Differences

This shows you the differences between two versions of the page.

--- bacteria:t3e:xopb [2019/09/05 22:53] – external edit 127.0.0.1
+++ bacteria:t3e:xopb [2025/01/27 22:29] (current) – [Conservation] jfpothier
@@ Line 1: / Line 1: @@
-Author: Ralf Koebnik
+====== The Type III Effector XopB from //Xanthomonas// ======
+Author: [[https://www.researchgate.net/profile/Ralf_Koebnik|Ralf Koebnik]]\\
+Internal reviewer: [[https://www.researchgate.net/profile/Nay_Dia|Nay C. Dia]]
 Class: 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)\\
 D structure: Unknown
-**Biological function**
+===== Biological function =====
+=== How discovered? ===
+XopB was discovered in a cDNA-AFLP screen (Noël //et al.//, 2001).
+=== (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).
+=== 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).
+=== 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).
+=== Localization ===
+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.
+=== Enzymatic function ===
+Unknown.
+=== Interaction partners ===
-//How discovered?// XopB was discovered in a cDNA-AFLP screen.<sup>[1]</sup>
+Unknown.
-//(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.<sup>[1]</sup> XopB belongs to translocation class B.<sup>[3]</sup> 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.<sup>[7]</sup>
+===== Conservation =====
-//Regulation:// The //xopB// gene was shown to be expressed in a //hrpG//- and //hrpX//-dependent manner.<sup>[1]</sup> Presence of a PIP and ‐10 box (TTCGB‐N<sub>15</sub>‐TTCGB‐N<sub>30–32</sub>‐YANNNT).<sup>[3]</sup>
+=== In xanthomonads ===
-//Phenotypes:// A deletion of //xopB// did not affect pathogenicity or bacterial growth in plants.<sup>[1]</sup> Later it was found that XopB contributes to disease symptoms and bacterial growth.<sup>[3,6]</sup> 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.<sup>[6]</sup>
+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 ===
-When expressed in yeast, XopB attenuated cell proliferation.<sup>[2]</sup> XopB caused a fast and confluent cell death when transiently expressed in the nonhost //Nicotiana benthamiana// leaves, whereas its expression in host tomato leaves did not result in a visible phenotype, even 7 days after agroinfiltration.<sup>[2]</sup> 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).<sup>[3]</sup> For instance, XopB inhibited the flg22-triggered burst of reactive oxygen species (ROS).<sup>[6]</sup> 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.<sup>[3]</sup> 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.<sup>[4]</sup> 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.<sup>[6]</sup>
+Yes (//e.g.//, //Pseudomonas// spp., //Ralstonia solanacearum//, //Acidovorax// spp., //Pantoea agglomerans//) (Schulze //et al.//, 2012).
+===== References =====
-//Localisation:// XopB localizes to the Golgi apparatus and cytoplasm of the plant cell and interferes with eukaryotic vesicle trafficking.<sup>[3]</sup>
+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]]
-//Enzymatic function:// Unknown
+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]]
-//Interaction partners:// Unknown
+Priller JPR, Reid 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 production. PLoS One 11: e0159107. DOI: [[https://doi.org/10.1371/journal.pone.0159107|10.1371/journal.pone.0159107]]
-**Conservation**
+Prochaska H, Thieme S, Daum 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 Pathol. 19: 2473-2487. DOI: [[https://doi.org/10.1111/mpp.12725|10.1111/mpp.12725]]
-//In xanthomonads:// Yes (e.g., //X. fragariae//, //X. gardneri//, //X. oryzae//, //X. vasicola//)<sup>[5]</sup>
+Salomon D, Dar D, Sreeramulu S, Sessa G (2011). Expression of //Xanthomonas campestris// pv. //vesicatoria// type III effectors in yeast affects cell growth and viability. Mol. Plant Microbe Interact. 24: 305-314. DOI: [[https://doi.org/10.1094/MPMI-09-10-0196|10.1094/MPMI-09-10-0196]]
-//In other plant pathogens/symbionts:// Yes (e.g., //Pseudomonas// spp., //Ralstonia solanacearum//, //Acidovorax// spp., //Pantoea agglomerans//)<sup>[3]</sup>
+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: 894-911. DOI: [[https://doi.org/10.1111/j.1469-8137.2012.04210.x|10.1111/j.1469-8137.2012.04210.x]]
-**References**
+Sonnewald S, Priller JPR, 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: e51763. DOI: [[https://doi.org/10.1371/journal.pone.0051763|10.1371/journal.pone.0051763]]
-  - 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(6): 1271-1281. doi: [[https://doi.org/10.1046/j.1365-2958.2001.02567.x|10.1046/j.1365-2958.2001.02567.x]].
+===== Acknowledgements =====
-  - Salomon D, Dar D, Sreeramulu S, Sessa G (2011). Expression of //Xanthomonas campestris// pv. //vesicatoria// type III effectors in yeast affects cell growth and viability. Mol. Plant Microbe Interact. 24(3): 305-314. doi: [[https://doi.org/10.1094/MPMI-09-10-0196|10.1094/MPMI-09-10-0196]].
-  - 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]].
-  - Sonnewald S, Priller 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]].
-  - Harrison J, Studholme DJ (2014). Draft genome sequence of //Xanthomonas axonopodis// pathovar //vasculorum// NCPPB 900. FEMS Microbiol. Lett. 360(2): 113-116. doi: [[https://doi.org/10.1111/1574-6968.12607|10.1111/1574-6968.12607]].
-  - Priller JP, Reid 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 production. PLoS One 11(7): e0159107. doi: [[https://doi.org/10.1371/journal.pone.0159107|10.1371/journal.pone.0159107]].
-  - Prochaska H, Thieme S, Daum 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 Pathol. 19(11): 2473-2487. doi: [[https://doi.org/10.1111/mpp.12725|10.1111/mpp.12725]].
+This fact sheet is based upon work from COST Action CA16107 EuroXanth, supported by COST (European Cooperation in Science and Technology).

EuroXanth DokuWiki

User Tools

Site Tools

Differences

Page Tools