Kiwifruit bacterial canker: novel insights on an old problem

Framework: Kiwifruit bacterial canker (KBC), caused by Pseudomonas syringae pv. actinidiae (PSA), is currently the most destructive disease of kiwifruit worldwide. It was introduced in Portugal in 2010, inducing production losses up to 80 %. Conversely, a closely related pathovar, P. syringae pv. actinidifoliorum (PSAF), only causes necrotic spots, not being associated with plant mortality. There is some evidence on the higher susceptibility of green kiwifruit (Actinidia deliciosa) cultivars to KBC, compared with the berry kiwi (A. arguta), but the reasons behind it are still largely unknown. The aim of this work was to evaluate how kiwi plants with reported distinct tolerance to the disease responded to artificial infection in terms of defence-related genes expression. Methods: Micropropagation of A. deliciosa cv. ‘Hayward’ and A. arguta cv. ‘Ken’s Red’ plants. Plant inoculation with a virulent Pseudomonas syringae pv. actinidiae strain (PSA) and with a low virulent P. syringae pv. actinidifoliorum strain (PSAF). Bacterial colony forming units (CFUs) determination in plant tissues 1, 2 and 5 days post inoculation (dpi). Defence-related gene expression analysis by reverse transcription polymerase chain reactions (qRT-PCR) at 1, 2 and 5 dpi. Conclusions: A. deliciosa cv. ‘Hayward’ seems to be much more susceptible to PSA infection than A. arguta cv. ‘Ken’s Red’. SOD expression was drastically increased in ‘Hayward’, whereas C AT was the most upregulated antioxidant-encoding gene in ‘Ken’s Red’. Jasmonic acid and ethylene precursors, LOX and SAM, were upregulated 2 dpi in ‘Hayward’ and already at 1 dpi in ‘Ken’s Red’. LOX1 and SAM transcriptional levels were higher in PSA-inoculated plants, compared with PSAF.