HopPtoN is a Pseudomonas syringae Hrp (type III secretion system) cysteine protease effector that suppresses pathogen‐induced necrosis associated with both compatible and incompatible plant interactions

Abstract

SummaryPseudomonas syringae pv. tomato DC3000 causes bacterial speck disease in tomato, and it elicits the hypersensitive response (HR) in non-host plants such as Nicotiana tabacum and Nicotiana benthamiana . The compatible and incompatible interactions of DC3000 with tomato and Nicotiana spp ., respectively, result in plant cell death, but the HR cell death occurs more rapidly and is associated with effective plant defense. Both interactions require the Hrp (HR and pathogenicity) type III secretion system (TTSS), which injects Hop (Hrp outer protein) effectors into plant cells. Here, we demonstrate that HopPtoN is translocated into tomato cells via the Hrp TTSS. A hopPtoN mutant produced eightfold more necrotic 'speck' lesions on tomato leaves than did DC3000, but the mutant and the wild-type strain grew to the same level in infected leaves. In non-host N. tabacum leaves, the hopPtoN mutant produced more cell death, whereas a DC3000 strain overexpressing HopPtoN produced less cell death and associated electrolyte leakage in comparison with wild-type DC3000. Transient expression of HopPtoN via infection with a PVX viral vector enabled tomato and N. benthamiana plants to tolerate, with reduced disease lesions, challenge infections with DC3000 and P. syringae pv. tabaci 11528, respectively. HopPtoN showed cysteine protease activity in vitro , and hopPtoN mutants altered in the predicted cysteine protease catalytic triad (C172S, H283A and D299A) lost HR suppression activity. These observations reveal that HopPtoN is a TTSS effector that can suppress plant cell death events in both compatible and incompatible interactions.

Ralstonia solanacearum requires F-box-like domain-containing type III effectors to promote disease on several host plants

“…Interestingly, even though GRS447 does not induce a wilting phenotype on Arabidopsis, this mutant can colonize the plant similarly to the wild-type strain, indicating that symptoms and bacterial internal growth could be dissociated. This observation has already been reported to be the case for two P. syringae T3SS effectors (43,44). For R. solanaceraum, development of wilt symptoms is directly associated with the obstruction of the xylem vessels by the exopolysaccharides (EPS) produced by the bacteria.…”

Genetic disassembly and combinatorial reassembly identify a minimal functional repertoire of type III effectors in Pseudomonas syringae

“…HopAA1-1 elicits cell death when expressed in yeast and plant cells (25). HopN1 is a cysteine protease that can suppress ETI-associated cell death (27). How these few T3Es function together to form a minimal repertoire may be complex, because T3Es can have multiple domains and interfering activities.…”

XopD SUMO Protease Affects Host Transcription, Promotes Pathogen Growth, and Delays Symptom Development inXanthomonas-Infected Tomato Leaves

“…The mechanisms by which HopN1 suppresses symptom production were not investigated. However, it was shown that HopN1 has Cys protease activity in vitro characteristic of papain-like enzymes, suggesting that it might cleave specific host targets associated with defense (Ló pez- Solanilla et al, 2004).…”