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--- bacteria:t3e:xopz [2020/08/02 22:49]
jfpothier
+++ bacteria:t3e:xopz [2020/08/02 23:04] (current)
jfpothier
@@ Line 18: / Line 18: @@
 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 and //Xanthomonas gardneri// strain 101 (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)
 === (Experimental) evidence for being a T3E ===
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 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).
 === Localization ===

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