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Salicylic Acid Signaling in Plant Immunity

EPA Grant Number: F07D10639
Title: Salicylic Acid Signaling in Plant Immunity
Investigators: Jones, Alexander M.
Institution: University of California - Berkeley
EPA Project Officer: Manty, Dale
Project Period: September 1, 2007 through September 1, 2010
RFA: STAR Graduate Fellowships (2007)
Research Category: Biology/Life Sciences , Fellowship - Biology/Life Sciences , Fellowship - Plant Biology , Academic Fellowships

Description:

Objective:

Plant diseases reduce crop yields and necessitate the use of toxic pesticides in crop production practices. Better pest management strategies are necessary to reduce or eliminate use of these toxic, though economically critical, chemicals released into the environment for the purpose of crop protection.

The outcome of a plant pathogen interaction, whether it is resistance or disease, is the result of an intricate and delicate duel between the plant immune system and pathogenic attack. The plant hormone salicylic acid (SA) is a key signal in the induction of the plant immune response to pathogens, and is therefore of great interest in plant pathology and crop protection. It is responsible for controlling critical aspects of both basal and resistance gene based immunity, and for promotion of the long lasting, broadly effective immunity termed systemic acquired resistance (SAR). In fact, analogs of SA have long been used on crops to modulate the immune response to pathogens, improve resistance, and reduce the need for other, more toxic pesticides. However, studies have shown that there are fitness costs associated with activation of these defenses. Therefore, a more targeted approach in which a subset of responses is activated may be superior to broad spectrum induction of the plant immune system. The research outlined below will uncover components of SA-based immunity and can guide more advanced and environmentally benign crop protection efforts.

Approach:

Molecular genetic and biochemical approaches will be combined to investigate two key steps in SA immunity, SA biosynthesis and SA activation of defense genes. In the model plant Arabidopsis thaliana, SA production in response to pathogens is induced through the increased expression of its biosynthetic enzyme, isochorismate synthase 1 (AtICS1). A high throughput assay system based on promoter-reporter (ICS1::Luciferase) transgenes will be used to discover cis-elements and cell machinery regulating AtICS1 and elucidate how the plant cell controls SA biosynthesis in response to chosen biotic and abiotic stresses. The WRKY38 transcription factor is rapidly and specifically activated by SA and is likely to regulate a subset of defense genes responsible for SA dependent immunity. WRKY38 mutant plants will be analyzed using pathogenesis assays to identify the functional relevance of WRKY38 regulation. This information will be combined with genome-wide transcriptional profiling (microarray) and target identification (chromatin immunoprecipitation) studies to identify the genes and mechanisms responsible for the WRKY38 node of plant immunity.

Expected Results:

The regulatory networks of SA signaling in plant immunity are complex. This is why targeted and detailed approaches as outlined above are needed to move forward in this field. As SA also mediates SAR in crop species, better understanding of the specific controls over Arabidopsis defense against pathogens will facilitate the design of more efficient and safer treatment and resistance in crop plants.

Supplemental Keywords:

Plant biology, plant immunity, crop resistance, Arabidopsis thaliana, salicylic acid, transcriptional regulation, transcription factor, AtICS1, AtWRKY38, pesticide reduction, crop protection, molecular genetics, biochemistry, promoter bashing, , Scientific Discipline

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The perspectives, information and conclusions conveyed in research project abstracts, progress reports, final reports, journal abstracts and journal publications convey the viewpoints of the principal investigator and may not represent the views and policies of ORD and EPA. Conclusions drawn by the principal investigators have not been reviewed by the Agency.


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