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bacteria:t3e:xopz [2025/07/04 23:49] – jfpothierbacteria:t3e:xopz [2025/07/24 22:55] (current) – jfpothier
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 RefSeq ID (XopZ1): [[https://www.ncbi.nlm.nih.gov/protein/WP_011259177.1|WP_011259177.1]] (1388 aa)\\ RefSeq ID (XopZ1): [[https://www.ncbi.nlm.nih.gov/protein/WP_011259177.1|WP_011259177.1]] (1388 aa)\\
 RefSeq ID (XopZ2): [[https://www.ncbi.nlm.nih.gov/protein/WP_039421390.1|WP_039421390.1]] (1317 aa)\\ RefSeq ID (XopZ2): [[https://www.ncbi.nlm.nih.gov/protein/WP_039421390.1|WP_039421390.1]] (1317 aa)\\
-Examples of other XopZ1 sequences: [[https://www.ncbi.nlm.nih.gov/protein/ACD59124.1|ACD59124.1]] and [[https://www.ncbi.nlm.nih.gov/protein/ACD59315.1|ACD59315.1]] (=PXO_01041 and PXO_06152, respectively, as strain PXO99<sup>A</sup>  contains two identical copies of the gene due to a 212-kb duplication in the genome) (Song //et al.//, 2010). These GenBank entries are only 1371 aa long whereas the first functional characterization proposes 1414 aa, thus positioning the PIP box (TTCTC-N<sub>15</sub>-TTCGC) 58 bp upstream of the predicted translation start site (Song and Yang, 2010). [[https://www.ncbi.nlm.nih.gov/protein/AAW75797.1|AAW75797.1]] (1414 aa) in strain KACC 10331 might be preferred.\\+Examples of other XopZ1 sequences: [[https://www.ncbi.nlm.nih.gov/protein/ACD59124.1|ACD59124.1]] and [[https://www.ncbi.nlm.nih.gov/protein/ACD59315.1|ACD59315.1]] (=PXO_01041 and PXO_06152, respectively, as strain PXO99<sup>A</sup> contains two identical copies of the gene due to a 212-kb duplication in the genome) (Song //et al.//, 2010). These GenBank entries are only 1371 aa long whereas the first functional characterization proposes 1414 aa, thus positioning the PIP box (TTCTC-N<sub>15</sub>-TTCGC) 58 bp upstream of the predicted translation start site (Song and Yang, 2010). [[https://www.ncbi.nlm.nih.gov/protein/AAW75797.1|AAW75797.1]] (1414 aa) in strain KACC 10331 might be preferred.\\
 Examples of other XopZ2 sequences: [[https://www.ncbi.nlm.nih.gov/protein/EGD18683.1|EGD18683.1]] (1318 aa)\\ Examples of other XopZ2 sequences: [[https://www.ncbi.nlm.nih.gov/protein/EGD18683.1|EGD18683.1]] (1318 aa)\\
 3D structure: Unknown. The N-terminus of XopZ<sub>PXO99</sub>, contains two Nuclear Localization Signals (NLS) and several Nuclear Export Signals (NES) (Zhou //et al.//, 2015). 3D structure: Unknown. The N-terminus of XopZ<sub>PXO99</sub>, contains two Nuclear Localization Signals (NLS) and several Nuclear Export Signals (NES) (Zhou //et al.//, 2015).
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 The first mention of XopZ as an homolog of HopAS1 in// Xanthomonas oryzae// MAFF311018 was made by Furutani //et al.// (2009). Indeed, the locustag XOO2402 ([[https://www.ncbi.nlm.nih.gov/protein/BAE69157.1|BAE69157.1]]; 1,288 aa) was shown to share homology with known Hrp outer proteins (Hops) of //Pseudomonas syringae// strains (Lindeberg //et al.//, 2005). The first mention of XopZ as an homolog of HopAS1 in// Xanthomonas oryzae// MAFF311018 was made by Furutani //et al.// (2009). Indeed, the locustag XOO2402 ([[https://www.ncbi.nlm.nih.gov/protein/BAE69157.1|BAE69157.1]]; 1,288 aa) was shown to share homology with known Hrp outer proteins (Hops) of //Pseudomonas syringae// strains (Lindeberg //et al.//, 2005).
  
