EuroXanth DokuWiki

User Tools

Site Tools

Trace:
bacteria:t3e:xopl

Differences

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

Link to this comparison view

Both sides previous revisionPrevious revision
Next revision		Previous revision
bacteria:t3e:xopl [2024/08/08 16:41] – [References] rkoebnikbacteria:t3e:xopl [2025/02/13 12:36] (current) – jfpothier
Line 16: Line 16:
 === How discovered? === === How discovered? ===
  
-XopL was first identified in //X. campestris// pv. //campestris// (//Xcc//) strain 8004 as a candidate T3E due to the presence of a plant-inducible promoter (PIP) box in its gene, XC_4273 (Jiang //et al.//, 2009). The CDS //XC_4273//, re-called XopXccLR (LR = leucine-rich repeat), in //X//. //campestris// pv. //campestris// 8004 was suggested to be a T3E has it harboured a N-terminal region possessing translocation signal with the functionality to target proteins into plant cells (Jiang //et al//., 2009). It was also shown to be required for //X//. //campestris// pv. //campestris// to proliferate well in hosts plant and thus essential for virulence (Jiang //et al//., 2009). It's only a few years later that the analysis of the genome sequence of //Xcv// strain 85-10 led to the identification of XCV3220 (//xopL//) as a new T3E candidate gene and to its more complete characterization (Singer //et al//., 2013). +XopL was first identified in //X. campestris// pv. //campestris// (//Xcc//) strain 8004 as a candidate T3E due to the presence of a plant-inducible promoter (PIP) box upstream of the CDS, //XC_4273// (Jiang //et al.//, 2009). The CDS //XC_4273//, re-called XopXccLR (LR = leucine-rich repeat) or XopL<sub>Xcc</sub> for the purposes of this article, in //Xcc// 8004 was suggested to be a T3E as it harboured a N-terminal region possessing a translocation signal that was able to target proteins into plant cells (Jiang //et al.//, 2009). It was also shown to be required for //Xcc// proliferation in hosts plant (Jiang //et al.//, 2009). It was only a few years later that the analysis of the genome sequence of //X.// //campestris// pv. //vesicatoria// (//Xcv//) strain 85-10 (synonymous with //X. euvesicatoria// 85-10; //Xe// 85-10) led to the identification of XCV3220 (//xopL<sub>Xe</sub> //) as a new T3E candidate gene and to its more complete characterization (Singer //et al//., 2013). XopL<sub>Xe</sub> was shown to have E3 ubiquitin ligase activity, conferred by a ligase domain with a novel fold (XL-box), capable of interacting with the plant host ubiquitination cascade (Singer //et al.//, 2023).
-=== (Experimental) evidence for being a T3E ===+
  
-Using an AvrBs1 reporter fusion, XopL<sub>Xcc8004</sub> was shown to be translated into plant cells in a //hrpF//- and //hpaB//-dependent manner (Jiang et al., 2009).+=== (Experimental) evidence for being a T3E ===
  
-XopL<sub>Xcv85-10</sub> contains a PIP box (plant inducible promoter) in its promoter (TTCG-N<sub>16</sub>-TTCG; genome position 3669238-261); co-regulation with the T3S system was confirmed by RT-PCR (Singer //et al//., 2013). Contains leucine-rich repeats (LRRs). Type III-dependent secretion and translocation was confirmed by //in vitro// secretion and //in vivo// translocation assays (Singer //et al//., 2013). Mutation of amino acids in the central cavity of the XL-box disrupts E3 ligase activity and prevents XopL-induced plant cell death. The lack of cysteine residues in the XL-box suggests the absence of thioester-linked ubiquitin-E3 ligase intermediates and a non-catalytic mechanism for XopL-mediated ubiquitination. The E3 ligase activity is required to provoke plant cell death, suppression of PAMP responses solely depends on the N-terminal LRR domain (Singer //et al//., 2013). XopL<sub>Xcc8004</sub> possesses features that are typical of T3Es: the promoter region of xopL<sub>Xcc8004</sub> gene contains a perfect plant inducible promoter (PIP) box followed by a 10 box similar sequence (TTCGC-N<sub>15</sub>-TTCGC-N<sub>31</sub>-ACGACA) and LRRs motif is characteristic of specific T3Es in pathogenic bacteria (Yan //et al//., 2019).+XopL<sub>Xcc</sub> possesses features that are typical of T3Es: the promoter region of the //xopL<sub>Xcc</sub>// gene contains a perfect plant inducible promoter (PIP) box followed by a 10 box similar sequence (TTCGC-N<sub>15</sub>-TTCGC-N<sub>31</sub>-ACGACA) and an LRR motif characteristic of T3Es in pathogenic bacteria (Yan //et al//., 2019). Using an AvrBs1 reporter fusion, XopL<sub>Xcc</sub> was shown to be translocated into plant cells in a //hrpF-// and //hpaB//-dependent manner (Jiang //et al//., 2009). XopL<sub>Xe</sub> also contains a PIP box (plant inducible promoter) in its promoter (TTCG-N<sub>16</sub>-TTCG; genome position 3669238-261) and co-regulation with the T3S system was confirmed by RT-PCR (Singer //et al.//, 2013). Type III-dependent secretion and translocation was confirmed by //in vitro//secretion and //in vivo//translocation assays (Singer //et al.//, 2013).
 === Regulation === === Regulation ===
  
