Genetic diversity ofPseudomonas syringaepv.actinidiae, pathogen of kiwifruit bacterial canker

Author:

Sawada H.1ORCID,Fujikawa T.2ORCID

Affiliation:

1. Genetic Resources Center National Agriculture and Food Research Organization (NARO) 2‐1‐2 Kannondai Tsukuba Ibaraki 305‐8602 Japan

2. Institute of Fruit Tree and Tea Science NARO 2‐1 Fujimoto Tsukuba Ibaraki 305‐8605 Japan

Abstract

Bacterial canker disease of kiwifruit currently occurs in at least 15 countries, causing serious damage. The causative agent of the disease isPseudomonas syringaepv.actinidiae(Psa), which is genetically diverse and is currently classified into five biovars, namely, biovars 1, 2, 3, 5 and 6. In Japan, four biovars except biovar 2 have been found so far. These biovars have been confirmed to have differences in the virulence and composition of pathogenicity‐related genes, such as toxin biosynthesis and typeIIIeffector genes. Biovars 1 and 6 possess thetoxisland, a genomic island of approximately 38 kb, which contains phaseolotoxin biosynthesis genes (argK‐toxcluster) and is confirmed to have been acquired from other bacteria through horizontal transfers. Also, on the megaplasmid possessed by biovar 6, there exist coronatine biosynthesis genes, and biovar 6 has the ability to produce two phytotoxins, phaseolotoxin and coronatine. In 2014, biovar 3, considered to be of foreign origin, was confirmed for the first time in Japan. Biovar 5, whose virulence is relatively weak, is distributed only in a limited area. In addition to thetoxisland and various plasmids, a large number of mobile genetic elements are confirmed to be present on the Psa genomes, which might have played a major role in helping Psa to acquire new features. In order to understand how Psa acquired the ability to infect kiwifruit systemically, it is important to make polyphasic comparisons with related pathovars, such asPsyringaepv.theaeand pv.actinidifoliorum.

Publisher

Wiley

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