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bacteria:t3e:xopr [2025/07/04 23:45] – jfpothierbacteria:t3e:xopr [2025/07/24 22:51] (current) – jfpothier
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 === (Experimental) evidence for being a T3E === === (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//</sub> was confirmed to have a functional type III secretion signal using a reporter fusion with AvrBs1 (Zhao //et al.//, 2013).
  
 === Regulation === === Regulation ===
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 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). 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).+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).
  
 === Phenotypes === === Phenotypes ===
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 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). 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 === === Localization ===
bacteria/t3e/xopr.txt · Last modified: 2025/07/24 22:51 by jfpothier

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