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The P seudomonas syringae type III effector H op D 1 suppresses effector‐triggered immunity, localizes to the endoplasmic reticulum, and targets the A rabidopsis transcription factor NTL 9
Author(s) -
Block Anna,
Toruño Tania Y.,
Elowsky Christian G.,
Zhang Chi,
Steinbrenner Jens,
Bey Jim,
Alfano James R.
Publication year - 2014
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.12626
Subject(s) - pseudomonas syringae , effector , endoplasmic reticulum , biology , virulence , mutant , microbiology and biotechnology , arabidopsis , pathogen , gene , genetics
SummaryP seudomonas 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 H op D 1 type III effector in A rabidopsis. H op D 1 contributes to P . syringae virulence in A rabidopsis and reduces effector‐triggered immunity ( ETI ) responses but not pathogen‐associated molecular pattern‐triggered immunity ( PTI ) responses. Plants expressing H op D 1 supported increased growth of ETI ‐inducing P . syringae strains compared with wild‐type A rabidopsis. We show that H op D 1 interacts with the membrane‐tethered A rabidopsis transcription factor NTL 9 and demonstrate that this interaction occurs at the endoplasmic reticulum ( ER ). A P . syringae hop D 1 mutant and ETI ‐inducing P . syringae strains exhibited enhanced growth on A rabidopsis ntl9 mutant plants. Conversely, growth of P . syringae strains was reduced in plants expressing a constitutively active NTL 9 derivative, indicating that NTL 9 is a positive regulator of plant immunity. Furthermore, H op D 1 inhibited the induction of NTL 9‐regulated genes during ETI but not PTI . H op D 1 contributes to P . syringae virulence in part by targeting NTL 9, resulting in the suppression of ETI responses but not PTI responses and the promotion of plant pathogenicity.