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--- bacteria:t3e:xopn [2025/07/24 22:46] – jfpothier
+++ bacteria:t3e:xopn [2025/12/11 12:25] (current) – jfpothier
@@ 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 ===
 Start codon of //xopN// was found downstream of a conserved cis-regulatory element, the plant-inducible promoter (PIP) box (TTCGG-N15-TTCTG). //xopN// is regulated by //hrpX// and //hrpG// genes (Jiang //et al//., 2008; Cheong //et al//., 2013).
-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).
+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 ===
@@ Line 35: / Line 32: @@
   * 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).
-  * //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).

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