====== The Type III Effector XopAA from //Xanthomonas// ======

Author: [[https://www.researchgate.net/profile/Ralf-Koebnik|Ralf Koebnik]]

Class: XopAA\\
Family: XopAA\\
Prototype: Ecf (//Xanthomonas euvesicatoria// pv. //euvesicatoria//, ex //Xanthomonas campestris// pv. //vesicatoria//; strain 75-3)\\
GenBank ID: [[https://www.ncbi.nlm.nih.gov/protein/AAW88576.1|AAW88576.1]] (688 aa)\\
RefSeq ID: [[https://www.ncbi.nlm.nih.gov/protein/WP_041855088.1|WP_041855088.1]] (688 aa)\\
Synonym: Ecf (early chlorosis factor)\\
3D structure: Unknown

===== Biological function =====

=== How discovered? ===

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).
=== (Experimental) evidence for being a T3E ===

Although //Xee// <sub>75-3</sub> 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).
=== Regulation ===

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).
=== Phenotypes ===

Transgenic rice plants expressing XopAA//<sub>Xoo</sub>// 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 XopAA<sub>//Xoo//</sub> 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 XopAA<sub>//Xoo//</sub> 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).
=== Localization ===

Unknown.

=== Enzymatic function ===

Unknown.

=== Interaction partners ===

A yeast two-hybrid experiment indicated that XopAA<sub>//Xoo//</sub> 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).

===== Conservation =====

=== In xanthomonads ===

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//.
=== In other plant pathogens/symbionts ===

Yes (//Mesorhizobium//). Weak homology (ca 25% sequence identity) to proteins in //Erwinia// and //Pseudomonas// (HopAE1/HopW family)

===== References =====

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: [[https://doi.org/10.1094/MPMI-10-14-0314-R|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: [[https://doi.org/10.1094/MPMI-18-0477|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: [[https://doi.org/10.1271/bbb.120929|10.1271/bbb.120929]]