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--- bacteria:t3e:xopr [2025/02/24 10:41] – [Biological function] rkoebnik
+++ bacteria:t3e:xopr [2025/07/28 15:17] (current) – [Biological function] rkoebnik
@@ Line 2: / Line 2: @@
 Author: [[https://www.researchgate.net/profile/Fernando_Tavares|Fernando Tavares]]\\
-Reviewer: [[https://www.researchgate.net/profile/Amandine_Cunty|Amandine Cunty]]
+Reviewer: [[https://www.researchgate.net/profile/Amandine_Cunty|Amandine Cunty]]\\
 Class: XopR\\
@@ Line 18: / Line 18: @@
 === (Experimental) evidence for being a T3E ===
-Evidence for T3SS-dependent secretion and translocation of XopR into plant cells was mainly based on calmodulin-dependent adenylate cyclase (Cya) reporter assays of fusion proteins (Furutani //et al.//, 2009). XopR<sub>//Xoo// </sub> was confirmed to have a functional type III secretion signal using a reporter fusion with AvrBs1 (Zhao //et al.//, 2013).
+Evidence for T3SS-dependent secretion and translocation of XopR into plant cells was mainly based on calmodulin-dependent adenylate cyclase (Cya) reporter assays of fusion proteins (Furutani //et al.//, 2009). XopR<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 ===
-Functional studies using //hrp//-inducing and non-//hrp//-inducing media and reverse-transcriptase PCR in wild type and //X. oryzae// pv. //oryzae// (//Xoo//) ∆//hrpX// mutants showed that the expression of //xopR// is //hrpX// dependent (Verma //et al.//, 2019). These results are indirectly supported by previous findings showing that //Xoo// mutants deficient for //xrvB//, a gene coding for a repressor of //hrp// gene expression, leads to an increase of XopR into plant cells (Kametani-Ikawa //et al.//, 2011).
+Functional studies using //hrp//-inducing and non-//hrp//-inducing media and reverse-transcriptase PCR in wild type and //X. oryzae// pv. //oryzae// (//Xoo//) ∆//hrpX// mutants showed that the expression of //xopR// is //hrpX// dependent (Verma //et al.//, 2019). These results are indirectly supported by previous findings showing that //Xoo// mutants deficient for //xrvB//, a gene coding for a repressor of //hrp// gene expression, leads to an increase of XopR secretion into plant cells (Kametani-Ikawa //et al.//, 2011).
 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 //Xoo// Δ//xrvC// mutant compared with those in the wild-type strain PXO99<sup>A</sup> , but this did not apply to //xopR// (Liu //et al.//, 2016).
@@ Line 30: / Line 30: @@
 A //xopR// deletion mutant in the Chinese //Xoo// strain 13751 showed a significant reduction in virulence in hybrid rice cv. Teyou63 compared to the wild type (Zhao //et al.//, 2013). However, the growth of the mutant in host plant rice was not affected. These results indicated that //xopR// was required for full virulence of //Xoo// strain 13751 by inducing rice disease tolerance (Zhao //et al.//, 2013).
-Later studies suggested that XopR suppress PAMP-triggered stomatal closure in transgenic //Arabidopsis// expressing XopR (Wang //et al.//, 2016). More recently, when compared with a //Xoo// wild type strain, //xopR// deficient mutants (//Xoo// ∆//xopR//) infiltrated in rice leaves led to an increase of callose deposits, and a significant higher production of reactive oxygen species (ROS), namely of hydrogen peroxide (H<sub>2</sub> O<sub>2</sub>) and superoxide anion (O<sub>2<sup>-</sup></sub>), known as the main components of the plant oxidative burst (Verma //et al.//, 2018). Furthermore, reverse transcriptase expression analyses of eight rice genes linked to plant disease resistance (//BRI1//, //GST1//, //PR2//, //PR5//, //RAC1//, //SERK1//, //WRKY29// and //WRKY71//) were shown to be up-regulated in rice leaves inoculated with //Xoo// ∆//xopR// (Verma //et al.//, 2018; Verma //et al.//, 2019). To further support these findings, complementation of //Xoo// ∆//xopR// with //xopR// was able to restore the disease phenotype of the wild type Xoo strain (Verma //et al.//, 2018; Verma //et al.//, 2019).
+Later studies suggested that XopR suppress PAMP-triggered stomatal closure in transgenic //Arabidopsis// expressing XopR (Wang //et al.//, 2016). More recently, when compared with a //Xoo// wild type strain, //xopR// deficient mutants (//Xoo// ∆//xopR//) infiltrated in rice leaves led to an increase of callose deposits, and a significant higher production of reactive oxygen species (ROS), namely of hydrogen peroxide (H<sub>2</sub> O<sub>2</sub>) and superoxide anion (O<sub>2<sup>-</sup>  </sub>), known as the main components of the plant oxidative burst (Verma //et al.//, 2018). Furthermore, reverse transcriptase expression analyses of eight rice genes linked to plant disease resistance (//BRI1//, //GST1//, //PR2//, //PR5//, //RAC1//, //SERK1//, //WRKY29// and //WRKY71//) were shown to be up-regulated in rice leaves inoculated with //Xoo// ∆//xopR// (Verma //et al.//, 2018; Verma //et al.//, 2019). To further support these findings, complementation of //Xoo// ∆//xopR// with //xopR// was able to restore the disease phenotype of the wild type Xoo strain (Verma //et al.//, 2018; Verma //et al.//, 2019).
 === Localization ===
@@ Line 47: / Line 47: @@
 Yes (e.g. //X. arboricola, X. axonopodis//, //X. campestris//, //X. citri//, //X. gardneri//, //X. oryzae//, //X. phaseoli//, //X. populi//, //X. vasicola//, //X. bromi//, //X. cucurbitae// inferred from a BlastP search for a query coverage higher than 90% and a percent identity over 35%).
 === In other plant pathogens/symbionts ===

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