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bacteria:t3e:xopb [2020/04/10 12:27] jfpothierbacteria:t3e:xopb [2025/01/27 22:29] (current) – [Conservation] jfpothier
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-====== XopB ======+====== The Type III Effector XopB from //Xanthomonas// ======
  
-Author: Ralf Koebnik\\ +Author: [[https://www.researchgate.net/profile/Ralf_Koebnik|Ralf Koebnik]]\\ 
-ReviewerFIXME\\ +Internal reviewer[[https://www.researchgate.net/profile/Nay_Dia|Nay C. Dia]]
-Expert reviewerFIXME+
  
 Class: XopB\\ Class: XopB\\
 Family: XopB\\ Family: XopB\\
-Prototype: XopB (//Xanthomonas euvesicatoria// pv. //euvesicatoria// aka //Xanthomonas campestris// pv. //vescicatoria//; strain 85-10)\\+Prototype: XCV0581 (//Xanthomonas euvesicatoria// pv. //euvesicatoria//, ex //Xanthomonas campestris// pv. //vesicatoria//; strain 85-10)\\ 
 +GenBank ID: [[https://www.ncbi.nlm.nih.gov/protein/CAJ22212.1|CAJ22212.1]] (613 aa)\\
 RefSeq ID: [[https://www.ncbi.nlm.nih.gov/protein/WP_039417318.1|WP_039417318.1]] (515 aa)\\ RefSeq ID: [[https://www.ncbi.nlm.nih.gov/protein/WP_039417318.1|WP_039417318.1]] (515 aa)\\
 3D structure: Unknown 3D structure: Unknown
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 === How discovered? === === How discovered? ===
-XopB was discovered in a cDNA-AFLP screen (Noël //et al.//, 2001). 
  
 +XopB was discovered in a cDNA-AFLP screen (Noël //et al.//, 2001).
 === (Experimental) evidence for being a T3E === === (Experimental) evidence for being a T3E ===
-A chimeric protein consisting of a C-terminally truncated XopB where the last 52 residues (5 kDa) were replaced by the triple c-myc epitope (5 kDa) was secreted into culture supernatants of a strain with a constitutively active form of //hrpG// in a type III secretion-dependent manner (Noël //et al.//, 2001). XopB belongs to translocation class B (Schulze //et al.//, 2012). Mutation studies of a putative translocation motif (TrM) showed that the proline/arginine-rich motif is required for efficient type III-dependent secretion and translocation of XopB and determines the dependence of XopB transport on the general T3S chaperone HpaB (Prochaska //et al.//, 2018). 
  
 +A chimeric protein consisting of a C-terminally truncated XopB where the last 52 residues (5 kDa) were replaced by the triple c-myc epitope (5 kDa) was secreted into culture supernatants of a strain with a constitutively active form of //hrpG// in a type III secretion-dependent manner (Noël //et al.//, 2001). XopB belongs to translocation class B (Schulze //et al.//, 2012). Mutation studies of a putative translocation motif (TrM) showed that the proline/arginine-rich motif is required for efficient type III-dependent secretion and translocation of XopB and determines the dependence of XopB transport on the general T3S chaperone HpaB (Prochaska //et al.//, 2018).
 === Regulation === === Regulation ===
-The //xopB// gene was shown to be expressed in a //hrpG//- and //hrpX//-dependent manner (Noël //et al.//, 2001). Presence of a PIP and ‐10 box (TTCGB‐N<sub>15</sub>‐TTCGB‐N<sub>30–32</sub>‐YANNNT) (Schulze //et al.//, 2012). 
  
