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SESSION 1 - Discovery - New horizons in plant pathology - page 38 / 65





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release of the PEDRo repository including several fungal proteome data sets will take place in March from http://pedro.man.ac.uk. A fungal plant pathogen EST database which now contains 42327 unisequences from 15 species of phytopathogen has been established and is accessible via the COGEME website. The Consortium units carry out development and maintenance of the various services and also have a role in training.   Both Transcriptome and Proteome units have expertise to act as research hotels for relevant experiments and are thus able to train members of the research community in both data generation and interpretation. We will describe the service provided in each of the Consortium facilities to inform the yeast community of the potential of our services. A new costing structure has been introduced with the transition to phase 2 of the IGF initiative. The structure and procedures for obtaining BBSRC funding to pay for the COGEME services will be explained.


Leptosphaeria biglobosa can induce higher resistance of Brassica napus to Phoma stem canker by triggering earlier JA/ET pathway and stronger SA pathway both locally and systematically

Renhu Liu, Shengyi Liu, Bruce D. L. Fitt*, Hans Cool, Akinwunmi Latunde-dada, Yongju Huang, Ziqin Li, John A. Lucas Rothamsted Research, Harpenden, Hertfordshire AL5 2JQ, UK

Phoma stem canker is one of the most seriously destructive diseases on worldwide winter oilseed rape. The disease was known to be caused by some fungi complex, which comprised at least A-group and B-group. A-group, which has been named as Leptosphaeria maculans recently, is highly aggressive and virulent, and causes destructive phoma stem canker at the stem base of oilseed rape. However, B-group is non-aggressive, just producing some lesions on the surface of upper stem, and now is called L. biglobosa.  Recent researches have shown that pre-inoculation with B-group fungus (L. biglobosa) can induce higher resistance of Brassica napus to A-group (L. maculans). In this research, we also confirmed that pre-inoculation of B-group could result in less damage from consequent A-group inoculation on Brassica napus cv. Madrigal by making smaller lesion size and less lesion number.  In order to research the defence signal pathway of this induced resistance, we chose some of the genes in the cascading of SA and JA/ET signal pathway respectively for realtime PCR, such as PDF 1.2 for JA/ET pathway, PR-1 for SA pathway. Results showed that JA/ET signal pathway could be induced 24 hours earlier than the controls both locally and systematically, while SA signal was still not earlier triggered, but much more strongly induced after 96 hours of inoculation both locally and systematically. Results also showed Chitinase gene expression could be only substantially locally induced on the inoculated leaves, and also much more strongly induced locally by B-group.  These results gave us a general impression on the genetic basis of the systematic acquired resistance on L. maculans induced by L. biglobosa.


Microsatellite markers distinguish genets of Heterobasidion annosum in a severely infected Sitka spruce stand in north east Scotland.

BODLES, W.J.A.1, ZAMPONI, L.3, BECKETT, E.1, WOODWARD, S.1 & CAPRETTI, P.3.  1: University of Aberdeen, School of Biological Sciences, Hilton Campus, Hilton Avenue, Aberdeen AB24 4FA, Scotland, UK, 2:  Dipartimento di Biotecnologie Agrarie, sez. Patologia Vegetale, piazzale delle Cascine 28, 50144 Firenze, Italy

A Sitka spruce (Picea sitchensis) site on the southern slopes of Bennachie in north east Scotland presenting a severe Heterobasidion annosum infection was investigated to determine (a) the history that lead to the development of conditions conducive to disease development and (b) the extent of genetic variation within the H. annosum population on the site.  Fifty one isolates of H. annosum were obtained.  Pairing heterokaryotic isolates from fruiting bodies suggested the presence of at least 22 genets on the site, affecting between one and five host trees, as judged on the basis of fruit body production.  The largest genets were approximately 22.5 m in length (based on 3 fruiting bodies), 17.5 m and 9 m, with likely ages in the region of 45, 35 and 18 years, respectively.  PCR amplification profiles obtained from the isolates using CCA and CGA minisatellite core sequences, were analysed. A phylogenetic dendrogram constructed with the UPGMA method differentiated the H. annosum population in different groups.  Data indicated several periods of recruitment into the H. annosum population on the site, although in the absence of thinning stumps, the source of the initial infections is unclear.  The localized severity of the infection probably arose due to former arable use of the land; the current low soil pH may have resulted from the build up of acidity from needle litter degradation.


Heterobasidion annosum genet size in a severely infected Norway spruce plantation following chemical thinning.

WOODWARD, S., HARAMBURU, E., BODLES, W.J.A. & JOHNSTON, D.H.  University of Aberdeen, School of Biological Sciences, Hilton Campus, Hilton Avenue, Aberdeen AB24 4FA, Scotland, UK

A very high incidence of Heterobasidion annosum infection was found in stands of Norway spruce (Picea abies) that had been chemically thinned (by injecting glyphosate into the stem), compared with conventionally thinned (one tree in three) and unthinned stands.  In the chemically thinned stand, 95 % of treated trees and at least 87% of untreated trees were infected by H. annosum. No standing trees in either the conventionally thinned or unthinned stands were infected, although 8% of stumps in the conventionally-thinned plots were colonised.  H. annosum genet sizes were examined in discrete plots within the chemically thinned stand to determine if the treatment resulted in enhanced tree-tree spread of individual genotypes of the pathogen.  The largest genet found was approximately 16.5 m in width; however, a number of genets occupying single trees or stumps were also observed.  Assuming thinning dates in 1985 – 88, the rate of spread of the largest genets was approximately 0.9 – 1.1 m per annum, higher than rates reported elsewhere.  The reason why chemically

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