-In 2009, the generation of mutants for 18 non-TAL type 3 effector genes in //Xoo// strain PXO99<sup>A</sup>  allowed to investigate the function of several T3Es. Among them XopZ (PXO_06152 and PXO_01041) was reported to contribute to the full virulence of the strain PXO99<sup>A</sup>  (Ryan //et al.//, 2009; Song and Yang, 2010).+In 2009, the generation of mutants for 18 non-TAL type 3 effector genes in //Xoo// strain PXO99<sup>A</sup> allowed to investigate the function of several T3Es. Among them XopZ (PXO_06152 and PXO_01041) was reported to contribute to the full virulence of the strain PXO99<sup>A</sup> (Ryan //et al.//, 2009; Song and Yang, 2010).
  
 XopZ2 was described in Potnis //et al.//, 2011 as a novel candidate effector gene upstream of //hrpW// in //Xanthomonas vesicatoria// strain 1111 (=ATCC 35937) ([[https://www.ncbi.nlm.nih.gov/protein/EGD08510.1|EGD08510.1]]=XVE_3221) and //Xanthomonas gardneri// strain 101 (=ATCC 19865) ([[https://www.ncbi.nlm.nih.gov/protein/EGD18683.1|EGD18683.1]]=XGA_2762; Potnis //et al.//, 2011). It was also shown to be functional i.e. as being translocated using a reporter gene assay (AvrBs2-based assay; Potnis //et al.//, 2011). The pairwise sequence identity below 50% warrants assigning these two proteins to a new family within the XopZ class, named XopZ2 (Potnis //et al.//, 2011). XopZ2 was described in Potnis //et al.//, 2011 as a novel candidate effector gene upstream of //hrpW// in //Xanthomonas vesicatoria// strain 1111 (=ATCC 35937) ([[https://www.ncbi.nlm.nih.gov/protein/EGD08510.1|EGD08510.1]]=XVE_3221) and //Xanthomonas gardneri// strain 101 (=ATCC 19865) ([[https://www.ncbi.nlm.nih.gov/protein/EGD18683.1|EGD18683.1]]=XGA_2762; Potnis //et al.//, 2011). It was also shown to be functional i.e. as being translocated using a reporter gene assay (AvrBs2-based assay; Potnis //et al.//, 2011). The pairwise sequence identity below 50% warrants assigning these two proteins to a new family within the XopZ class, named XopZ2 (Potnis //et al.//, 2011).
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 === (Experimental) evidence for being a T3E === === (Experimental) evidence for being a T3E ===
  
-The secretion of XopZ //in planta// was shown using a //B. pertussis// Cya translocation reporter assay (Furutani //et al.//, 2009). With a PIP box 58 bp upstream of the predicted translation start site, //xopZ// <sub>PXO99</sub> gene is certainly inducible //in planta// and regulated through the hypersensitive reaction and pathogenicity (Hrp) regulatory network (Song and Yang, 2010). PXO99<sup>A</sup>  and an //hrpG// mutant were grown in nutrient broth (NB) or //Xanthomonas hrp//-inducing medium (XOM2) (Song and Yang, 2010). The expression of //xopZ// <sub>PXO99</sub> was only observed, by RT-PCR, in XOM2 medium and was //hrpG// dependent (Song and Yang, 2010).+The secretion of XopZ //in planta// was shown using a //B. pertussis// Cya translocation reporter assay (Furutani //et al.//, 2009). With a PIP box 58 bp upstream of the predicted translation start site, //xopZ// <sub>PXO99</sub> gene is certainly inducible //in planta// and regulated through the hypersensitive reaction and pathogenicity (Hrp) regulatory network (Song and Yang, 2010). PXO99<sup>A</sup> and an //hrpG// mutant were grown in nutrient broth (NB) or //Xanthomonas hrp//-inducing medium (XOM2) (Song and Yang, 2010). The expression of //xopZ// <sub>PXO99</sub> was only observed, by RT-PCR, in XOM2 medium and was //hrpG// dependent (Song and Yang, 2010).
  
 === Regulation === === Regulation ===
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 The //xopZ// gene was shown to be expressed in a //hrpG//-dependent manner. A PIP box (TTCTC-N<sub>15</sub>-TTCGC) was identified 58 bp upstream of the predicted translation start site (Song and Yang, 2010). The //xopZ// gene was shown to be expressed in a //hrpG//-dependent manner. A PIP box (TTCTC-N<sub>15</sub>-TTCGC) was identified 58 bp upstream of the predicted translation start site (Song and Yang, 2010).
  
-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//), including //xopZ//, were significantly reduced in the //Xanthomonas oryzae// pv. //oryzae// Δ//xrvC// mutant compared with those in the wild-type strain PXO99<sup>A</sup>  (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//), including //xopZ//, were significantly reduced in the //Xanthomonas oryzae// pv. //oryzae// Δ//xrvC// mutant compared with those in the wild-type strain PXO99<sup>A</sup> (Liu //et al.//, 2016).
  
