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--- bacteria:t3e:xops [2020/09/10 17:13] – [Conservation] rkoebnik
+++ bacteria:t3e:xops [2025/02/21 13:37] (current) – [Biological function] rkoebnik
@@ Line 1: / Line 1: @@
-====== XopS ======
+====== The Type III Effector XopS from //Xanthomonas// ======
 Author: [[https://www.researchgate.net/profile/Gabor_Rakhely|Gábor Rákheli]]\\
@@ Line 7: / Line 7: @@
 Class: XopS\\
 Family: XopS\\
-Prototype: XopS (//Xanthomonas euvesicatoria// pv. //euvesicatoria//, ex //Xanthomonas campestris// pv. //vesicatoria//; strain 85-10)\\
+Prototype: XCV0324 (//Xanthomonas euvesicatoria// pv. //euvesicatoria//, ex //Xanthomonas campestris// pv. //vesicatoria//; strain 85-10)\\
-RefSeq ID: -\\
+GenBank ID: [[https://www.ncbi.nlm.nih.gov/protein/CAJ21955.1|CAJ21955.1]] (308 aa, perhaps 5 aa too long)\\
+RefSeq ID: [[https://www.ncbi.nlm.nih.gov/protein/WP_039418869.1|WP_039418869.1]] (292 aa, perhaps 11 aa too short)\\
 D structure: Unknown
@@ Line 15: / Line 16: @@
 === How discovered? ===
-Although no homology was found between XopS and other T3E effectors, //xopS //was putatively identified by the presence of a plant-induced promoter (PIP) box, a lower G+C content suggesting acquisition by HGT, and co-expression with other T3E genes (Schulze //et al.//, 2012). Deficient mutants and overexpression studies revealed that XopB and XopS contribute to disease symptoms and bacterial growth, and suppress plant defense gene expression (Schulze //et al.//, 2012).
+The //xopS// gene was identified as a candidate type III effector (T3E) by the presence of a plant-induced promoter (PIP) box, a lower G+C content suggesting acquisition by HGT, and co-expression with other T3E genes (Schulze //et al.//, 2012). Deficient mutants and overexpression studies revealed that XopB and XopS contribute to disease symptoms and bacterial growth, and suppress plant defense gene expression (Schulze //et al.//, 2012).
 === (Experimental) evidence for being a T3E ===
@@ Line 26: / Line 27: @@
 === Phenotypes ===
-To study the contribution of the T3Es to bacterial virulence, the effector gene was individually deleted in //Xcv// strain 85‐10, and the mutant was inoculated into leaves of susceptible ECW pepper plants. In addition, induction of the HR in pepper ECW‐10R was analyzed, which is based on the recognition of the T3E AvrBs1 by the Bs1 resistance gene (Schulze //et al//., 2012). Schulze et al. 2012 studied XopS along with XopB in their study. Deletion of //xopB// or //xopS// led to significantly reduced disease symptoms, whereas the HR induction was not impaired. The mutant phenotypes of 85-10Δ//xopB// and 85-10Δ//xopS// were complemented by ectopic expression of the respective effector gene, suggesting that reduced virulence was not caused by polar effects of the deletions on downstream genes. Although the growth of both individual effector mutants in ECW plants did not differ significantly from that of the wild‐type strain), multiplication of an 85‐10Δ//xopB//Δ//xopS// double mutant was reduced significantly, suggesting that XopB and XopS fulfill redundant functions. To identify additional virulence phenotypes, as well as defense reactions, mediated by the analyzed T3Es, leaves of pepper ECW, //N. benthamiana// and //N. tabacum// were inoculated with //Agrobacterium// strains mediating the in planta expression of the effector genes fused to GFP. These experiments confirmed that XopS (similar to XopB, XopG, XopM) trigger cell death in different //Solanaceae// (Schulze //et al//., 2012). XopS is involved in the severity of disease symptoms, the promotion of bacterial growth and the suppression of PTI (Schulze //et al//., 2012).
