RESUMEN
Understanding the mode of gene action that controls seed yield and Sclerotinia stem rot resistance in Indian mustard is critical for boosting yield potential. In a line × tester mating design, ten susceptible lines and four resistant testers were used to conduct genetic analysis. The significance of general combining ability (GCA) and specific combining ability (SCA) variances revealed that both additive and non-additive gene actions were involved in the inheritance of Sclerotinia stem rot resistance and yield attributing traits. In addition to 1000-seed weight and number of primary and secondary branches/plant, the genotypes RH 1569 (line) and DRMR 2035 (tester) appeared to be the strongest general combiners for Sclerotinia stem rot resistance. RH 1657 × EC 597317 was the only cross among several that demonstrated a significant desired SCA value for Sclerotinia rot resistance. Regarding SCA effects for yield and component traits, the cross RH 1658 × EC 597328 performed best, with a non-significant but acceptable negative SCA effect for resistance. DRMR 2035, RH 1222-28, RH 1569, RH 1599-41, RH 1657, RH 1658, and EC 597328 are promising genotypes to use as parents in future heterosis breeding and for obtaining populations with high yield potential and greater resistance to Sclerotinia stem rot disease in Indian mustard, based on GCA effects of parents, per se performance, and SCA effects of hybrids. Days to 50% flowering, number of primary branches/plant, main shoot length, and 1000-seed weight all had a high genotypic coefficient of variability (GCV), broad-sense heritability (h2bs), and genetic advance as percent of the mean (GAM) values, as well as significant and desirable correlations and direct effects on seed yield. As a result, these traits have been recognized as the most critical selection criterion for Indian mustard breeding programs.
RESUMEN
Sclerotinia stem rot is one of the utmost important disease of mustard, causing considerable losses in seed yield and oil quality. The study of the genetic and proteomic basis of resistance to this disease is imperative for its effective utilization in developing resistant cultivars. Therefore, the genetic pattern of Sclerotinia stem rot resistance in Indian mustard was studied using six generations (P1, P2, F1, F2, BC1P1, and BC1P2) developed from the crossing of one resistant (RH 1222-28) and two susceptible (EC 766300 and EC 766123) genotypes. Genetic analysis revealed that resistance was governed by duplicate epistasis. Comparative proteome analysis of resistant and susceptible genotypes indicated that peptidyl-prolyl cis-trans isomerase (A0A078IDN6 PPIase) showed high expression in resistant genotype at the early infection stage while its expression was delayed in susceptible genotypes. This study provides important insight to mustard breeders for designing effective breeding programs to develop resistant cultivars against this devastating disease.
Asunto(s)
Planta de la Mostaza/genética , Inmunidad de la Planta , Proteoma/genética , Ascomicetos/patogenicidad , Planta de la Mostaza/metabolismo , Planta de la Mostaza/microbiología , Isomerasa de Peptidilprolil/genética , Isomerasa de Peptidilprolil/metabolismo , Proteínas de Plantas/genética , Proteínas de Plantas/metabolismo , Proteoma/metabolismoRESUMEN
Productivity of Indian mustard, an important oilseed crop of India, is affected by several pathogens. Among them, the hemibiotroph Sclerotinia sclerotiorum, which causes sclerotinia rot disease, is the most devastating fungal pathogen causing up to 90% yield losses. The availability of host resistance is the only efficient approach to control and understand the host-pathogen interaction. Therefore, the present investigation was carried out using six Indian mustard genotypes with contrasting behavior towards sclerotinia rot to study the antioxidant resistance mechanism against S. sclerotiorum. The plants at post-flowering stage were inoculated with five-day-old pure culture of S. sclerotiorum using artificial stem inoculation method. Disease evaluation revealed significant genotypic differences for mean lesion length among the tested genotypes, where genotype DRMR 2035 was found highly resistant, while genotypes RH 1569 and RH 1633 were found highly susceptible. The resistant genotypes had more phenolics and higher activities of peroxidase, catalase and polyphenol oxidase which provide them more efficient and strong antioxidant systems as compared with susceptible genotypes. Studies of antioxidative mechanisms validate the results of disease responses.