====== AvrBs1 ======

Author: [[https://www.researchgate.net/profile/Mariya_Stoyanova|Mariya Stoyanova]]\\
Internal reviewer: Yael Helman\\
Expert reviewer: FIXME

Class: AvrBs1\\
Family: AvrBs1\\
Prototype: AvrBs1 (//Xanthomonas euvesicatoria// pv. //euvesicatoria//, ex //Xanthomonas campestris// pv. //vesicatoria//; strain E3) (Swanson //et al.//, 1988)\\
RefSeq ID: [[https://www.ebi.ac.uk/ena/browser/view/CAJ19916|CAJ19916.1]] (445 aa)\\
3D structure: [[https://swissmodel.expasy.org/repository/uniprot/Q3C000|Q3C000_XANC5]] (homology model)

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

=== How discovered? ===

Dahlbeck and Stall (1979) demonstrated that pepper race 2 strains of //X//. //campestris// pv. //vesicatoria// (//Xcv//) spontaneously mutate from avirulence to virulence (race 1) at a high frequency (4×10<sup>-4</sup>  per cell per division) when inoculated into a pepper cultivar containing the //Bs1// locus. Later, avirulence loci were found to be located in a plasmid during trials to transmit the copper resistence loci by conjugation (Stall //et al.//, 1986). In further studies an avirulence gene in race 2 strains was cloned and molecularly characterized by restriction enzyme mapping, subcloning and deletion analysis. The gene, //avrBs1,// was localized to a 5.3-kb fragment of DNA, located in the self-transmissible copper resistance plasmid pXvCu1. A single cosmid clone, pXv2000, was identified to specifically convert virulent race 1 isolates of //Xcv// to avirulence when inoculated into the pepper cultivar ECW10R containing the dominant resistance gene //Bs1//. It was demonstrated that the cloned wild type avirulence gene //avrBs1//, which encodes encodes a 50-kD protein, can complement race 2 spontaneous race-change mutants (Ronald & Staskawicz, 1988; Swanson //et al.//, 1988).
=== (Experimental) evidence for being a T3E ===

Epitope tagged AvrBs1 proteins were detected in culture supernatants only in the presence of a functional type III apparatus and not in a //hrcV// mutant, showing that the AvrBs1 proteins are secreted by //Xcv// in an //hrp//-dependent manner (Escolar //et al.//, 2001).
=== Regulation ===

In 2001, in tests whether //avrBs1// promoter activity depends on the //hrp// regulatory genes, //hrpG// and //hrpX//, promoter constructs containing only avrBs1 ORF2 were conjugated into wild-type Xcv race 2 strains deleted in //hrpX// or //hrpG//. The mutations did not significantly alter the GUS activity, indicating that //avrBs1// expression is not under the control of these hrp gene regulators (Escolar //et al.//, 2001). However, gene expression analysis using β-glucuronidase as reporter in another study in 2006 showed 7.3-fold reduction in GUS activity indicating that //avrBs1// was regulated by hrpG (Rongqi //et al.//, 2006). In 2010 it was reported that AvrBsT suppresses AvrBs1-elicited HR from X. //campestris// pv. //vesicatoria// in resistant pepper plants. HR suppression occurs inside the plant cell and depends on a conserved predicted catalytic residue of AvrBsT (Szczesny //et al.//, 2010).
=== Phenotypes ===

AvrBs1 specifies avirulence on pepper cultivars containing the resistance gene Bs1 observed as hypersensitive response (HR) induction (Ronald & Staskawicz, 1988). Transient expression of avrBs1 and avrBsT in resistant host plants using //Agrobacterium tumefaciens//-mediated gene transfer resulted in the induction of a specific HR (Escolar //et al.//, 2001). Studies with expression of //avrBs1// in //N. benthamiana// showed a decrease in the starch content in chloroplasts and an increased number of vesicles, indicating an enlargement of the central vacuole and the cell wall. These changes resulted in a swelling of the upper epidermis and bloating of the palisade cells in the mesophyll, thus changing their shape and leading to a decrease in the intercellular spaces. A significant increase in ion leakage, as well as dead cells in //avrBs1//-expressing tissue were also detected. Macroscopically, chlorosis and weak necrotic reactions in //N. benthamiana// were observed (Gürlebeck //et al.//, 2009).
=== Localization ===

