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--- bacteria:t3e:avrbs1 [2023/02/17 16:13] – [AvrBs1] rkoebnik
+++ bacteria:t3e:avrbs1 [2025/02/17 22:34] (current) – jfpothier
@@ Line 1: / Line 1: @@
-====== AvrBs1 ======
+====== The Type III Effector AvrBs1 from //Xanthomonas// ======
 Author: [[https://www.researchgate.net/profile/Mariya_Stoyanova|Mariya Stoyanova]]\\
-Internal reviewer: Yael Helman\\
+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)\\
-GenBank ID: [[https://www.ncbi.nlm.nih.gov/protein/CAJ19916.1|CAJ19916.1]] (445 aa)\\
+GenBank ID: [[https://www.ncbi.nlm.nih.gov/protein/P19520.1|P19520.1]] (445 aa)\\
 RefSeq ID: [[https://www.ncbi.nlm.nih.gov/protein/WP_011037255.1|WP_011037255.1]] (445 aa)\\
 D structure: [[https://swissmodel.expasy.org/repository/uniprot/Q3C000|Q3C000_XANC5]] (homology model)
@@ 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 (Ronald & Staskawicz, 1988; Swanson //et al.//, 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 22: / Line 21: @@
 === 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).
+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).
+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 ===
@@ Line 39: / Line 38: @@
 === 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> )
+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: ===
-//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), //Xylophilus ampelinus// (Nyembe, 2014).
+//Acidovorax citrulli//, //Pseudomonas amygdali// <sup>[Acc.No: [[https://www.ncbi.nlm.nih.gov/protein/EGH05685.1|EGH05685.1]]]</sup> , homolog of AvrA from //Pseudomonas syringae// pv. //glycinea// (Napoli & Staskawicz, 1987; Ronald & Staskawicz, 1988), //Xylophilus ampelinus// (Nyembe, 2014).
 ===== References =====
@@ Line 76: / Line 74: @@
 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]]
+===== Acknowledgements =====
+This fact sheet is based upon work from COST Action CA16107 EuroXanth, supported by COST (European Cooperation in Science and Technology).

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