Genetic basis of control of Rhynchosporium secalis infection and symptom expression in barley

The genetic basis of several different components of resistance to Rhynchosporium secalis in barley was investigated in a mapping population derived from a cross between winter and spring barley types. Both the severity of visual disease symptoms and amount of R. secalis DNA in leaf tissues were assessed in field trials in Scotland in the 2007/2008 and 2008/2009 growing seasons. Relative expression of symptoms was defined as the residual values from a linear regression of amount of R. secalis DNA against visual plot disease score at GS 50. Amount of R. secalis DNA and visual disease score were highly correlated traits and identified nearly identical QTL. The genetic control of relative expression of symptoms was less clear. However, a QTL on chromosome 7H was identified as having a significant effect on the expression of visual disease symptoms relative to overall amount of R. secalis colonisationPeer reviewedFinal Accepted Versio

Characterisation of barley resistance to rhynchosporium on chromosome 6HS

Key Message: Major resistance gene to rhynchosporium, Rrs18, maps close to the telomere on the short arm of chromosome 6H in barley. Rhynchosporium or barley scald caused by a fungal pathogen Rhynchosporium commune is one of the most destructive and economically important diseases of barley in the world. Testing of Steptoe × Morex and CIho 3515 × Alexis doubled haploid populations has revealed a large effect QTL for resistance to R. commune close to the telomere on the short arm of chromosome 6H, present in both populations. Mapping markers flanking the QTL from both populations onto the 2017 Morex genome assembly revealed a rhynchosporium resistance locus independent of Rrs13 that we named Rrs18. The causal gene was fine mapped to an interval of 660 Kb using Steptoe × Morex backcross 1 S₂ and S₃ lines with molecular markers developed from Steptoe exome capture variant calling. Sequencing RNA from CIho 3515 and Alexis revealed that only 4 genes within the Rrs18 interval were transcribed in leaf tissue with a serine/threonine protein kinase being the most likely candidate for Rrs18.Max Coulter, Bianca Büttner, Kerstin Hofmann, Micha Bayer, Luke Ramsay, Günther Schweizer, Robbie Waugh, Mark E. Looseley, Anna Avrov

Identification and molecular mapping of a single Arabidopsis thaliana locus determining resistance to a phytopathogenic Pseudomonas syringae isolate

Debener T, Lehnackers H, Dangl JL. Identification and molecular mapping of a single Arabidopsis thaliana locus determining resistance to a phytopathogenic Pseudomonas syringae isolate. Plant journal. 1991;11(1):289-302

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

E. F. boys, S. E. roques, J. S. West, C. P. Werner, G. J. King, P. S. Dyer, B. D. L. Fitt, '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 (3): 543-554, August 2011, available online at doi: 10.1111/j.1365-3059.2011.02529.x. © 2011 The Authors. Plant Pathology © 2011 BSPPThe 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 caracterized. 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.Peer reviewe

Fine mapping, physical mapping and development of diagnostic markers for the Rrs2 scald resistance gene in barley

The Rrs2 gene confers resistance to the fungal pathogen Rhynchosporium secalis which causes leaf scald, a major barley disease. The Rrs2 gene was fine mapped to an interval of 0.08 cM between markers 693M6_6 and P1D23R on the distal end of barley chromosome 7HS using an Atlas (resistant) x Steffi (susceptible) mapping population of 9,179 F(2)-plants. The establishment of a physical map of the Rrs2 locus led to the discovery that Rrs2 is located in an area of suppressed recombination within this mapping population. The analysis of 58 barley genotypes revealed a large linkage block at the Rrs2 locus extending over several hundred kb which is present only in Rrs2 carrying cultivars. Due to the lack of recombination in the mapping population and the presence of a Rrs2-specific linkage block, we assume a local chromosomal rearrangement (alien introgression or inversion) in Rrs2 carrying varieties. The variety analysis led to the discovery of eight SNPs which were diagnostic for the Rrs2 phenotype. Based on these SNPs diagnostic molecular markers (CAPS and pyrosequencing markers) were developed which are highly useful for marker-assisted selection in resistance gene pyramiding programmes for Rhynchosporium secalis resistance in barley