Pseudomonas syringae pv. actinidiae ICMP 18884 biovar 3 (Psa3) produces necrotic lesions during infection of its kiwifruit host. Bacterial growth in planta and lesion formation are dependent upon a functional type III secretion system (T3S), which translocates multiple effector proteins into host cells. Associated with the T3S locus is the conserved effector locus (CEL), which has been characterized and shown to be essential for the full virulence in other P. syringae pathovars. Two effectors at the CEL, hopM1 and avrE1, as well as an avrE1‐related non‐CEL effector, hopR1, have been shown to be redundant in the model pathogen P. syringae pv. tomato DC3000 (Pto), a close relative of Psa. However, it is not known whether CEL‐related effectors are required for Psa pathogenicity. The Psa3 allele of hopM1, and its associated chaperone, shcM, have diverged significantly from their orthologs in Pto. Furthermore, the CEL effector hopAA1‐1, as well as a related non‐CEL effector, hopAA1‐2, have both been pseudogenized. We have shown that HopM1 does not contribute to Psa3 virulence due to a truncation in shcM, a truncation conserved in the Psa lineage, probably due to the need to evade HopM1‐triggered immunity in kiwifruit. We characterized the virulence contribution of CEL and related effectors in Psa3 and found that only avrE1 and hopR1, additively, are required for in planta growth and lesion production. This is unlike the redundancy described for these effectors in Pto and indicates that these two Psa3 genes are key determinants essential for kiwifruit bacterial canker disease.

中文翻译：

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丁香假单胞菌pv的AvrE1和HopR1。猕猴桃的完全毒性还需要添加猕猴桃。

丁香假单胞菌PV。猕猴桃ICMP 18884 biovar 3（Psa3）在其猕猴桃宿主感染期间产生坏死性病变。植物中细菌的生长和病变的形成取决于功能性III型分泌系统（T3S），该系统将多种效应蛋白转运到宿主细胞中。与T3S基因座相关的是保守的效应基因座（CEL），其已被表征并显示出对于其他丁香假单胞菌病原体的全部毒力至关重要。CEL的两个效应子HopM1和avrE1以及与avrE1相关的非CEL效应子hopR1在模型病原体丁香假单胞菌pv中被证明是多余的。番茄DC3000（Pto），Psa的近亲。但是，尚不清楚Psa致病性是否需要CEL相关效应子。的PSA3等位基因hopM1，及其相关的伴侣，shcM，从他们在PTO同源基因显著分歧。此外，CEL效应子hopAA1-1和相关的非CEL效应子hopAA1-2均已被伪生成。我们已经证明，由于shcM的截短（在Psa谱系中保守的截短），HopM1对Psa3的毒力没有贡献，这可能是由于需要避开猕猴桃中HopM1触发的免疫力所致。我们表征了CEL和相关效应子在Psa3中的毒性贡献，发现只有avrE1另外，hopR1对于植物生长和病变生产是必需的。这不同于在Pto中为这些效应子描述的冗余，并表明这两个Psa3基因是猕猴桃细菌性溃疡病必不可少的关键决定因素。