<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>27(3)</volume><submitter>Lauber E</submitter><funding>French National Research Agency</funding><pubmed_abstract>Molecular mechanisms underlying quantitative variations of pathogenicity remain elusive. Here, we identified the &lt;i>Xanthomonas campestris&lt;/i> XopJ6 effector that triggers disease resistance in cauliflower and &lt;i>Arabidopsis thaliana&lt;/i>. XopJ6 is a close homolog of the &lt;i>Ralstonia&lt;/i>&lt;i>pseudo&lt;/i>&lt;i>solanacearum&lt;/i> PopP2 YopJ family acetyltransferase. XopJ6 is recognized by the RRS1-R/RPS4 NLR pair that integrates a WRKY decoy domain mimicking effector targets. We identified a XopJ6 natural variant carrying a single residue substitution in XopJ6 WRKY-binding site that disrupts interaction with WRKY proteins. This mutation allows XopJ6 to evade immune perception while retaining some XopJ6 virulence functions. Interestingly, &lt;i>xopJ6&lt;/i> resides in a Tn&lt;i>3&lt;/i>-family transposon likely co</pubmed_abstract><journal>iScience</journal><pagination>109224</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10909901</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Bacterial host adaptation through sequence and structural variations of a single type III effector gene.</pubmed_title><pmcid>PMC10909901</pmcid><pubmed_authors>Noel LD</pubmed_authors><pubmed_authors>Vicedo C</pubmed_authors><pubmed_authors>Carrere S</pubmed_authors><pubmed_authors>Pichereaux C</pubmed_authors><pubmed_authors>Lauber E</pubmed_authors><pubmed_authors>Escouboue M</pubmed_authors><pubmed_authors>Gris C</pubmed_authors><pubmed_authors>Pouzet C</pubmed_authors><pubmed_authors>Jauneau A</pubmed_authors><pubmed_authors>Deslandes L</pubmed_authors><pubmed_authors>Zhang ZM</pubmed_authors><pubmed_authors>Gonzalez-Fuente M</pubmed_authors><pubmed_authors>Luneau JS</pubmed_authors></additional><is_claimable>false</is_claimable><name>Bacterial host adaptation through sequence and structural variations of a single type III effector gene.</name><description>Molecular mechanisms underlying quantitative variations of pathogenicity remain elusive. Here, we identified the &lt;i>Xanthomonas campestris&lt;/i> XopJ6 effector that triggers disease resistance in cauliflower and &lt;i>Arabidopsis thaliana&lt;/i>. XopJ6 is a close homolog of the &lt;i>Ralstonia&lt;/i>&lt;i>pseudo&lt;/i>&lt;i>solanacearum&lt;/i> PopP2 YopJ family acetyltransferase. XopJ6 is recognized by the RRS1-R/RPS4 NLR pair that integrates a WRKY decoy domain mimicking effector targets. We identified a XopJ6 natural variant carrying a single residue substitution in XopJ6 WRKY-binding site that disrupts interaction with WRKY proteins. This mutation allows XopJ6 to evade immune perception while retaining some XopJ6 virulence functions. Interestingly, &lt;i>xopJ6&lt;/i> resides in a Tn&lt;i>3&lt;/i>-family transposon likely co</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Mar</publication><modification>2026-07-15T00:10:23.56Z</modification><creation>2025-04-19T22:02:56.936Z</creation></dates><accession>S-EPMC10909901</accession><cross_references><pubmed>38439954</pubmed><doi>10.1016/j.isci.2024.109224</doi></cross_references></HashMap>