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Molecular Diagnosis and Diversity for Regulated Xanthomonas
Bacterial virulence factors
This DokuWiki is based upon work from COST Action CA16107 EuroXanth, supported by COST (European Cooperation in Science and Technology)
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Author: Ralf Koebnik
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Class: XopAA
Family: XopAA
Prototype: Ecf (Xanthomonas euvesicatoria pv. euvesicatoria, ex Xanthomonas campestris pv. vesicatoria; strain 75-3)
GenBank ID: AAW88576.1 (688 aa)
RefSeq ID: WP_041855088.1 (688 aa)
Synonym: Ecf (early chlorosis factor)
3D structure: Unknown
The xopAA gene, at that time called ecf for early chlorosis factor, was identified as a novel locus from X. euvesicatoria pv. euvesicatoria (Xee) that induces early chlorosis in tomato and several nonhosts (Morales et al., 2005). To examine the factor(s) that induce(s) the response of bean to Xee tomato races, a library of DNA from Xee strain 75-3 was screened in the bean pathogen X. phaseoli pv. phaseoli strain 85-6. One cosmid clone, containing the xopAA gene, converted the host response from a normal watersoaking to a bright yellow chlorosis on bean cvs. Sprite and Bush Blue Lake (Morales et al., 2005).
Although Xee 75-3 induced chlorosis on susceptible tomato lines, none of the 75-3 hrp mutants tested induced a chlorotic response on tomato. This result suggested the possibility that XopAA is normally translocated by the Hrp T3SS into host cells (Morales et al., 2005).
Transient expression of xopAA in planta using an Agrobacterium tumefaciens-mediated expression system induced a chlorotic phenotype independent of Xanthomonas, This demonstration that xopAA induces chlorosis when directly expressed by the host cell suggested that the loss of chlorosis induction in the hrp mutants was a direct effect of preventing T3SS-dependent translocation (Morales et al., 2005).
Xanthomonas bacteria carrying a translational fusion of XopAA to the calmodulin-dependent adenylate cyclase Cya produced approximately 30 times more cAMP in tomato leaves at 8 hpi when compared to bacteria with a mutation in the T3SS gene hrcV or bacteria that harbour a recA:cya fusion. These results indicated that the xopAA gene product is translocated to host cells in a T3SS-dependent manner (Morales et al., 2005).
RT-PCR expression analyses suggested that, although translocation of XopAA is dependent on the Hrp T3SS apparatus, xopAA expression does not depend on nutritional conditions that induce hrp gene expression in Xee (Morales et al., 2005).
Transgenic rice plants expressing XopAAXoo exhibited semi-dwarfism and a reduction in Brassinolide-dependent laminar inclination, characteristics of brassinosteroid (BR)-insensitive mutants caused by mutations of the BR receptor (Yamaguchi et al., 2013).
Rice plants inoculated with a T3SS-deficient hrpX mutant of X. oryzae pv. oryzae (Xoo) did not develop disease lesions. In contrast, a transgenic rice line overexpressing xopAA showed severe lesions when inoculated with the Xoo hrpX mutant and the bacterial population of the hrpX mutant was 100-fold higher in the transgenic plants than in wild-type plants. This observation led the authors conclude that XopAAXoo inhibits resistance to Xoo, which was probably caused by suppression of host PTI (Yamaguchi et al., 2013). However, a xopAA knock-out strain of Xoo did not exhibit any defect in virulence (Yamaguchi et al., 2013).
Expression of XopAAXoo in Arabidopsis cells activated host immune responses, suggesting the presence of intracellular immune receptors that recognize XopAA (Yamaguchi et al., 2013).
Xanthomonas oryzae pv. oryzicola bacteria with a deletion of xopAA were found to cause enhanced virulence to a certain rice cultivar (Li et al., 2015).
Unknown.
Unknown.
A yeast two-hybrid experiment indicated that XopAAXoo interacted with OsBAK1, an essential component of both microbe-associated molecular patterns (MAMPs) and BR receptors, suggesting that the virulent activity of XopAA is mediated by inhibition of OsBAK1 (Yamaguchi et al., 2013).
DNA hybridization experiments had suggested that xopAA might be highly specific to Xee (Morales et al., 2005). However, genomic comparisons showed that xopAA homologs are present in other xanthomonads, such as X. hortorum, X. hydrangeae, X. oryzae, X. populi, X. translucens, and X. vasicola.
Yes (Mesorhizobium). Weak homology (ca 25% sequence identity) to proteins in Erwinia and Pseudomonas (HopAE1/HopW family)
Li S, Wang Y, Wang S, Fang A, Wang J, Liu L, Zhang K, Mao Y, Sun W (2015). The type III effector AvrBs2 in Xanthomonas oryzae pv. oryzicola suppresses rice immunity and promotes disease development. Mol. Plant Microbe Interact. 28: 869-880. DOI: 10.1094/MPMI-10-14-0314-R
Morales CQ, Posada J, Macneale E, Franklin D, Rivas I, Bravo M, Minsavage J, Stall RE, Whalen MC (2005). Functional analysis of the early chlorosis factor gene. Mol. Plant Microbe Interact. 18: 477-486. DOI: 10.1094/MPMI-18-0477
Yamaguchi K, Nakamura Y, Ishikawa K, Yoshimura Y, Tsuge S, Kawasaki T (2013). Suppression of rice immunity by Xanthomonas oryzae type III effector Xoo2875. Biosci. Biotechnol. Biochem. 77: 796-801. DOI: 10.1271/bbb.120929
