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--- bacteria:t3e:avrbs1 [2020/07/08 17:51]
rkoebnik [AvrBs1]
+++ bacteria:t3e:avrbs1 [2022/05/09 11:30] (current)
rkoebnik [Further reading]
@@ Line 7: / Line 7: @@
 Class: AvrBs1\\
 Family: AvrBs1\\
-Prototype: //Xanthomonas euvesicatoria// pv. //euvesicatoria//, ex //Xanthomonas campestris// pv. //vesicatoria//; strain 85-10 (Thieme //et al.//, 2005)
+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)\\
-D structure: [[https://swissmodel.expasy.org/repository/uniprot/Q3C000|Q3C000_XANC5]] //Xanthomonas campestris// pv. //vesicatoria// (strain 85-10)
+D structure: [[https://swissmodel.expasy.org/repository/uniprot/Q3C000|Q3C000_XANC5]] (homology model)
 ===== Biological function =====
@@ Line 16: / Line 15: @@
 === 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 (Swanson //et al.//, 1988; Ronald & Staskawicz, 1988).
+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 ===
@@ Line 25: / Line 24: @@
 === 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 (Gurlebeck //et al.//, 2009).
+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 (Gurlebeck //et al.//, 2009).
+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 (Tepper //et al.//, 2015).
+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 ===
@@ Line 37: / Line 36: @@
 ===== Conservation =====
-In xanthomonads:
+=== 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> )
@@ Line 56: / Line 55: @@
 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.
+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]]
@@ Line 62: / Line 61: @@
 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.
+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]]
@@ Line 74: / Line 73: @@
 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]]
+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]]

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