 === Phenotypes === === Phenotypes ===
  
-PXO99<sup>A</sup>  contains two identical copies of the gene due to a duplication of 212 kb in the genome. However, a deletion of one //xopZ// gene did not affect pathogenicity or bacterial growth in plants, while strains with mutations in both copies of //xopZ// <sub>PXO99</sub> displayed reduced virulence in terms of lesion length and bacterial multiplication compared with the wild type strain PXO99<sup>A</sup> . The introduction of one genomic copy of //xopZ// <sub>PXO99</sub> restores the mutant to full virulence. To test whether XopZ<sub>PXO99</sub> inhibits the host cell-wall-associated defense responses (PTI), leaves of //Nicotiana benthamiana// were infiltrated with //Agrobacterium// cells with and without //xopZ// <sub>PXO99</sub> under the control of the cauliflower mosaic virus 35S promoter 24 hours preceding inoculation of the same leaves with a T3SS mutant of PXO99<sup>A</sup>  (ME7). Twenty-four hours after inoculation, leaves inoculated with ME7 had more callose depositions than the leaves inoculated with //Agrobacterium// spp. expressing //xopZ// <sub>PXO99</sub>. This results suggesting a role for XopZ<sub>PXO99</sub> in interfering with host innate immunity (PTI) during //X. oryzae// pv. //oryzae// infection (Song //et al.//, 2010). Besides, Western blot analysis with p44/42 MAP kinase antibody clearly showed that XopN, XopV and XopZ inhibited the peptidoglycan(PNG)-induced phosphorylation of OsMAPKs. Expression of all Xop effectors were verified by immunoblotting with anti-HA antibody. Thus, expression of three Xop effectors from PXO99<sup>A</sup>  in rice protoplasts results in compromised OsMAPK activation induced by PGN, highlighting their putative virulence functions during pathogenesis (Long //et al.//, 2018).+PXO99<sup>A</sup> contains two identical copies of the gene due to a duplication of 212 kb in the genome. However, a deletion of one //xopZ// gene did not affect pathogenicity or bacterial growth in plants, while strains with mutations in both copies of //xopZ// <sub>PXO99</sub> displayed reduced virulence in terms of lesion length and bacterial multiplication compared with the wild type strain PXO99<sup>A</sup> . The introduction of one genomic copy of //xopZ// <sub>PXO99</sub> restores the mutant to full virulence. To test whether XopZ<sub>PXO99</sub> inhibits the host cell-wall-associated defense responses (PTI), leaves of //Nicotiana benthamiana// were infiltrated with //Agrobacterium// cells with and without //xopZ// <sub>PXO99</sub> under the control of the cauliflower mosaic virus 35S promoter 24 hours preceding inoculation of the same leaves with a T3SS mutant of PXO99<sup>A</sup> (ME7). Twenty-four hours after inoculation, leaves inoculated with ME7 had more callose depositions than the leaves inoculated with //Agrobacterium// spp. expressing //xopZ// <sub>PXO99</sub>. This results suggesting a role for XopZ<sub>PXO99</sub> in interfering with host innate immunity (PTI) during //X. oryzae// pv. //oryzae// infection (Song //et al.//, 2010). Besides, Western blot analysis with p44/42 MAP kinase antibody clearly showed that XopN, XopV and XopZ inhibited the peptidoglycan(PNG)-induced phosphorylation of OsMAPKs. Expression of all Xop effectors were verified by immunoblotting with anti-HA antibody. Thus, expression of three Xop effectors from PXO99<sup>A</sup> in rice protoplasts results in compromised OsMAPK activation induced by PGN, highlighting their putative virulence functions during pathogenesis (Long //et al.//, 2018).
  
 A role of XopZ in full virulence was also clearly shown in //Xanthomonas axonopodis// pv. //manihotis// CIO151 but not in PTI or ETI supression, at least under the tested conditions, as on the contrary to XopZ of //X. oryzae// pv. //oryzae// PXO99, no reduction of callose deposition was observed (Medina //et al.//, 2017). A role of XopZ in full virulence was also clearly shown in //Xanthomonas axonopodis// pv. //manihotis// CIO151 but not in PTI or ETI supression, at least under the tested conditions, as on the contrary to XopZ of //X. oryzae// pv. //oryzae// PXO99, no reduction of callose deposition was observed (Medina //et al.//, 2017).
bacteria/t3e/xopz.1751669383.txt.gz · Last modified: 2025/07/04 23:49 by jfpothier

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