University of Hertfordshire

From the same journal

By the same authors

  • Emily F. Boys
  • Jon S. West
  • C. Peter Werner
  • Graham J. King
  • Paul S. Dyer
  • Bruce D.L. Fitt
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Original languageEnglish
Pages (from-to)100
JournalActa Phytopathologica Sinica
Journal publication dateAug 2013
Volume43
IssueSupp
Publication statusPublished - Aug 2013
Event10th International Congress of Plant Pathology - Beijing, China
Duration: 25 Aug 201330 Aug 2013

Abstract

The phenotype of a form of Brassica napus (oilseed rape) R gene-mediated resistance against the hemibiotrophic plant pathogen Pyrenopeziza brassicae, cause of light leaf spot, was investigated. Using a doubled haploid B. napus mapping population that segregated for resistance against P. brassicae, development of visual symptoms was characterised and asymptomatic growth was followed using quantitative PCR and scanning electron microscopy on leaves of resistant/susceptible lines inoculated with suspensions of P. brassicae conidia. A new phenotype of resistance was observed in lines derived from B. napus cv. Imola. 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 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 susceptible cv. Apex.
However, when leaf tissues senesced, there was a rapid increase in amount of P. brassicae DNA in the resistant but not susceptible cultivar and sexual sporulation (apothecia) was abundant on senescent tissues of both. These results were supported by results of controlled environment 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.

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