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--- bacteria:t3e:xopbh [2025/05/07 08:43] – [Biological function] rkoebnik
+++ bacteria:t3e:xopbh [2025/05/07 09:45] (current) – [References] rkoebnik
@@ Line 1: / Line 1: @@
 ====== The Type III Effector XopBH from //Xanthomonas// ======
-Author: Naama Wagner\\
+Author: [[https://www.researchgate.net/profile/Naama-Wagner|Naama Wagner]]\\
 Internal reviewer: [[https://www.researchgate.net/profile/Ralf_Koebnik|Ralf Koebnik]]
 Class: XopBH\\
-Family: XopB\\
+Family: XopBH\\
-Prototype: XCV0581 (//Xanthomonas euroxanthea//, strain 85-10)\\
+Prototype: XTG_RS02340 (//Xanthomonas euroxanthea//, strain CPBF 424) Attention: The prototype sequence is too long because codons 18 to 39 overlap with the plant-inducible promoter (see below; Koebnik //et al.//, 2006).\\
-GenBank ID: [[https://www.ncbi.nlm.nih.gov/protein/CAJ22212.1|CAJ22212.1]] (613 aa)\\
+GenBank ID: [[https://www.ncbi.nlm.nih.gov/protein/CAE1133144.1|CAJ22212.1]] (286 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_212580660.1|WP_039417318.1]] (216 aa)\\
 D structure: Unknown
@@ Line 15: / Line 15: @@
 === How discovered? ===
-XopB was discovered in a cDNA-AFLP screen (Noël //et al.//, 2001).
+XopBH was discovered by a [[https://effectidor.tau.ac.il|Effectidor II]], a pan-genomic AI-based algorithm for the prediction of type III secretion system effectors (Wagner //et al.//, 2025). The //xopBH// gene of strain CPBF 424 is located near the T3SS gene cluster, next to [[:bacteria:t3e:xopz|xopZ]] and [[:bacteria:t3e:xopf|xopF]], which are all encoded between //hrpE// and //hrpF// (Huguet & Bonas, 1997; Weber //et al.//, 2005).
 === (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).
+XopBH was shown to have a functional type III secretion signal using a reporter fusion with AvrBs1 (Zhao //et al.//, 2013).
 === 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 presence of a PIP box and a properly spaced ‐10 promoter motif (TTCGB‐N<sub>15</sub> ‐TTCGB‐N<sub>30–32</sub> ‐YANNNT) suggests that the //xopBH// gene is under control of HrpG and HrpX (Wengelnik & Bonas, 1996; Wengelnik //et al.//, 1996; Koebnik //et al.//, 2006).
 === 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).
+Unknown.
 === Localization ===
@@ Line 41: / Line 42: @@
 === In xanthomonads ===
-Yes (//e.g.//, //X. fragariae//, //X. cynarae// pv. //gardneri// (syn. //X. gardneri//), //X. oryzae//, //X. vasicola//) (Harrison //et al.//, 2014).
+Yes (//e.g.//, //X. arboricola//, //X. campestris// pv. //papavericola//, //X. hortorum//).
 === In other plant pathogens/symbionts ===
-Yes (//e.g.//, //Pseudomonas// spp., //Ralstonia solanacearum//, //Acidovorax// spp., //Pantoea agglomerans//) (Schulze //et al.//, 2012).
+No.
 ===== References =====
+Huguet E, Bonas U (1997). //hrpF// of //Xanthomonas campestris// pv. //vesicatoria// encodes an 87-kDa protein with homology to NoIX of //Rhizobium fredii//. Mo.l Plant Microbe Interact. 10: 488-498. DOI: [[https://doi.org/10.1094/MPMI.1997.10.4.488|10.1094/MPMI.1997.10.4.488]]
 Koebnik R, Krüger A, Thieme F, Urban A, Bonas U (2006). Specific binding of the //Xanthomonas campestris// pv. //vesicatoria// AraC-type transcriptional activator HrpX to plant-inducible promoter boxes. J. Bacteriol. 188: 7652-7660. DOI: [[https://doi.org/10.1128/JB.00795-06|10.1128/JB.00795-06]]
 Wagner N, Baumer E, Lyubman I, Shimony Y, Bracha N, Martins L, Potnis N, Chang JH, Teper D, Koebnik R, Pupko T (2025). Effectidor II: A pan-genomic AI-based algorithm for the prediction of type III secretion system effectors. Bioinformatics, in press. DOI: [[https://doi.org/10.1093/bioinformatics/btaf272|10.1093/bioinformatics/btaf272]]
+Weber E, Ojanen-Reuhs T, Huguet E, Hause G, Romantschuk M, Korhonen TK, Bonas U, Koebnik R (2005). The type III-dependent Hrp pilus is required for productive interaction of //Xanthomonas campestris// pv. //vesicatoria// with pepper host plants. J. Bacteriol. 187: 2458-2468. DOI: [[https://doi.org/10.1128/JB.187.7.2458-2468.2005|10.1128/JB.187.7.2458-2468.2005]]
+Wengelnik K, Bonas U (1996). HrpXv, an AraC-type regulator, activates expression of five of the six loci in the hrp cluster of //Xanthomonas campestris// pv. //vesicatoria//. J. Bacteriol. 178: 3462-3469. DOI: [[https://doi.org/10.1128/jb.178.12.3462-3469.1996|10.1128/jb.178.12.3462-3469.1996]]
+Wengelnik K, Van den Ackerveken G, Bonas U (1996). HrpG, a key hrp regulatory protein of //Xanthomonas campestris// pv. //vesicatoria// is homologous to two-component response regulators. Mol. Plant Microbe Interact. 9: 704-712. DOI: [[https://doi.org/10.1094/mpmi-9-0704|10.1094/mpmi-9-0704]]
+Zhao S, Mo WL, Wu F, Tang W, Tang JL, Szurek B, Verdier V, Koebnik R, Feng JX (2013). Identification of non-TAL effectors in //Xanthomonas oryzae// pv. //oryzae// Chinese strain 13751 and analysis of their role in the bacterial virulence. World J. Microbiol. Biotechnol. 29: 733-744. DOI: [[https://doi.org/10.1007/s11274-012-1229-5|10.1007/s11274-012-1229-5]]
 ===== Acknowledgements =====

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