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bacteria:t3e:xopr

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bacteria:t3e:xopr [2025/02/24 10:41] – [Biological function] rkoebnikbacteria:t3e:xopr [2025/02/24 10:45] (current) – [Biological function] rkoebnik
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 === Regulation === === 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).+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 ===
  
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 Co-immunoprecipitation assays indicate that XopR associates with various receptor-like cytoplasmic kinases (RLCKs), including BIK1 known to be involved in pathogen-associated molecular patterns (PAMP) to triggered stomatal closure (Wang //et al.//, 2016). //In vitro// kinase assays indicate that XopR is phosphorylated by BIK1 likely affecting BIK1 targets, and possibly impairing PAMP-triggered stomatal immunity (Wang //et al.//, 2016). Co-immunoprecipitation assays indicate that XopR associates with various receptor-like cytoplasmic kinases (RLCKs), including BIK1 known to be involved in pathogen-associated molecular patterns (PAMP) to triggered stomatal closure (Wang //et al.//, 2016). //In vitro// kinase assays indicate that XopR is phosphorylated by BIK1 likely affecting BIK1 targets, and possibly impairing PAMP-triggered stomatal immunity (Wang //et al.//, 2016).
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 ===== Conservation ===== ===== Conservation =====
  
bacteria/t3e/xopr.1740393665.txt.gz · Last modified: 2025/02/24 10:41 by rkoebnik