Line 28: Line 27:
 qRT-PCR revealed that transcript levels of 15 out of 18 tested non-TAL effector genes (as well as the regulatory genes //hrpG// and //hrpX//), including //xopL//, were significantly reduced in the //Xanthomonas oryzae// pv. //oryzae// Δ//xrvC// mutant compared with those in the wild-type strain PXO99<sup>A</sup>  (Liu //et al.//, 2016). qRT-PCR revealed that transcript levels of 15 out of 18 tested non-TAL effector genes (as well as the regulatory genes //hrpG// and //hrpX//), including //xopL//, were significantly reduced in the //Xanthomonas oryzae// pv. //oryzae// Δ//xrvC// mutant compared with those in the wild-type strain PXO99<sup>A</sup>  (Liu //et al.//, 2016).
  
-The expression of //xopL// <sub>Xcc8004</sub> gene is positively regulated by HrpG/HrpX (Yan //et al//., 2019).+The expression of //xopL<sub>Xcc</sub>// gene is positively regulated by HrpG/HrpX (Yan //et al//., 2019).
 === Phenotypes === === Phenotypes ===
  
-  * XopL<sub>Xcv85-10</sub>  displays E3 ubiquitin ligase activity and inhibits expression of the elf18- and flg22-induced defense gene pNHL10 in //Arabidopsis//  mesophyll protoplasts, triggers cell death in //Nicotiana benthamiana//  and suppresses PTI in host plants (Singer //et al//., 2013; Popov //et al//., 2016). +  * XopL<sub>//Xe//</sub>  from //X. euvesicatoria//  85-10 (previously referred to as //X. campestris// pv. //euvesicatoria//; //Xcv//) displays E3 ubiquitin ligase activity (Singer //et al.//, 2013). 
-  * In contrast, XopL<sub>Xoc</sub>  does not induce cell death in //N. benthamiana//. FIXME +  * XopL//<sub>Xe</sub>// inhibits expression of the elf18- and flg22-induced defense gene pNHL10 in //Arabidopsis// mesophyll protoplasts independent of E3 ligase function (Singer //et al.//, 2013). 
-  * XopL<sub>Xcc8004</sub>  is required for full virulence and growth of //X. campestris//  pv. //campestris//  in the host plant Chinese radish (Jiang //et al.//, 2009). +  * XopL//<sub>Xe</sub>// suppresses ABA responsive reporter //pRD29b:GUS// and PTI reporter //pFRK1:LUC// in //Arabidopsis// protoplasts (Popov //et al//., 2016). 
-  * XopL<sub>Xcv85-10</sub>  suppresses PAMP-related defense gene expression and is an E3 ubiquitin ligase (Singer //et al//., 2013). +  * XopL//<sub>Xcc</sub>// interferes with innate immunity (Yan //et al.//, 2019; Huang //et al.//, 2024a) and SA signaling in //Arabidopsis// (Huang //et al.//, 2024). 
-  * Transient expression of XopL, led to a nearly complete elimination of stromules and the relocation of plastids to the nucleus and further characterization of XopL revealed that the E3 ligase activity is essential for two plastid phenotypes (Erickson //et al//., 2016). +  * XopL//<sub>Xe</sub>// triggers cell death in //Nicotiana benthamiana// in an E3 ligase dependant manner (Singer //et al.//, 2013). XopL<sub>Xoc</sub> from //X. oryzae// pv. //oryzicola// and XopL<sub>Xoo</sub> from //X. oryzae// pv. //oryzae// PX099A also cause cell death in this model (Ma //et al.//, 2020). 
