Page 286 - PC2019 Program & Proceedings
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PLANT CANADA 2019

               P145. Variation between Ilyonectria mors-panacis and I. robusta isolates causing root rot in Panax
               quinquefolius
                             *
               Behdarvandi, B ; M. Valliani; P. Goodwin
               University of Guelph

               Ilyonectria mors-panacis is associated with ginseng replant disease causing disappearing root rot in
               replant soil versus only 2-5% rot in non-replant soils. Ilyonectria mors-panacis may be more common in
               ginseng roots because it is more virulent than other species, and isolates from roots in replant soil may be
               more virulent than from non-replant soil. One type of fungal virulence factor is small secreted proteins
               (SSPs) that can induce or suppress host triggered immunity. Measuring lesion size following inoculation
               of wounded ginseng roots with spores showed that virulence of three I. mors-panacis isolates from roots
               in replant soil was not significantly different from six isolates from roots in non-replant soil, and the
               average virulence of twelve I. mors-panacis isolates was not significantly different than that of four I.
               robusta isolates. Following genome sequencing, predicted homologs of SSPs were classified based on
               size, cysteine number and isoelectric point. PCA analyses of the SSPs showed that the twelve I. mors-
               panacis isolates clustered into two groups and the four I. robusta isolates clustered into two other groups
               with one isolate being more similar to I. europaea. There was no evidence that virulence of I. mors-
               panacis differed between isolates from replant and non-replant soils or that I. mors-panacis was more
               virulent than I. robusta, and clustering of isolates based on predicted SSPs was unrelated to virulence or
               replant/non-replant soil type.

               Behrang Behdarvandi (bbehdarv@uoguelph.ca)




               P146. Para-aminobenzoic acid (PABA) reducing Botrytis cinerea disease in leaves of Nicotiana
               benthamiana plants
               Costa, L.; A. Munawar; P. Goodwin
               University of Guelph)

               Para-aminobenzoic acid (PABA) is a folate precursor previously shown to induce resistance against
               Xanthomonas axonopodis pv. vesicatoria and cucumber mosaic virus in the field when pepper seedlings
               were dipped into 1 mM PABA. Induced resistance by PABA was demonstrated by up-regulation of the
               salicylic (SA) regulated genes, CaPR4 and CaPR9, during the growing season. In this study, 18 mM
               PABA was applied 3 times weekly to soil around Nicotiana benthamiana seedlings. Seven days after the
               last application, leaves were inoculated with spores of the necrotroph, Botrytis cinerea. PABA-treated
               plants had 50% smaller lesions compared to water treated plants. No effects on plant growth were
               measured. Following treatment, up-regulation occurred only after inoculation for the SA regulated genes
               for acidic NbPR-1a, Nb-ACC3 (1-aminocyclopropane-1-carboxylate oxidase3) and acidic NbPR-2,
               indicating priming. Up-regulation after treatment, but before inoculation, was observed for the SA
               regulated genes for acidic NbPR-4B, NbSAR8.2a (systemic acquired resistance protein 8.2a), and Nb-CHn
               (atypical basic endochitinase), indicating induction. Induction was also observed for NbCP23 (cysteine
               protease 23) expression, which is not under ethephon (ET) or jasmonate (JA) regulation. Expression of
               the ET and JA-regulated genes for basic NbPRb-1b, basic NbPR-2 were not affected by PABA, indicating
               that they were not involved in signaling resistance. This study showed that PABA can induce resistance
               against B. cinerea, which is due to both induction and priming of SA-regulated genes.


               Lucio Costa (lucio@uoguelph.ca)








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