AvrBs1-GFP localizes exclusively to the cytoplasm of the plant cells (Gürlebeck //et al.//, 2009).
=== Enzymatic function ===

Unknown. It was found that AvrBs1 suppresses the activation of the high osmolarity glycerol (HOG) MAP kinase pathway in yeast, suggesting that this effector targets a signaling component that is conserved in eukaryotic organisms (Teper //et al.//, 2015).
=== Interaction partners ===

Gene silencing experiments revealed that SNF1-related kinase 1 (SnRK1) is required for the induction of the AvrBs1-specific HR. It was speculated that SnRK1 is involved in the AvrBsT-mediated suppression of the AvrBs1-specific HR (Szczesny //et al.//, 2010).
===== Conservation =====

=== In xanthomonads: ===

Yes (//X//. //campestris// pv. //campestris// (Ronald & Staskawicz, 1988), //X//. //campestris// pv. //vitians// (Ronald & Staskawicz, 1988), //X//. //arboricola// pv//. juglandis// <sup>[Acc.No: [[https://www.ncbi.nlm.nih.gov/protein/SYZ61276.1|SYZ61276.1]]] </sup> )

=== In other plant pathogens/symbionts: ===

//Xylophilus ampelinus// (Nyembe, 2014), //Acidovorax citrulli//, //Pseudomonas amygdali// <sup> </sup>  <sup>[Acc.No: [[https://www.ncbi.nlm.nih.gov/protein/EGH05685.1|EGH05685.1]]]</sup>  <sup> </sup>  ,<sup> </sup>  homolog of AvrA from //Pseudomonas syringae// pv. //glycinea// (Napoli & Staskawicz, 1987; Ronald & Staskawicz, 1988).
===== References =====

Dahlbeck D, Stall RE (1979). Mutations for change of race in cultures of //Xanthomonas vesicatoria//. Phytopathology 69: 634-636. DOI: [[https://doi.org/10.1094/Phyto-69-634|10.1094/Phyto-69-634]]

Escolar L, Van Den Ackerveken G, Pieplow S, Rossier O, Bonas U (2001). Type III secretion and //in planta// recognition of the //Xanthomonas// avirulence proteins AvrBs1 and AvrBsT. Mol. Plant Pathol. 2: 287-296. DOI: [[https://doi.org/10.1046/j.1464-6722.2001.00077.x|10.1046/j.1464-6722.2001.00077.x]]

Gürlebeck D, Jahn S, Gürlebeck N, Szczesny R, Szurek B, Hahn S, Hause G, Bonas U (2009). Visualization of novel virulence activities of the //Xanthomonas// type III effectors AvrBs1, AvrBs3 and AvrBs4. Mol. Plant Pathol. 10: 175-188. DOI: [[https://doi.org/10.1111/j.1364-3703.2008.00519.x|10.1111/j.1364-3703.2008.00519.x]]

Napoli C, Staskawicz BJ (1987). Molecular characterization of an avirulence gene from race 6 of //Pseudomonas syringae// pv. //glycinea//. J. Bacteriol. 169: 572-578. DOI: [[https://doi.org/10.1128/jb.169.2.572-578.1987|10.1128/jb.169.2.572-578.1987]]

Nyembe NPP (2014). Development of a reporter system for the analysis of //Xylophilus ampelinus// type III secreted effectors. Doctoral Thesis, University of the Western Cape, South Africa. PDF: [[https://etd.uwc.ac.za/handle/11394/4325|etd.uwc.ac.za/handle/11394/4325]]