-  * XopL<sub>Xap</sub>  is a T3E which supports //X. axonopodis//  pv. //punicae//  for multiplication in pomegranate by suppressing plant immune responses including plant cell death (Soni //et al//., 2017). +  * Distantly related XopL homolog XopL//<sub>Xcc</sub>// from //Xcc// 8004 failed to cause plant cell death. (Ortmann //et al.//, 2023). 
-  * XopL<sub>Xcc8004</sub>  interferes with innate immunity of //Arabidopsis//  (Yan //et al//., 2019). +  * XopL//<sub>Xcc</sub>// is required for full virulence and growth of //Xcc// 8004 in the host plant Chinese radish (Jiang //et al.//, 2009) but not in //Arabidopsis// (Huang et al, 2024). However a mutant for 17 effectors (Δ//17E//) supplemented with //xopL<sub>Xcc</sub> // did grow better than Δ//17E//. 
-  * //Xcv//  strain 85-10 suppresses host autophagy by utilizing type-III effector XopL. Intriguingly, XopL is targeted for degradation by defense-related selective autophagy mediated by NBR1/Joka2, revealing a complex antagonistic interplay between XopL and the host autophagy machinery (Leong //et al.//, 2022). +  * XopL//<sub>Xcc</sub>// constitutive overexpression in //Arabidopsis// led to enhanced //Xcc// 8004 virulence and suppressed callose deposition and oxidative burst (Huang //et al.//, 2024). 
-  * XopL from //X. euvesicatoria//  pv. //euvesicatoria //  (XopL<sub>Xee</sub>) was found to cause strong cell death upon transient expression in //N. benthamiana//, whereas the distantly related //X. campestris//  pv. //campestris//  XopL homolog (XopL<sub>Xcc</sub>) failed to cause plant cell death. (Ortmann //et al.//, 2023). +  * XopL//<sub>Xe</sub>// is required for full virulence of //Xe// 85-10 on tomato (Leong et al., 2022). 
 +  * XopL//<sub>Xap</sub>// supports //X. axonopodis //pv.// punicae //multiplication in pomegranate by suppressing plant immune responses including plant cell death (Soni //et al//., 2017). 
 +  * Transient expression of XopL//<sub>Xe</sub> //, led to a nearly complete elimination of stromules and the relocation of plastids to the nucleus and further characterization revealed that the E3 ligase activity is essential for the two plastid phenotypes (//Erickson et al//., 2018). 
 +  * //Xe //85-10 suppresses host autophagy by utilizing type-III effector XopL//<sub>Xe</sub> //. Intriguingly, XopL//<sub>Xe</sub>// is targeted for degradation by defense-related selective autophagy mediated by NBR1/Joka2, revealing a complex antagonistic interplay between XopL and the host autophagy machinery (Leong// et al.//, 2022).
 === Localization === === Localization ===
  
-Possibly plasma membrane. The transiently expressed XopL<sub>Xap</sub>::EYFP fusion protein was localized to the plasma membrane, indicating the possible site of its action (Soni //et al//., 2017). XopL from //X. euvesicatoria//  pv. //euvesicatoria //  (XopL<sub>Xee</sub>) was found to directly associate with plant microtubules, whereas the distantly related //X. campestris//  pv. //campestris//  XopL homolog (XopL<sub>Xcc</sub>) failed to localize to microtubules (Ortmann //et al.//, 2023).+Several localization patterns have been reported for XopL proteins in epidermal cells with some strain dependent differences. XopLs are most often tagged at the C-terminus, with the exception of the studies by Leong //et al//., 2022 and Yan //et al.//, 2019.
  
