The Pseudomonas syringae type III effector HopD1 suppresses effector‐triggered immunity, localizes to the endoplasmic reticulum, and targets the Arabidopsis transcription factor NTL9. Issue 4 (12th December 2013)

• Record Type: Journal Article
• Authors: Block, Anna; Toruño, Tania Y.; Elowsky, Christian G.; Zhang, Chi; Steinbrenner, Jens; Beynon, Jim; Alfano, James R.
• Is Part Of: New phytologist. Volume 201:Issue 4(2014)
• Page Start: 1358
• Page End: 1370
• Publication Date: 2013-12-12
• Subjects: Botany -- Periodicals; 580
• DOI: 10.1111/nph.12626
• Languages: English
• ISSNs: 0028-646X

Abstract

<abstract abstract-type="main" id="nph12626-abs-0001"> <title>Summary</title> <p> <list id="nph12626-list-0001" list-type="bullet"> <list-item> <p> <italic>Pseudomonas syringae</italic> 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.</p> </list-item> <list-item> <p>We used genetic, molecular, and cell biology methods to characterize the activities, localization, and target of the HopD1 type III effector in Arabidopsis.</p> </list-item> <list-item> <p>HopD1 contributes to <italic>P. syringae</italic> 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 <italic>P. syringae</italic> 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 <italic>P. syringae hopD1</italic> mutant and ETI‐inducing <italic>P. syringae</italic> strains exhibited enhanced growth on Arabidopsis <italic>ntl9</italic> mutant plants. Conversely, growth of <italic>P. syringae</italic> 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.</p> </list-item> <list-item> <p>HopD1 contributes to <italic>P. syringae</italic> virulence in part by targeting NTL9, resulting in the suppression of ETI responses but not PTI responses and the promotion of plant pathogenicity.</p> </list-item> </list> </p> </abstract>