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--- bacteria:t3e:xopn [2025/07/24 22:46] – jfpothier
+++ bacteria:t3e:xopn [2026/06/22 10:25] (current) – [References] rkoebnik
@@ Line 2: / Line 2: @@
 Author: [[https://www.researchgate.net/profile/Jakub_Pecenka|Jakub Pečenka]]\\
-Internal reviewer: [[https://www.researchgate.net/profile/Joana_Vicente2|Joana G. Vicente]]\\
+Internal reviewer: [[https://www.researchgate.net/profile/Joana_Vicente2|Joana G Vicente]]\\
 Class: XopN\\
@@ Line 16: / Line 16: @@
 XopN was identified in a genetic screen, using a Tn//5//-based transposon construct harboring the coding sequence for the HR-inducing domain of AvrBs2, but devoid of the effectors' T3SS signal, that was randomly inserted into the genome of //X. campestris// pv. //vesicatoria// (//Xcv//) strain 85-10. The XopN::AvrBs2 fusion protein triggered a //Bs2//-dependent hypersensitive response (HR) in pepper leaves (Roden //et al//., 2004).
 === (Experimental) evidence for being a T3E ===
-Type III-dependent secretion was confirmed using a calmodulin-dependent adenylate cyclase reporter assay, with a Δ//hrpF// mutant strain serving as negative control (Roden //et al.//, 2004). XopR<sub>//Xoo//</sub> was confirmed to have a functional type III secretion signal using a reporter fusion with AvrBs1 (Zhao //et al.//, 2013).
+Type III-dependent secretion was confirmed using a calmodulin-dependent adenylate cyclase reporter assay, with a Δ//hrpF// mutant strain serving as negative control (Roden //et al.//, 2004). XopN<sub>//Xoo//13751</sub> was confirmed to have a functional type III secretion signal using a reporter fusion with AvrBs1 (Zhao //et al.//, 2013).
 === Regulation ===
@@ Line 26: / Line 24: @@
 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//) were significantly reduced in the //Xanthomonas oryzae// pv. //oryzae// Δ//xrvC// mutant compared with those in the wild-type strain PXO99<sup>A</sup> , but this did not apply to //xopN// (Liu //et al.//, 2016).
 === Phenotypes ===
-  * XopN<sub>Xcv</sub> is required for the pathogens' maximal growth in the leaf tissue of tomato and pepper plants (Roden //et al//., 2004).
+  * XopN<sub>Xcv</sub>  is required for the pathogens' maximal growth in the leaf tissue of tomato and pepper plants (Roden //et al//., 2004).
-  * Its homolog XopN <sub>Xcc</sub> was found as well to be required for full virulence on Chinese radish (Jiang //et al//., 2008).
+  * Its homolog XopN <sub>Xcc</sub>  was found as well to be required for full virulence on Chinese radish (Jiang //et al//., 2008).
-  * XopN has been shown to play a role in host defence systems causing the reduction of PAMP-triggered immune responses and reduce the callose deposition in the host tissue. Moreover the deletion of //xopN// open reading frame (ORF) reduced the //Xcv// strain virulence exhibited by lower bacterial spot symptoms occurrence (Kim //et al//., 2009).
+  * XopN has been shown to play a role in host defence systems causing the reduction of PAMP-triggered immune responses and reduce the callose deposition in the host tissue. Moreover the deletion of //xopN//  open reading frame (ORF) reduced the //Xcv//  strain virulence exhibited by lower bacterial spot symptoms occurrence (Kim //et al//., 2009).
   * The role of XopN in X. oryzae pv. oryzae is dependent on leaf stage (Cheong et al., 2013).
-  * XopN has been shown to be required for maximal pathogenicity of //X. axonopodis// pv. //punicae// (//Xap//) in pomegranate (Kumar and Mondal, 2013). The deletion of XopN from Xap caused higher accumulation of reactive oxygen species showing that XopN suppresses ROS-mediated defense responses during blight pathogenesis in pomegranate (Kumar //et al.//, 2016).
+  * XopN has been shown to be required for maximal pathogenicity of //X. axonopodis//  pv. //punicae//  (//Xap//) in pomegranate (Kumar and Mondal, 2013). The deletion of XopN from Xap caused higher accumulation of reactive oxygen species showing that XopN suppresses ROS-mediated defense responses during blight pathogenesis in pomegranate (Kumar //et al.//, 2016).
-  * A Δ//xopN//–Δ//xopQ// double knock-out mutant in //X. phaseoli// pv. //manihotis// (//Xpm//) was less aggressive in the cassava host plant than its single mutation counterparts. In addition, //in planta// bacterial growth was reduced at 5 dpi in the double mutant with respect to the wild-type strain CIO151 and individual knock-out strains. The phenotype of the double mutant could be complemented when transforming a plasmid containing //xopQ//. These results confirmed that //xopN// and //xopQ //are functionally redundant in //Xpm// (Medina //et al.//, 2017).
+  * A Δ//xopN//–Δ//xopQ//  double knock-out mutant in //X. phaseoli//  pv. //manihotis//  (//Xpm//) was less aggressive in the cassava host plant than its single mutation counterparts. In addition, //in planta//  bacterial growth was reduced at 5 dpi in the double mutant with respect to the wild-type strain CIO151 and individual knock-out strains. The phenotype of the double mutant could be complemented when transforming a plasmid containing //xopQ//. These results confirmed that //xopN//  and //xopQ //are functionally redundant in //Xpm//  (Medina //et al.//, 2017).
