Unravelling Actinidia molecular mechanisms against Pseudomonas syringae pv. actinidiae and P. syringae pv. actinidifoliorum - first steps

Kiwifruit bacterial canker (KBC), caused by Pseudomonas syringae pv. actinidiae (Psa), is currently the most destructive disease of kiwifruit worldwide. In contrast, the closely related pathovar P. syringae pv. actinidifoliorum (Psaf) only causes necrotic spots, not being associated with plant mortality. Moreover, there is some evidence for greater susceptibility of Actinidia deliciosa cultivars to KBC, compared with Actinidia arguta, but the reasons behind this observation are still largely unknown. In this work, micropropagated female plants of A. deliciosa ‘Hayward’ and A. arguta ‘Ken’s Red’ were inoculated with Psa or with Psaf (10⁷ CFU mL^-1). Disease development was monitored at 1, 2 and 5 days post-inoculation (dpi) through CFU determination and gene expression analysis of plant defence-related genes (APX, CAT, SOD, LOX1, SAM and TLP1). At 5 dpi, Psa and Psaf CFU were 17.4- and 2.8-fold higher, respectively, in ‘Hayward’ compared with ‘Ken’s Red’. Expression of antioxidant enzyme-related genes was very distinct between the two species: SOD expression was drastically increased in ‘Hayward’ (up to 1.1-fold), whereas, in ‘Ken’s Red’, CAT was the most upregulated gene (up to 0.7-fold). LOX1, involved in jasmonic acid biosynthesis, was upregulated in both species, but at different time-points: up to 1.2-fold in ‘Hayward’ at 2 dpi and 0.9-fold in ‘Ken’s Red’ at 1 dpi. These results demonstrate that ‘Ken’s Red’ seems to be much more tolerant of Psa than ‘Hayward’ and that the resistance mechanisms between the two species involve specific defence pathways being triggered at distinct moments after plant infection.

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