Title

Effects of R gene-mediated resistance in Brassica napus (oilseed rape) on asexual and sexual sporulation of Pyrenopeziza brassicae (light leaf spot)

Document Type

Article

Publication details

Boys, EF, Roques, SE, West, JS, Werner, CP, King, GJ, Dyer, PS & Fitt, BDL 2011, 'Effects of R gene-mediated resistance in Brassica napus (oilseed rape) on asexual and sexual sporulation of Pyrenopeziza brassicae (light leaf spot)', Plant Pathology, vol. 61, no. 3, pp. 543-54.

Published version available from:

http://dx.doi.org/10.1111/j.1365-3059.2011.02529.x

Peer Reviewed

Peer-Reviewed

Abstract

The phenotype of the R gene-mediated resistance derived from oilseed rape (Brassica napus) cv. Imola against the light leaf spot plant pathogen, Pyrenopeziza brassicae, was characterized. Using a doubled haploid B. napus mapping population that segregated for resistance against P. brassicae, development of visual symptoms was characterized and symptomless growth was followed using quantitative PCR and scanning electron microscopy on leaves of resistant/susceptible lines inoculated with suspensions of P. brassicae conidia. Initially, in controlled-environment experiments, growth of P. brassicae was unaffected; then from 8 days post-inoculation (dpi) some epidermal cells collapsed (‘black flecking’) in green living tissue of cv. Imola and from 13 to 36 dpi there was no increase in the amount of P. brassicae DNA and no asexual sporulation (acervuli/pustules). By contrast, during this period there was a 300-fold increase in P. brassicae DNA and extensive asexual sporulation in leaves of the susceptible cv. Apex. However, when leaf tissue senesced, the amount of P. brassicae DNA increased rapidly in the resistant but not in the susceptible cultivar and sexual sporulation (apothecia) was abundant on senescent tissues of both. These results were consistent with observations from both controlled condition and field experiments with lines from the mapping population that segregated for this resistance. Analysis of results of both controlled-environment and field experiments suggested that the resistance was mediated by a single R gene located on chromosome A1.