The Xanthomonas effector XopK harbours E3 ubiquitin-ligase activity that is required for virulence
© 2018 The Authors. New Phytologist © 2018 New Phytologist Trust.
Veröffentlicht in: | The New phytologist. - 1979. - 220(2018), 1 vom: 15. Okt., Seite 219-231 |
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1. Verfasser: | |
Weitere Verfasser: | , , , , , , , , , |
Format: | Online-Aufsatz |
Sprache: | English |
Veröffentlicht: |
2018
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Zugriff auf das übergeordnete Werk: | The New phytologist |
Schlagworte: | Journal Article Research Support, Non-U.S. Gov't Xanthomonas OsSERK2 effector plant immunity ubiquitination Bacterial Proteins Pathogen-Associated Molecular Pattern Molecules Plant Proteins mehr... |
Zusammenfassung: | © 2018 The Authors. New Phytologist © 2018 New Phytologist Trust. Xanthomonas oryzae pv. oryzae is the causative agent of rice bacterial leaf blight. While the type III secretion system of X. oryzae pv. oryzae is essential for virulence, the biochemical activities and virulence mechanisms of non-transcription activator-like (non-TAL) effectors delivered by this system are largely unknown. Here, by screening for non-TAL effectors that contribute to X. oryzae pv. oryzae virulence, we revealed that Xanthomonas outer protein K (XopK) inhibits pathogen-associated molecular pattern-triggered immunity upstream of mitogen-activated protein kinase cascades. Specifically, XopK interacted with and directly ubiquitinated rice somatic embryogenic receptor kinase 2 (OsSERK2), resulting in its degradation. Accordingly, mutation of a putative ubiquitin-conjugation enzyme (E2) binding site abolished XopK-induced degradation of OsSERK2 and compromised XopK-dependent virulence. As crucial immune regulators associated with a multitude of immune receptors, SERKs have been shown to be perturbed by Pseudomonas effectors via different mechanisms. Our study revealed a distinct perturbation mechanism of SERK activity via ubiquitination achieved by Xanthomonas non-TAL effector |
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Beschreibung: | Date Completed 01.10.2019 Date Revised 30.09.2020 published: Print-Electronic Citation Status MEDLINE |
ISSN: | 1469-8137 |
DOI: | 10.1111/nph.15287 |