 +  * __Cytosolic localization__ has been reported for XopL//<sub>Xe</sub>// (Erickson //et al.//, 2018), XopL//<sub>Xcc</sub>// (Yan //et al//., 2019; Ortmann //et al//. 2023), XopL<sub>//Xoo//</sub> (Ma //et al//., 2020; Ortmann //et al//., 2023), and XopL//<sub>Xac</sub> //  from //X. citri// pv. //citri// (Ortmann et al. 2023) in //N. benthamiana//.
 +  * __Nuclear localization__ was reported for XopL//<sub>Xe</sub>//, XopL<sub>//Xcc//</sub> (Yan //et al.//, 2019; Ortmann //et al//., 2023) and XopL//<sub>Xac</sub>// in //N. benthamiana// (Ortmann et al. 2023), but not for XopL//<sub>Xoo</sub>// in //N. benthamiana// or XopL//<sub>Xap</sub>// from //X. axonopodis// pv. //punicae// in //Arabidopsis// protoplasts (Soni //et al.//, 2017; Ortmann //et al.,// 2023).
 +  * __Plasma membrane localization__ has been reported for XopL<sub>//Xap//</sub> transiently expressed in //N. benthmiana// (Soni //et al//., 2017) and XopL//<sub>Xcc</sub>// expressed in //Arabidopsis// protoplasts (Huang //et al//. 2024b; Yan //et al.// , 2019) and //N. benthamiana// leaves (Yan //et al//., 2019).
 +  * __Microtubule localization__ has been reported for XopL//<sub>Xe</sub>//, XopL<sub>//Xoo//</sub> and XopL//<sub>Xac</sub>//, whereas the distantly related XopL//<sub>Xcc</sub>// failed to localize to microtubules in //N. benthamiana// (Ortmann //et al.//, 2023).
 +  * __Autophagosome localization__ has been reported for XopL//<sub>Xe</sub>// (co-localizes with autophagy markers RFP-ATG8e and SH3P2-RFP; Leong //et al//., 2022).
 === Enzymatic function === === Enzymatic function ===
  
-E3 ubiquitin ligase activity (Singer //et al//., 2013).+XopL<sub>Xe</sub> harbours an unstructured N-terminus, followed by three alpha helices, an leucine-rich repeat (LRR) domain and an XL-box. Mutation of amino acids in the central cavity of the XL-box disrupt E3 ligase activity and prevent XopL-induced plant cell death. The lack of cysteine residues in the XL-box suggest that thioester-linked ubiquitin-E3 ligase intermediates are not formed during XopL-mediated ubiquitination. Suppression of PAMP responses solely depends on the N-terminal LRR domain (Singer //et al//., 2013), while microtubule binding relies on a proline-rich region in the unstructured region and the alpha-helical region (Ortman //et al//., 2023).
  
 === Interaction partners === === Interaction partners ===
  
-XopL<sub>//Xcv//85-10</sub>  interacts with and degrades the autophagy component SH3P2 via its E3 ligase activity to promote infection (Leong //et al.//, 2022).+XopL<sub>Xe</sub> interacts with and degrades the autophagy component SH3P2 via its E3 ligase activity to promote infection (Leong //et al.//, 2022). XopL<sub>Xoo</sub> interacts with and degrades ferredoxin from //N. benthamiana//, part of the electron transport chain (Ma //et al.//, 2020). XopLXcc interaction with proton pump interactor 1 (PPI1) in //Arabidopsis// (Huang //et al//., 2024b).
  
 ===== Conservation ===== ===== Conservation =====
Line 57: Line 63:
 === In xanthomonads === === In xanthomonads ===
  
-Yes (//e.g.//, //X. euvesicatoria//, //X. citri//, //X. axonopodis//, //X. oryzae//, //X. oryzicola//, //X//. //fragariae//, //X//. //perforans, X. gardneri//, //X. campestris//  pv. //campestris//, but not //X. campestris//  pv. //raphani//, in some //X. arboricola//  pathovars). See for example [[https://doi.org/10.1094/MPMI-22-11-1401|Table 2]] in Jiang //et al//. (2009) and [[https://doi.org/10.1371/journal.ppat.1003121.s001|Figure S1]] in Singer //et al//. (2013).+Yes (//e.g.//, //X. euvesicatoria//, //X. citri//, //X. axonopodis//, //X. oryzae//, //X. oryzicola//, //X//. //fragariae//, //X//. //perforans, X. gardneri//, //X. campestris// pv. //campestris//, but not //X. campestris// pv. //raphani//, in some //X. arboricola// pathovars). See for example [[https://doi.org/10.1094/MPMI-22-11-1401|Table 2]] in Jiang //et al//. (2009) and [[https://doi.org/10.1371/journal.ppat.1003121.s001|Figure S1]] in Singer //et al//. (2013).
  
