AI Article Synopsis
- Researchers identified a protein called XopJ6 that helps cauliflower resist disease, which is related to a known family of acetyltransferases.
- A mutation in XopJ6 affects its ability to interact with proteins involved in plant immunity, allowing it to avoid detection while still being somewhat effective in causing disease.
- The study suggests that variations in the genetic sequence and structure of this effector protein play a significant role in how bacteria adapt to their plant hosts, especially through changes in gene copy numbers.
Article Abstract
Molecular mechanisms underlying quantitative variations of pathogenicity remain elusive. Here, we identified the XopJ6 effector that triggers disease resistance in cauliflower and . XopJ6 is a close homolog of the 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, resides in a Tn-family transposon likely contributing to copy number variation (CNV). Using synthetic biology, we demonstrate that CNV tunes pathogen virulence on Arabidopsis through gene dosage-mediated modulation of expression Together, our findings highlight how sequence and structural genetic variations restricted at a particular effector gene contribute to bacterial host adaptation.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10909901 | PMC |
| http://dx.doi.org/10.1016/j.isci.2024.109224 | DOI Listing |
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