Ronald PC, Staskawicz BJ (1988). The avirulence gene //avrBs1// from //Xanthomonas campestris// pv. //vesicatoria// encodes a 50-kD protein. Mol. Plant Microbe Interact. 1: 191-198. DOI: [[https://doi.org/10.1094/MPMI-1-191|10.1094/MPMI-1-191]]

Rongqi X, Xianzhen L, Hongyu W, Bole J, Kai L, Yongqiang H, Jiaxun F, Jiliang T (2006). Regulation of eight avr by hrpG and hrpX in //Xanthomonas campestris// pv. //campestris// and their role in pathogenicity. Progress in Natural Science 16: 1288-1294. DOI: [[https://doi.org/10.1080/10020070612330143|10.1080/10020070612330143]]

Stall RE, Loschke DC, Jones JB (1986). Linkage of copper resistance and avirulence loci on a self-transmissible plasmid in //Xanthomonas campestris// pv. //vesicatoria//. Phytopathology 76: 240-243. DOI: [[https://doi.org/10.1094/Phyto-76-240|10.1094/Phyto-76-240]]

Swanson J, Kearney B, Dahlbeck D, Staskawicz B (1988). Cloned avirulence gene of //Xanthomonas campestris// pv. //vesicatoria// complements spontaneous race-change mutants. Mol. Plant Microb. Interact. 1: 5-9. DOI: [[https://doi.org/10.1094/MPMI-1-005|10.1094/MPMI-1-005]]

Szczesny R, Büttner D, Escolar L, Schulze S, Seiferth A, Bonas U (2010). Suppression of the AvrBs1-specific hypersensitive response by the YopJ effector homolog AvrBsT from //Xanthomonas// depends on a SNF1-related kinase. New Phytol. 187: 1058-1074. DOI: [[https://doi.org/10.1111/j.1469-8137.2010.03346.x|10.1111/j.1469-8137.2010.03346.x]]

Teper D, Sunitha S, Martin GB, Sessa G (2015). Five //Xanthomonas// type III effectors suppress cell death induced by components of immunity associated MAP kinase cascades. Plant Signal. Behav. 10: e1064573. DOI: [[https://doi.org/10.1080/15592324.2015.1064573|10.1080/15592324.2015.1064573]]

Thieme F, Koebnik R, Bekel T, Berger C, Boch J, Büttner D, Caldana C, Gaigalat L, Goesmann A, Kay S, Kirchner O, Lanz C, Linke B, McHardy AC, Meyer F, Mittenhuber G, Nies DH, Niesbach-Klösgen U, Patschkowski T, Ruckert C, Rupp O, Schneiker S, Schuster SC, Vorhölter FJ, Weber E, Pühler A, Bonas U, Bartels D, Kaiser O (2005). Insights into genome plasticity and pathogenicity of the plant pathogenic bacterium //Xanthomonas campestris// pv. //vesicatoria// revealed by the complete genome sequence. J. Bacteriol. 187: 7254-7266. [[https://dx.doi.org/10.1128/JB.187.21.7254-7266.2005|10.1128/JB.187.21.7254-7266.2005]]

===== Further reading =====

Kearney B, Staskawicz BJ (1990). Characterization of IS//476// and its role in bacterial spot disease of tomato and pepper. J. Bacteriol. 172: 143-148. DOI: [[https://doi.org/10.1128/jb.172.1.143-148.1990|10.1128/jb.172.1.143-148.1990]]. Erratum in: J. Bacteriol. (1990) 172: 2199.

O'Garro LW, Gibbs H, Newton A (1997). Mutation in the //avrBs1// avirulence gene of //Xanthomonas campestris// pv. //vesicatoria// influences survival of the bacterium in soil and detached leaf tissue. Phytopathology 87: 960-966. DOI: [[https://doi.org/10.1094/PHYTO.1997.87.9.960|10.1094/PHYTO.1997.87.9.960]]