+To study the contribution of the T3Es to bacterial virulence, the effector gene was individually deleted in //Xcv// strain 85‐10, and the mutant was inoculated into leaves of susceptible ECW pepper plants. In addition, induction of the HR in pepper ECW‐10R was analyzed, which is based on the recognition of the T3E AvrBs1 by the Bs1 resistance gene (Schulze //et al//., 2012). Schulze et al. 2012 studied XopS along with XopB in their study. Deletion of //xopB// or //xopS// led to significantly reduced disease symptoms, whereas the HR induction was not impaired. The mutant phenotypes of 85-10Δ//xopB// and 85-10Δ//xopS// were complemented by ectopic expression of the respective effector gene, suggesting that reduced virulence was not caused by polar effects of the deletions on downstream genes. Although the growth of both individual effector mutants in ECW plants did not differ significantly from that of the wild‐type strain), multiplication of an 85‐10Δ//xopB//Δ//xopS// double mutant was reduced significantly, suggesting that XopB and XopS fulfill redundant functions. To identify additional virulence phenotypes, as well as defense reactions, mediated by the analyzed T3Es, leaves of pepper ECW, //Nicotiana benthamiana// and //N. tabacum// were inoculated with //Agrobacterium// strains mediating the in planta expression of the effector genes fused to GFP. These experiments confirmed that XopS (similar to XopB, XopG, XopM) trigger cell death in different //Solanaceae// (Schulze //et al//., 2012). XopS is involved in the severity of disease symptoms, the promotion of bacterial growth and the suppression of PTI (Schulze //et al//., 2012).
+XopS<sub>//Xcv//85-10</sub> inhibited proteasomal degradation of WRKY40, a transcriptional regulator of defense gene expression. Virus-induced gene silencing of WRKY40 in pepper enhanced plant tolerance to //Xcv// infection, indicating that WRKY40 represses immunity. Stabilization of WRKY40 by XopS reduced the expression of its targets, which included salicylic acid-responsive genes and the jasmonic acid signaling repressor JAZ8. //Xcv// bacteria lacking XopS displayed significantly reduced virulence when surface inoculated onto susceptible pepper leaves. XopS delivery by //Xcv//, as well as ectopic expression of XopS in //Arabidopsis thaliana// or //Nicotiana benthamiana//, prevented stomatal closure in response to bacteria and biotic elicitors. Silencing WRKY40 in pepper or //N. benthamiana// abolished XopS’s ability to prevent stomatal closure. These findings suggests that XopS interferes with both preinvasion and apoplastic defense by manipulating WRKY40 stability and downstream gene expression, eventually altering phytohormone crosstalk to promote pathogen proliferation (Raffeiner //et al.//, 2022).
 === Localization ===
-Unknown.
+A XopS-GFP fusion has a nucleo-cytoplasmic distribution on epidermal cells of //N. benthamiana// (Raffeiner //et al.//, 2022).
 === Enzymatic function ===
@@ Line 37: / Line 39: @@
 === Interaction partners ===
-Unknown.
+XopS<sub>//Xcv//85-10</sub> interacts with WRKY40, a transcriptional regulator of defense gene expression (Raffeiner //et al.//, 2022).
 ===== Conservation =====
@@ Line 53: / Line 55: @@
 Fonseca NP, Patané JSL, Varani AM, Felestrino EB, Caneschi WL, Sanchez AB, Cordeiro IF, Lemes CGC, Assis RAB, Garcia CCM, Belasque Jr. J, Martins Jr J, Facincani AP, Ferreira RM, Jaciani FJ, Almeida NF, Ferro JA, Moreira LM, Setubal JC (2019). Analyses of seven new genomes of //Xanthomonas citri// pv. //aurantifolii// strains, causative agents of citrus canker B and C, show a reduced repertoire of pathogenicity genes. Front Microbiol. 10: 2361. DOI: [[https://doi.org/10.3389/fmicb.2019.02361|10.3389/fmicb.2019.02361]]
+Raffeiner M, Üstün S, Guerra T, Spinti D, Fitzner M, Sonnewald S, Baldermann S, Börnke F (2022). The //Xanthomonas// type-III effector XopS stabilizes CaWRKY40a to regulate defense responses and stomatal immunity in pepper (//Capsicum annuum//). Plant Cell 34: 1684-1708. DOI: [[https://doi.org/10.1093/plcell/koac032|10.1093/plcell/koac032]]
 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]]
+===== 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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