-  * //Agrobacterium// mediated transient transfer of the gene for XopN resulted in suppression of rice innate immune responses induced by LipA, a hydrolitic enzyme secreted by //X. oryzae// pv. //oryzae// (Xoo), but a //xopN// <sup>//-// </sup> mutant of //Xoo//retains the ability to suppress these innate immune responses indicating other functionally redundant proteins; XopQ, XopX and XopZ were shown to be suppressors of LipA induced innate immune responses; mutation in any one of the //xopN, xopQ, xopX or xopZ// genes causes partial virulence deficiency (Sinha et al., 2013). XopN was shown to contribute significantly to //X. oryzae// pv. //oryzae// (Xoo) virulence on a susceptible rice variety Nipponbare. XopN was shown to be highly translocated to suppress rice defense responses (Mo //et al.//, 2020).
+  * //Agrobacterium//  mediated transient transfer of the gene for XopN resulted in suppression of rice innate immune responses induced by LipA, a hydrolitic enzyme secreted by //X. oryzae//  pv. //oryzae//  (Xoo), but a //xopN// <sup>//-// </sup>   mutant of //Xoo//retains the ability to suppress these innate immune responses indicating other functionally redundant proteins; XopQ, XopX and XopZ were shown to be suppressors of LipA induced innate immune responses; mutation in any one of the //xopN, xopQ, xopX or xopZ//  genes causes partial virulence deficiency (Sinha et al., 2013). XopN was shown to contribute significantly to //X. oryzae//  pv. //oryzae//  (Xoo) virulence on a susceptible rice variety Nipponbare. XopN was shown to be highly translocated to suppress rice defense responses (Mo //et al.//, 2020).
-  * XopN and AvrBS2 were shown to significantly contribute to virulence of //X. oryzae// pv. //oryzicola// (Xoc GX01) (Liao //et al.//, 2020).
+  * XopN and AvrBS2 were shown to significantly contribute to virulence of //X. oryzae//  pv. //oryzicola//  (Xoc GX01) (Liao //et al.//, 2020).
+  * XopN<sub>//Xoc// </sub>  acts as a critical suppressor of rice basal immunity, perhaps by disrupting the formation of the OsRACK1B-OsRap2.6 immune module (Wang //et al.//, 2026).
 === Localization ===
@@ Line 44: / Line 42: @@
 === Enzymatic function ===
-XopN binds TARK1, a tomato atypical receptor kinase required for PTI. Taylor //et al.// (2012) showed that XopN promotes TARK1/TFT1 complex formation //in vitro// and //in planta// by functioning as a molecular scaffold.TFT proteins are involved in immune signaling during //X. euvesicatoria// infection and can interact with multiple effectors including XopN (Dubrow //et al.//, 2018). TARK1 was shown to interact with proteins predicted to be associated with stomatal closure (Guzman et al., 2020).
+XopN binds TARK1, a tomato atypical receptor kinase required for PTI. Taylor //et al.//  (2012) showed that XopN promotes TARK1/TFT1 complex formation //in vitro//  and //in planta//  by functioning as a molecular scaffold.TFT proteins are involved in immune signaling during //X. euvesicatoria//  infection and can interact with multiple effectors including XopN (Dubrow //et al.//, 2018). TARK1 was shown to interact with proteins predicted to be associated with stomatal closure (Guzman et al., 2020).
 Three effectors (XopZ, XopN and XopV) were shown to be able to supress the peptidoglycan-triggered MAPK activation and a triple mutant of Xoo lacking these genes showed additively reduced virulence (Long et al., 2018).
@@ Line 52: / Line 50: @@
 XopN interact with two types of proteins in tomato: Tomato Atypical Receptor-like Kinase1 (TARK1) and four Tomato Fourteen-Three-Three isoforms (TFT1, TFT3, TFT5, and TFT6) (Kim //et al//., 2009). XopN interacts with the tomato 14-3-3 isoform TFT1 that functions in PTI and is a XopN virulence target (Taylor //et al.//, 2012).
-Two rice proteins, OsVOZ2 and a putative thiamine synthase (OsXNP) were identified as targets of XopN<sub>KXO85</sub> by yeast two-hybrid screening (Cheong et al., 2012).
+Two rice proteins, OsVOZ2 and a putative thiamine synthase (OsXNP) were identified as targets of XopN<sub>KXO85</sub>  by yeast two-hybrid screening (Cheong et al., 2012).
+Using yeast two-hybrid screening, bimolecular fluorescence complementation, and pull-down assays, the WD40-repeat scaffold protein OsRACK1B was identified as a direct target of XopN<sub>//Xoc// </sub>  (Wang //et al.//, 2026).
 ===== Conservation =====
@@ Line 95: / Line 95: @@
 Taylor KW, Kim JG, Su XB, Aakre CD, Roden JA, Adams CM, Mudgett MB (2012). Tomato TFT1 is required for PAMP-triggered immunity and mutations that prevent T3S effector XopN from binding to TFT1 attenuate //Xanthomonas// virulence. PLoS Pathog. 8: e1002768. DOI: [[https://doi.org/10.1371/journal.ppat.1002768|10.1371/journal.ppat.1002768]]
+Wang J, Ni Z, Chen X, Zhang Y, Qin H, Wang H, He Y, Tang J, Huang S (2026). //Xanthomonas// type III effector XopN targets scaffold protein OsRACK1B to suppress rice immunity. Mol. Plant Pathol. 27: e70300. DOI: [[https://doi.org/10.1111/mpp.70300|10.1111/mpp.70300]]
 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]]

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