Inheritance of Prehaustorial Resistance to Puccinia graminis f. sp. avenae in Barley (Hordeum vulgare L.).
Dracatos, P.M., Ayliffe, M.A., Khatkar, S., Fetch Jr., T.G., Singh, D., and Park, R.F. (2014). "Inheritance of Prehaustorial Resistance to Puccinia graminis f. sp. avenae in Barley (Hordeum vulgare L.).", Molecular Plant-Microbe Interactions, 27(11), pp. 1253-1262. doi : 10.1094/MPMI-05-14-0140-R Access to full text
Rust pathogens within the genus Puccinia cause some of the most economically significant diseases of crops. Different formae speciales of P. graminis have co-evolved to mainly infect specific grass hosts; however, some genotypes of other closely related cereals can also be infected. This study investigated the inheritance of resistance to three diverse pathotypes of the oat stem rust pathogen (P. graminis f. sp. avenae) in the ‘Yerong’ ✕ ‘Franklin’ (Y/F) barley doubled haploid (DH) population, a host with which it is not normally associated. Both parents, ‘Yerong’ and ‘Franklin’, were immune to all P. graminis f. sp. avenae pathotypes; however. there was transgressive segregation within the Y/F population, in which infection types (IT) ranged from complete immunity to mesothetic susceptibility, suggesting the presence of heritable resistance. Both QTL and marker-trait association (MTA) analysis was performed on the Y/F population to map resistance loci in response to P. graminis f. sp. avenae. QTL on chromosome 1H (‘Yerong’ Rpga1 and Rpga2) were identified using all forms of analysis, while QTL detected on 5H (‘Franklin’ Rpga3 and Rpga4) and 7H (Rpga5) were only detected using MTA or composite interval mapping–single marker regression analysis respectively. Rpga1 to Rpga5 were effective in response to all P. graminis f. sp. avenae pathotypes used in this study, suggesting resistance is not pathotype specific. Rpga1 co-located to previously mapped QTL in the Y/F population for adult plant resistance to the barley leaf scald pathogen (Rhynchosporium secalis) on chromosome 1H. Histological evidence suggests that the resistance observed within parental and immune DH lines in the population was prehaustorial and caused by callose deposition within the walls of the mesophyll cells, preventing hyphal penetration.
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