Differences

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

--- bacteria:t3e:xopj5 [2020/07/08 18:08] – [References] rkoebnik
+++ bacteria:t3e:xopj5 [2025/02/13 11:49] (current) – jfpothier
@@ Line 1: / Line 1: @@
-====== XopJ5 ======
+====== The Type III Effector XopJ5 from //Xanthomonas// ======
 Author: [[https://www.researchgate.net/profile/Alexandre_Menezes6|Alexandre B. de Menezes]]\\
-Internal reviewer: [[https://www.researchgate.net/profile/Katarina_Gasic|Katarina Gašić]]\\
+Internal reviewer: [[https://www.researchgate.net/profile/Katarina_Gasic|Katarina Gašić]]
-Expert reviewer: FIXME
 Class: XopJ\\
 Family: XopJ5\\
 Prototype: AvrXccB (//Xanthomonas campestris// pv. //campestris//; strain ATCC 33913)\\
-RefSeq ID: [[https://www.ncbi.nlm.nih.gov/protein/NP_639077|NP_639077]] (235 aa)\\
+GenBank ID: [[https://www.ncbi.nlm.nih.gov/protein/AAM42989.1|AAM42989.1]] (235 aa)\\
+RefSeq ID: [[https://www.ncbi.nlm.nih.gov/protein/WP_228442257.1|WP_228442257.1]] (360 aa)\\
 Synonym: AvrXccB\\
 D structure: Unknown
@@ Line 20: / Line 20: @@
 === (Experimental) evidence for being a T3E ===
-T3E-defective mutant was not capable of secreting the effector protein when carrying the plasmid-borne gene encoding for AvrXccB.
+Using the HR-inducing domain AvrBs1<sub>59-445</sub> as a type-3 translocation reporter, the N-terminal region of XopJ5<sub>Xcc8004</sub> was found to act as a type 3 secretion signal, since the translational reporter fusion triggered a //Bs1//-specific hypersensitive response in a //hrpF//- and //hpaB//-dependent manner (Jiang et al., 2009).
+AvrXccB, fused to a HA tag, was shown to be secreted into culture supernatants by Western blot analysis using an anti‐haemagglutinin (HA) antibody. In contrast, a T3E-defective mutant was not capable of secreting this effector (Liu //et al//., 2017).
 === Regulation ===
-The //xopE1// <sub>Xcc8004</sub> gene (//avrXccB//) contains a PIP box and was shown to be controlled by //hrpG// and //hrpX// (Jiang et al., 2009). (Rongqi //et al//., 2006; Jiang //et al//., 2009).
+The //xopE1// <sub>Xcc8004</sub> gene (//avrXccB//) contains a PIP box and was shown to be controlled by //hrpG// and //hrpX// (Rongqi //et al//., 2006; Jiang et al., 2009).
 === Phenotypes ===
-AvrXccB (XopJ5<sub>Xcc8004</sub>) is not required for full virulence and growth of //Xcc// in the host plant Chinese radish (Jiang //et al.//, 2009). Experimental evidence using heterologous expression of //avrXccB// suggests that this protein is involved in the suppression of plant immunity. Immunity suppression in //Arabidopsis// involved multiple mechanisms: ectopic expression of //avrXccB// reduced flg22-induced callose deposition and ROS production, while //avrXccB// expression in //Arabidopsis// protoplasts inhibited the promoter activity of resistance gene //NHO1//. Heterologous expression of //avrXccB// led to an increase in the in-planta population of //Xcc// B186 and //Pst// DC300 in //Arabidopsis//. Conversely, //avrXccB// mutants were compromised in their ability to inhibit MAMP-induced immunity (callose deposition, ROS production and defence-related genes in //Arabidopsis// protoplasts) (Liu //et al//., 2017).
+  * AvrXccB (XopJ5<sub>Xcc8004</sub>) is not required for full virulence and growth of //Xcc// in the host plant Chinese radish (Jiang //et al.//, 2009).
+  * XopJ5 was found to be associated with variations in disease symptoms when testing a set of 45 //X. campestris// pv. //campestris// strains on two //Arabidopsis// natural accessions (Guy //et al.//, 2013).
+  * Experimental evidence using heterologous expression of //avrXccB// suggests that this protein is involved in the suppression of plant immunity. Immunity suppression in //Arabidopsis// involved multiple mechanisms: ectopic expression of //avrXccB// reduced flg22-induced callose deposition and ROS production, while //avrXccB// expression in //Arabidopsis// protoplasts inhibited the promoter activity of resistance gene //NHO1//. Heterologous expression of //avrXccB// led to an increase in the //in planta// population of //Xcc// B186 and //Pst// DC300 in //Arabidopsis//. Conversely, //avrXccB// mutants were compromised in their ability to inhibit MAMP-induced immunity (callose deposition, ROS production and defence-related genes in //Arabidopsis// protoplasts) (Liu //et al//., 2017).
 === Localization ===
-Membrane, confirmed experimentally through GFP-tagged AvrXccB expression in transgenic //Arabidopsis// (Liu //et al//., 2017; Thieme //et al//., 2007)
+Plant plasma membrane, confirmed experimentally through GFP-tagged AvrXccB expression in transgenic //Arabidopsis//. The putative //N//‐myristoylation motif is essential for its localization (Thieme //et al//., 2007; Liu //et al//., 2017).
