ABSTRACT
Pathogen susceptibility and defence gene inducibility were compared between the Actinidia arguta cultivar 'Hortgem Tahi' and the two cultivars of A. chinensis 'Hayward' and 'Zesy002'. Plants were treated with acibenzolar-s-methyl (ASM) or methyl jasmonate (MeJA) one week before inoculation with Pseudomonas syringae pv. actinidiae (Psa biovar3) or Sclerotinia sclerotiorum, or secondary induction with chitosan+glucan (Ch-Glu) as a potential pathogen proxy. Defence expression was evaluated by measuring the expression of 18 putative defence genes. 'Hortgem Tahi' was highly susceptible to sclerotinia and very resistant to Psa, whereas 'Zesy002' was highly resistant to both, and 'Hayward' was moderately susceptible to both. Gene expression in 'Hayward' and 'Zesy002' was alike but differed significantly from 'Hortgem Tahi' which had higher basal levels of PR1-i, PR5-i, JIH1, NPR3 and WRKY70 but lower expression of RD22 and PR2-i. Treatment with ASM caused upregulation of NIMIN2, PR1-i, WRKY70, DMR6 and PR5-i in all cultivars and induced resistance to Psa in 'Zesy002' and 'Hayward' but decreased resistance to sclerotinia in 'Zesy002'. MeJA application caused upregulation of LOX2 and downregulation of NIMIN2, DMR6 and PR2-i but did not affect disease susceptibility. The Ch-Glu inducer induced PR-gene families in each cultivar, highlighting its possible effectiveness as an alternative to actual pathogen inoculation. The significance of variations in fundamental and inducible gene expression among the cultivars is explored.
Subject(s)
Actinidia , Ascomycota , Pseudomonas syringae/physiology , Actinidia/genetics , Plant Diseases/geneticsABSTRACT
The plant defence inducer Actigard® (acibenzolar-S-methyl [ASM]) is applied before flowering and after fruit harvest to control bacterial canker in kiwifruit caused by Pseudomonas syringae pv. actinidiae. Pre-flowering application of ASM is known to upregulate defence gene expression; however, the effect of postharvest ASM on defence gene expression in the vine is unknown. In this study, the expression of eight "defence marker" genes was measured in the leaves of Actinidia chinensis var. chinensis, "Zesy002," and Actinidia chinensis var. deliciosa, "Hayward," vines after postharvest treatment with ASM and/or copper. There were two orchards per cultivar with harvest dates approximately three weeks apart for investigating potential changes in responsiveness to ASM during the harvest period. In all trials, postharvest ASM induced the expression of salicylic-acid-pathway defence genes PR1, PR2, PR5, BAD, DMR6, NIMIN2, and WRKY70. Gene upregulation was the greatest at 1 day and 7 days after treatment and declined to the control level after 3 weeks. In "Zesy002", the ASM-induced response was greater at the early harvest site than at the late harvest site. This decline was concomitant with leaf yellowing and a reduction in RNA yield. Effects of postharvest ASM on gene expression did not persist into the following spring, nor were vines conditioned to respond more strongly to pre-flowering ASM application.
