Minisymposium 26: Plant Pathogen Interactions
Add
this abstract to my Itinerary
Abs #
M2603: A Small Number of WRKY Transcription Factors Mediate Defense Responses Downstream of NPR1
|
|
Presenter: |
Wang, Dong Contact Presenter |
Authors | Wang, Dong (A) Amornsiripanitch, Nita (A) Dong, Xinnian (A) | | Affiliations: |
(A): Development, Cell, and Molecular Biology Group, Department of Biology, Duke University, Durham, NC 27708, USA
|
|
|
Systemic Acquired Resistance (SAR) is an important form of inducible plant defense response against a broad spectrum of pathogens. In Arabidopsis, SAR is preceded by the accumulation of the small signaling molecule salicylic acid (SA), which through a redox switch activates the central regulator protein NPR1. NPR1 plays a multi-facet role in establishing SAR. On one hand, it induces the expression of myriad genes required for broad-spectrum resistance. On the other hand, NPR1 also prevents excessive accumulation of SA to mitigate its cytotoxic effect. Some NPR1 target genes encode transcriptional regulators and thus may represent important nodes of an intricate regulatory network. Using a genomic approach, we discovered that NPR1 directly induces eight WRKY transcription factors, members of a large gene family implicated in diverse defense responses against plant pathogens. Reverse genetic analysis defined the roles of several of these WRKY factors. One central player is WRKY18, which when disrupted resulted in impaired resistance to a bacterial pathogen. Transcriptional profiling revealed a few hundred NPR1-dependent genes under the control of WRKY18, which may explain the observed defects. The ability of NPR1 to negatively regulate the levels of SA is carried out by WRKY70 and its close homolog WRKY54: knocking out both genes caused SA to accumulate to abnormally high levels. Finally, WRKY53 and WRKY58 play positive and negative roles respectively in fine-tuning the final defense response output. Taken together, our results reveal an intricate transcriptional regulatory network underlying the onset of SAR.