The Pseudomonas syringae type III effector HopD1 suppresses effector-triggered immunity, localizes to the endoplasmic reticulum, and targets the Arabidopsis transcription factor NTL9
No claim to original US Government works. New Phytologist © 2013 New Phytologist Trust.
Veröffentlicht in: | The New phytologist. - 1979. - 201(2014), 4 vom: 16. März, Seite 1358-1370 |
---|---|
1. Verfasser: | |
Weitere Verfasser: | , , , , , |
Format: | Online-Aufsatz |
Sprache: | English |
Veröffentlicht: |
2014
|
Zugriff auf das übergeordnete Werk: | The New phytologist |
Schlagworte: | Journal Article Research Support, N.I.H., Extramural Research Support, U.S. Gov't, Non-P.H.S. bacterial pathogens plant defense plant disease plant immunity type III effector Arabidopsis Proteins Bacterial Proteins mehr... |
Zusammenfassung: | No claim to original US Government works. New Phytologist © 2013 New Phytologist Trust. • Pseudomonas syringae type III effectors are known to suppress plant immunity to promote bacterial virulence. However, the activities and targets of these effectors are not well understood. • We used genetic, molecular, and cell biology methods to characterize the activities, localization, and target of the HopD1 type III effector in Arabidopsis. • HopD1 contributes to P. syringae virulence in Arabidopsis and reduces effector-triggered immunity (ETI) responses but not pathogen-associated molecular pattern-triggered immunity (PTI) responses. Plants expressing HopD1 supported increased growth of ETI-inducing P. syringae strains compared with wild-type Arabidopsis. We show that HopD1 interacts with the membrane-tethered Arabidopsis transcription factor NTL9 and demonstrate that this interaction occurs at the endoplasmic reticulum (ER). A P. syringae hopD1 mutant and ETI-inducing P. syringae strains exhibited enhanced growth on Arabidopsis ntl9 mutant plants. Conversely, growth of P. syringae strains was reduced in plants expressing a constitutively active NTL9 derivative, indicating that NTL9 is a positive regulator of plant immunity. Furthermore, HopD1 inhibited the induction of NTL9-regulated genes during ETI but not PTI. • HopD1 contributes to P. syringae virulence in part by targeting NTL9, resulting in the suppression of ETI responses but not PTI responses and the promotion of plant pathogenicity |
---|---|
Beschreibung: | Date Completed 29.09.2014 Date Revised 17.04.2021 published: Print-Electronic Citation Status MEDLINE |
ISSN: | 1469-8137 |
DOI: | 10.1111/nph.12626 |