 +The //xopB// gene was shown to be expressed in a //hrpG//- and //hrpX//-dependent manner (Noël //et al.//, 2001). Presence of a PIP and ‐10 box (TTCGB‐N<sub>15</sub> ‐TTCGB‐N<sub>30–32</sub> ‐YANNNT) (Schulze //et al.//, 2012).
 === Phenotypes === === Phenotypes ===
 +
 A deletion of //xopB// did not affect pathogenicity or bacterial growth in plants (Noël //et al.//, 2001). Later it was found that XopB contributes to disease symptoms and bacterial growth (Schulze //et al.//, 2012; Priller //et al.//, 2016). Infection of susceptible pepper plants with a strain lacking //xopB// resulted in increased formation of salicylic acid (SA) and expression of pathogenesis-related (PR) genes (Priller //et al.//, 2016). When expressed in yeast, XopB attenuated cell proliferation (Salomon //et al.//, 2011). XopB caused a fast and confluent cell death when transiently expressed in the non-host //Nicotiana benthamiana// leaves, whereas its expression in host tomato leaves did not result in a visible phenotype, even seven days after agroinfiltration (Salomon //et al.//, 2011). XopB suppresses pathogen‐associated molecular pattern (PAMP)‐triggered plant defense gene expression and inhibits cell death reactions induced by different T3Es, thus suppressing defense responses related to both PAMP‐triggered immunity (PTI) and effector‐triggered immunity (ETI) (Schulze //et al.//, 2012). For instance, XopB inhibited the flg22-triggered burst of reactive oxygen species (ROS) (Priller //et al.//, 2016). Interestingly, a XopB point mutant derivative was defective in the suppression of ETI‐related responses, but still interfered with vesicle trafficking and was only slightly affected with regard to the suppression of defense gene induction, suggesting that XopB‐mediated suppression of PTI and ETI is dependent on different mechanisms that can be functionally separated (Schulze //et al.//, 2012). A deletion of //xopB// caused a prominent increase in cell wall-bound invertase activity, which might be linked to defense responses because an increase in the apoplastic hexose-to-sucrose ratio has been suggested to strengthen plant defense (Sonnewald //et al.//, 2012). Expression of //xopB// in //Arabidopsis thaliana// promoted the growth of the virulent //Pseudomonas syringae// pv. //tomato// DC3000 strain, which was paralleled by a decreased salicylic acid (SA)-pool and a lower induction of SA-dependent pathogenicity-related (PR) gene expression (Priller //et al.//, 2016). A deletion of //xopB// did not affect pathogenicity or bacterial growth in plants (Noël //et al.//, 2001). Later it was found that XopB contributes to disease symptoms and bacterial growth (Schulze //et al.//, 2012; Priller //et al.//, 2016). Infection of susceptible pepper plants with a strain lacking //xopB// resulted in increased formation of salicylic acid (SA) and expression of pathogenesis-related (PR) genes (Priller //et al.//, 2016). When expressed in yeast, XopB attenuated cell proliferation (Salomon //et al.//, 2011). XopB caused a fast and confluent cell death when transiently expressed in the non-host //Nicotiana benthamiana// leaves, whereas its expression in host tomato leaves did not result in a visible phenotype, even seven days after agroinfiltration (Salomon //et al.//, 2011). XopB suppresses pathogen‐associated molecular pattern (PAMP)‐triggered plant defense gene expression and inhibits cell death reactions induced by different T3Es, thus suppressing defense responses related to both PAMP‐triggered immunity (PTI) and effector‐triggered immunity (ETI) (Schulze //et al.//, 2012). For instance, XopB inhibited the flg22-triggered burst of reactive oxygen species (ROS) (Priller //et al.//, 2016). Interestingly, a XopB point mutant derivative was defective in the suppression of ETI‐related responses, but still interfered with vesicle trafficking and was only slightly affected with regard to the suppression of defense gene induction, suggesting that XopB‐mediated suppression of PTI and ETI is dependent on different mechanisms that can be functionally separated (Schulze //et al.//, 2012). A deletion of //xopB// caused a prominent increase in cell wall-bound invertase activity, which might be linked to defense responses because an increase in the apoplastic hexose-to-sucrose ratio has been suggested to strengthen plant defense (Sonnewald //et al.//, 2012). Expression of //xopB// in //Arabidopsis thaliana// promoted the growth of the virulent //Pseudomonas syringae// pv. //tomato// DC3000 strain, which was paralleled by a decreased salicylic acid (SA)-pool and a lower induction of SA-dependent pathogenicity-related (PR) gene expression (Priller //et al.//, 2016).
 +=== Localization ===
  
