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--- bacteria:t3e:avrbs1 [2020/07/03 10:23]
rkoebnik
+++ 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// aka //Xanthomonas campestris// pv. //vescicatoria//; 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 =====
 === 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 24: / 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 36: / 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 55: / 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 61: / 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 68: / Line 68: @@
 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]]

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