 === In other plant pathogens/symbionts === === In other plant pathogens/symbionts ===
Line 65: Line 71:
 ===== References ===== ===== References =====
  
-Adlung N (2016). Charakterisierung der Avirulenzaktivität von XopQ und Identifizierung möglicher Interaktoren von XopL aus //Xanthomonas campestris// pv. //vesicatoria//. Doctoral Thesis. Martin-Luther-Universität Halle-Wittenberg, Germany. PDF: [[https://d-nb.info/1116951061/34|d-nb.info/1116951061/34]] FIXME+Adlung N (2016). Charakterisierung der Avirulenzaktivität von XopQ und Identifizierung möglicher Interaktoren von XopL aus //Xanthomonas campestris// pv. //vesicatoria//. Doctoral Thesis. Martin-Luther-Universität Halle-Wittenberg, Germany. PDF: [[https://d-nb.info/1116951061/34|d-nb.info/1116951061/34]]FIXME
  
 Erickson JL, Adlung N, Lampe C, Bonas U, Schattat MH (2018). The //Xanthomonas// effector XopL uncovers the role of microtubules in stromule extension and dynamics in //Nicotiana benthamiana//. Plant J. 93: 856-870. DOI:[[https://doi.org/10.1111/tpj.13813|10.1111/tpj.13813]] Erickson JL, Adlung N, Lampe C, Bonas U, Schattat MH (2018). The //Xanthomonas// effector XopL uncovers the role of microtubules in stromule extension and dynamics in //Nicotiana benthamiana//. Plant J. 93: 856-870. DOI:[[https://doi.org/10.1111/tpj.13813|10.1111/tpj.13813]]
  
-Huang J, Zhou H, Zhou M, Li N, Jiang B, He Y (2024). Functional analysis of type III effectors in //Xanthomonas campestris// pv. //campestris// reveals distinct roles in modulating //Arabidopsis// innate immunity. Pathogens 13: 448. DOI: [[https://doi.org/10.3390/pathogens13060448|10.3390/pathogens13060448]]+Huang J, Dong Y, Li N, He Y, Zhou H (2024a). The type III effector XopL//<sub>Xcc</sub>// in //Xanthomonas campestris// pv. //campestris// targets the proton pump interactor 1 and suppresses innate immunity in //Arabidopsis//. Int. J. Mol. Sci. 25: 9175. DOI: [[https://doi.org/10.3390/ijms25179175|10.3390/ijms25179175]] 
 + 
 +Huang J, Zhou H, Zhou M, Li N, Jiang B, He Y (2024b). Functional analysis of type III effectors in //Xanthomonas campestris// pv. //campestris// reveals distinct roles in modulating //Arabidopsis// innate immunity. Pathogens 13: 448. DOI: [[https://doi.org/10.3390/pathogens13060448|10.3390/pathogens13060448]]
  
 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]] 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 76: Line 84:
  
 Liu Y, Long J, Shen D, Song C (2016). //Xanthomonas oryzae// pv. //oryzae// requires H-NS-family protein XrvC to regulate virulence during rice infection. FEMS Microbiol. Lett. 363: fnw067. DOI: [[https://doi.org/10.1093/femsle/fnw067|10.1093/femsle/fnw067]] Liu Y, Long J, Shen D, Song C (2016). //Xanthomonas oryzae// pv. //oryzae// requires H-NS-family protein XrvC to regulate virulence during rice infection. FEMS Microbiol. Lett. 363: fnw067. DOI: [[https://doi.org/10.1093/femsle/fnw067|10.1093/femsle/fnw067]]
 +
 +Ma W, Xu X, Cai L, Cao Y, Haq F, Alfano JR, Zu B, Zou L, Chen G (2020). A //Xanthomonas oryzae// type III effector XopL causes cell death through mediating ferredoxin degradation in //Nicotiana benthamiana//. Phytopathol Res. 2: 16. DOI: 10.1186/s42483-020-00055-w
  
 Ortmann S, Marx J, Lampe C, Handrick V, Ehnert TM, Zinecker S, Reimers M, Bonas U, Erickson JL (2023). A conserved microtubule-binding region in //Xanthomonas// XopL is indispensable for induced plant cell death reactions. PLoS Pathog. 19: e1011263. DOI: [[https://doi.org/10.1371/journal.ppat.1011263|10.1371/journal.ppat.1011263]] Ortmann S, Marx J, Lampe C, Handrick V, Ehnert TM, Zinecker S, Reimers M, Bonas U, Erickson JL (2023). A conserved microtubule-binding region in //Xanthomonas// XopL is indispensable for induced plant cell death reactions. PLoS Pathog. 19: e1011263. DOI: [[https://doi.org/10.1371/journal.ppat.1011263|10.1371/journal.ppat.1011263]]
bacteria/t3e/xopl.1723131683.txt.gz · Last modified: 2024/08/08 16:41 by rkoebnik

Page Tools

Except where otherwise noted, content on this wiki is licensed under the following license: CC Attribution-Share Alike 4.0 International
CC Attribution-Share Alike 4.0 International Donate Powered by PHP Valid HTML5 Valid CSS Driven by DokuWiki