-=== Localisation === +XopB localizes to the Golgi apparatus and cytoplasm of the plant cell and interferes with eukaryotic vesicle trafficking (Schulze //et al.//, 2012). Interestingly, a short ORF is found between the PIP box/-10 promoter region and the predicted translation start codon of //xopB// in Xcv<sub>85-10</sub>, which encodes a 25-aa peptide (MGLCSSKPRVQAQLNIMRPRHRAD) with a strong palmitoylation signal (Koebnik, unpublished). Whether this peptide once belonged to XopB or to another candidate effector, if at all, remains unknown.
-XopB localizes to the Golgi apparatus and cytoplasm of the plant cell and interferes with eukaryotic vesicle trafficking (Schulze //et al.//, 2012). +
 === Enzymatic function === === Enzymatic function ===
 +
 Unknown. Unknown.
  
 === Interaction partners === === Interaction partners ===
 +
 Unknown. Unknown.
  
-===== Conservation ===== +===== Conservation =====
  
-=== In xanthomonads ===  +=== In xanthomonads ===
-Yes (e.g., //X. fragariae//, //X. gardneri//, //X. oryzae//, //X. vasicola//) (Harrison //et al.//, 2014).+
  
 +Yes (//e.g.//, //X. fragariae//, //X. cynarae// pv. //gardneri// (syn. //X. gardneri//), //X. oryzae//, //X. vasicola//) (Harrison //et al.//, 2014).
 === In other plant pathogens/symbionts === === In other plant pathogens/symbionts ===
-Yes (e.g., //Pseudomonas// spp., //Ralstonia solanacearum//, //Acidovorax// spp., //Pantoea agglomerans//) (Schulze //et al.//, 2012). 
  
-===== References ===== +Yes (//e.g.//, //Pseudomonas// spp., //Ralstonia solanacearum//, //Acidovorax// spp., //Pantoea agglomerans//) (Schulze //et al.//, 2012). 
 +===== References ===== 
 + 
 +Harrison J, Studholme DJ (2014). Draft genome sequence of //Xanthomonas axonopodis// pathovar //vasculorum// NCPPB 900. FEMS Microbiol. Lett. 360: 113-116. DOI: [[https://doi.org/10.1111/1574-6968.12607|10.1111/1574-6968.12607]] 
 + 
 +Noël L, Thieme F, Nennstiel D, Bonas U (2001). cDNA-AFLP analysis unravels a genome-wide //hrpG//-regulon in the plant pathogen //Xanthomonas campestris// pv. //vesicatoria//. Mol. Microbiol. 41: 1271-1281. DOI: [[https://doi.org/10.1046/j.1365-2958.2001.02567.x|10.1046/j.1365-2958.2001.02567.x]]
  
-Harrison JStudholme DJ (2014). Draft genome sequence of //Xanthomonas axonopodis// pathovar //vasculorum// NCPPB 900FEMS Microbiol. Lett. 360(2)113-116. DOI: [[https://doi.org/10.1111/1574-6968.12607|10.1111/1574-6968.12607]].+Priller JPRReid S, Konein P, Dietrich P, Sonnewald S (2016). The //Xanthomonas campestris// pv. //vesicatoria// type-3 effector XopB inhibits plant defence responses by interfering with ROS productionPLoS One 11e0159107. DOI: [[https://doi.org/10.1371/journal.pone.0159107|10.1371/journal.pone.0159107]]
  