 === Enzymatic function ===
 Cysteine protease/acetyltransferase (putative) (Liu //et al//., 2017). Point mutations in the catalytic triad (conserved with other YopJ-like proteins which also function as protease/acetyltransferases) compromised //NOH1// promoter activity and were deprived of their abilities to suppress flg22-induced callose deposition and ROS production (Liu //et al//., 2017).
 === Interaction partners ===
-AvrXccB interacts with SAM-MT1 in //Arabidopsis//, through SAM-MT1's C-terminal domain. AvrXccB-SAM-MT1 interaction was determined experimentally using in-vitro pull-down assays and Co-IP assays (Liu //et al//., 2017).
+AvrXccB interacts with //S//‐adenosyl‐L‐methionine‐dependent methyltransferases SAM‐MT1 and SAM‐MT2 in //Arabidopsis//. Interaction with SAM-MT1 in //Arabidopsis// occurs through SAM-MT1's C-terminal domain. AvrXccB-SAM-MT1 interaction was determined experimentally using in-vitro pull-down assays and Co-IP assays (Liu //et al//., 2017).
 ===== Conservation =====
@@ Line 42: / Line 49: @@
 Yes. YopJ-like effectors such as AvrBsT in //Xcv// or //Xcc//, XopJ in //Xcv//.
 === In other plant pathogens/symbionts ===
 Yes. YopJ-like effectors HopZ1a in //P. syringae// and Pop2 in //R. solanacearum//.
 ===== References =====
 da Silva AC, Ferro JA, Reinach FC, Farah CS, Furlan LR, Quaggio RB, Monteiro-Vitorello CB, Van Sluys MA, Almeida NF, Alves LM, do Amaral AM, Bertolini MC, Camargo LE, Camarotte G, Cannavan F, Cardozo J, Chambergo F, Ciapina LP, Cicarelli RM, Coutinho LL, Cursino-Santos JR, El-Dorry H, Faria JB, Ferreira AJ, Ferreira RC, Ferro MI, Formighieri EF, Franco MC, Greggio CC, Gruber A, Katsuyama AM, Kishi LT, Leite RP, Lemos EG, Lemos MV, Locali EC, Machado MA, Madeira AM, Martinez-Rossi NM, Martins EC, Meidanis J, Menck CF, Miyaki CY, Moon DH, Moreira LM, Novo MT, Okura VK, Oliveira MC, Oliveira VR, Pereira HA, Rossi A, Sena JA, Silva C, de Souza RF, Spinola LA, Takita MA, Tamura RE, Teixeira EC, Tezza RI, Trindade dos Santos M, Truffi D, Tsai SM, White FF, Setubal JC, Kitajima JP (2002). Comparison of the genomes of two //Xanthomonas// pathogens with differing host specificities. Nature 417: 459-463. DOI: [[https://doi.org/10.1038/417459a|10.1038/417459a]]
+Guy E, Genissel A, Hajri A, Chabannes M, David P, Carrere S, Lautier M, Roux B, Boureau T, Arlat M, Poussier S, Noël LD (2013). Natural genetic variation of //Xanthomonas campestris// pv. //campestris// pathogenicity on //Arabidopsis// revealed by association and reverse genetics. mBio 4: e00538-12. DOI: [[https://doi.org/10.1128/mBio.00538-12|10.1128/mBio.00538-12]]. Erratum in: MBio (2013) 4: e00978-13.
 Jiang W, Jiang BL, Xu RQ, Huang JD, Wei HY, Jiang GF, Cen WJ, Liu J, Ge YY, Li GH, Su LL, Hang XH, Tang DJ, Lu GT, Feng JX, He YQ, Tang JL (2009). Identification of six type III effector genes with the PIP box in //Xanthomonas campestris// pv. //campestris// and five of them contribute individually to full pathogenicity. Mol. Plant Microbe Interact. 22: 1401-1411. DOI: [[https://doi.org/10.1094/mpmi-22-11-1401|10.1094/mpmi-22-11-1401]]
@@ Line 57: / Line 68: @@
 Thieme F, Szczesny R, Urban A, Kirchner O, Hause G, Bonas U (2007). New type III effectors from //Xanthomonas campestris// pv. //vesicatoria// trigger plant reactions dependent on a conserved N-myristoylation motif. Mol. Plant Microbe Interact. 20: 1250-1261. DOI: [[https://doi.org/10.1094/MPMI-20-10-1250|10.1094/MPMI-20-10-1250]]
-===== Further reading =====
+===== Acknowledgements =====
-Guy E, Genissel A, Hajri A, Chabannes M, David P, Carrere S, Lautier M, Roux B, Boureau T, Arlat M, Poussier S, Noël LD (2013). Natural genetic variation of //Xanthomonas campestris// pv. //campestris// pathogenicity on arabidopsis revealed by association and reverse genetics. mBio 4: e00538-12. DOI: [[https://doi.org/10.1128/mBio.00538-12|10.1128/mBio.00538-12]]. Erratum in: MBio (2013) 4: e00978-13.
+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