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Molecular Diagnosis and Diversity for Regulated Xanthomonas
Bacterial virulence factors
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Author: Ralf Koebnik
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Class: XopB
Family: XopB
Prototype: XopB (Xanthomonas euvesicatoria pv. euvesicatoria aka Xanthomonas campestris pv. vescicatoria; strain 85-10)
RefSeq ID: WP_039417318.1 (515 aa)
3D structure: Unknown
Biological function
How discovered? XopB was discovered in a cDNA-AFLP screen.[1]
(Experimental) evidence for being a T3E: A chimeric protein consisting of a C-terminally truncated XopB where the last 52 residues (5 kDa) were replaced by the triple c-myc epitope (5 kDa) was secreted into culture supernatants of a strain with a constitutively active form of hrpG in a type III secretion-dependent manner.[1] XopB belongs to translocation class B.[3] Mutation studies of a putative translocation motif (TrM) showed that the proline/arginine-rich motif is required for efficient type III-dependent secretion and translocation of XopB and determines the dependence of XopB transport on the general T3S chaperone HpaB.[7]
Regulation: The xopB gene was shown to be expressed in a hrpG- and hrpX-dependent manner.[1] Presence of a PIP and ‐10 box (TTCGB‐N15‐TTCGB‐N30–32‐YANNNT).[3]
Phenotypes: A deletion of xopB did not affect pathogenicity or bacterial growth in plants.[1] Later it was found that XopB contributes to disease symptoms and bacterial growth.[3,6] Infection of susceptible pepper plants with a strain lacking xopB resulted in increased formation of salicylic acid (SA) and expression of pathogenesis-related (PR) genes.[6]
When expressed in yeast, XopB attenuated cell proliferation.[2] XopB caused a fast and confluent cell death when transiently expressed in the nonhost Nicotiana benthamiana leaves, whereas its expression in host tomato leaves did not result in a visible phenotype, even 7 days after agroinfiltration.[2] XopB suppresses pathogen‐associated molecular pattern (PAMP)‐triggered plant defense gene expression and inhibits cell death reactions induced by different T3Es, thus suppressing defense responses related to both PAMP‐triggered immunity (PTI) and effector‐triggered immunity (ETI).[3] For instance, XopB inhibited the flg22-triggered burst of reactive oxygen species (ROS).[6] Interestingly, a XopB point mutant derivative was defective in the suppression of ETI‐related responses, but still interfered with vesicle trafficking and was only slightly affected with regard to the suppression of defense gene induction, suggesting that XopB‐mediated suppression of PTI and ETI is dependent on different mechanisms that can be functionally separated.[3] A deletion of xopB caused a prominent increase in cell wall-bound invertase activity, which might be linked to defense responses because an increase in the apoplastic hexose-to-sucrose ratio has been suggested to strengthen plant defense.[4] Expression of xopB in Arabidopsis thaliana promoted the growth of the virulent Pseudomonas syringae pv. tomato DC3000 strain, which was paralleled by a decreased salicylic acid (SA)-pool and a lower induction of SA-dependent pathogenicity-related (PR) gene expression.[6]
Localisation: XopB localizes to the Golgi apparatus and cytoplasm of the plant cell and interferes with eukaryotic vesicle trafficking.[3]
Enzymatic function: Unknown
Interaction partners: Unknown
Conservation
In xanthomonads: Yes (e.g., X. fragariae, X. gardneri, X. oryzae, X. vasicola)[5]
In other plant pathogens/symbionts: Yes (e.g., Pseudomonas spp., Ralstonia solanacearum, Acidovorax spp., Pantoea agglomerans)[3]
References