-Noël L, Thieme FNennstiel D, Bonas U (2001). cDNA-AFLP analysis unravels a genome-wide //hrpG//-regulon in the plant pathogen //Xanthomonas campestris// pv. //vesicatoria//. Mol. Microbiol41(6)1271-1281. DOI: [[https://doi.org/10.1046/j.1365-2958.2001.02567.x|10.1046/j.1365-2958.2001.02567.x]].+Prochaska H, Thieme SDaum S, Grau J, Schmidtke C, Hallensleben M, John P, Bacia K, Bonas U (2018). A conserved motif promotes HpaB-regulated export of type III effectors from //Xanthomonas//. Mol. Plant Pathol192473-2487. DOI: [[https://doi.org/10.1111/mpp.12725|10.1111/mpp.12725]]
  
-Priller JPReid S, Konein P, Dietrich P, Sonnewald S (2016). The //Xanthomonas campestris// pv. //vesicatoria// type-3 effector XopB inhibits plant defence responses by interfering with ROS productionPLoS One 11(7)e0159107. DOI: [[https://doi.org/10.1371/journal.pone.0159107|10.1371/journal.pone.0159107]].+Salomon DDar D, Sreeramulu S, Sessa G (2011). Expression of //Xanthomonas campestris// pv. //vesicatoria// type III effectors in yeast affects cell growth and viabilityMol. Plant Microbe Interact. 24305-314. DOI: [[https://doi.org/10.1094/MPMI-09-10-0196|10.1094/MPMI-09-10-0196]]
  
-Prochaska H, Thieme S, Daum S, Grau J, Schmidtke CHallensleben MJohn PBacia K, Bonas U (2018). A conserved motif promotes HpaB-regulated export of type III effectors from //Xanthomonas//MolPlant Pathol. 19(11)2473-2487. DOI: [[https://doi.org/10.1111/mpp.12725|10.1111/mpp.12725]].+Schulze S, Kay S, Büttner D, Egler M, Eschen-Lippold L, Hause G, Krüger A, Lee J, Müller OScheel DSzczesny RThieme F, Bonas U (2012). Analysis of new type III effectors from //Xanthomonas// uncovers XopB and XopS as suppressors of plant immunityNew Phytol195894-911. DOI: [[https://doi.org/10.1111/j.1469-8137.2012.04210.x|10.1111/j.1469-8137.2012.04210.x]]
  
-Salomon DDar DSreeramulu S, Sessa G (2011). Expression of //Xanthomonas campestris// pv. //vesicatoria// type III effectors in yeast affects cell growth and viabilityMol. Plant Microbe Interact. 24(3)305-314. DOI: [[https://doi.org/10.1094/MPMI-09-10-0196|10.1094/MPMI-09-10-0196]].+Sonnewald S, Priller JPR, Schuster J, Glickmann EHajirezaei MRSiebig S, Mudgett MB, Sonnewald U (2012). Regulation of cell wall-bound invertase in pepper leaves by //Xanthomonas campestris// pv. //vesicatoria// type three effectors. PLoS One 7e51763. DOI: [[https://doi.org/10.1371/journal.pone.0051763|10.1371/journal.pone.0051763]]
  
-Schulze S, Kay S, Büttner D, Egler M, Eschen-Lippold L, Hause G, Krüger A, Lee J, Müller O, Scheel D, Szczesny R, Thieme F, Bonas U (2012). Analysis of new type III effectors from //Xanthomonas// uncovers XopB and XopS as suppressors of plant immunity. New Phytol. 195(4): 894-911. DOI: [[https://doi.org/10.1111/j.1469-8137.2012.04210.x|10.1111/j.1469-8137.2012.04210.x]].+===== Acknowledgements =====
  
-Sonnewald SPriller JP, Schuster J, Glickmann E, Hajirezaei MR, Siebig S, Mudgett MB, Sonnewald U (2012). Regulation of cell wall-bound invertase in pepper leaves by //Xanthomonas campestris// pv. //vesicatoria// type three effectors. PLoS One 7(12): e51763. DOI: [[https://doi.org/10.1371/journal.pone.0051763|10.1371/journal.pone.0051763]].+This fact sheet is based upon work from COST Action CA16107 EuroXanthsupported by COST (European Cooperation in Science and Technology).
  
bacteria/t3e/xopb.1586518045.txt.gz · Last modified: 2023/01/09 10:20 (external edit)