87.12% and 2.26 to 36.80% for the two crosses, respectively. The highest phenotypic variations in AUDPC (2,504.10 to 5,833.14) for segregating progenies (B(1), B(2), and F(2)) represent that the character was highly influenced by the environment. The experimental results of the two crosses indicate that resistance to stripe rust is under control of two major genes in association with several polygene rather than cytoplasmic inheritance.
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