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--- bacteria:t3e:xopz [2024/08/06 15:25] – rkoebnik
+++ bacteria:t3e:xopz [2025/02/24 10:23] (current) – jensboch
@@ Line 2: / Line 2: @@
 Author: Marlène Lachaux\\
-Internal reviewer: [[https://www.researchgate.net/profile/Joel_Pothier2|Joël F. Pothier]]\\
+Internal reviewer: [[https://www.researchgate.net/profile/Joel_Pothier2|Joël F. Pothier]]
-Expert reviewer: **WANTED!**
 Class: XopZ\\
-Family: XopZ1, XopZ2\\
+Families: XopZ1, XopZ2\\
 Prototype: XOO2402 (//Xanthomonas oryzae// pv. o//ryzae//; strain T7174)\\
 GenBank ID (XopZ1): [[https://www.ncbi.nlm.nih.gov/protein/BAE69157.1|BAE69157.1]] (1288 aa)\\
@@ Line 34: / Line 33: @@
 === 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).
@@ Line 50: / Line 49: @@
 === In xanthomonads ===
-Yes, found to be conserved in all //Xanthomonas//spp. (whose genomes have been sequenced) with the exception of some clade-1 strains (//e.g.// //X. albilineans//) (Song and Yang, 2010; Sinha //et al.//, 2013).
+Yes, found to be conserved in all //Xanthomonas //spp. (whose genomes have been sequenced) with the exception of some clade-1 strains (//e.g.//, //X. albilineans//) (Song and Yang, 2010; Sinha //et al.//, 2013).
 === In other plant pathogens/symbionts ===

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