Plants and animals respond to PAMPs (pathogen-associated molecular patterns) that are indicative of pathogens. Oligogalacturonides (OGs), plant cell wall fragments generated by pathogen polygalacturonases, function as a PAMP in Arabidopsis thaliana. We hypothesize that OG-activated innate immune response pathways are among the most ancient and are most similar to so-called """"""""Toll-like"""""""" innate immune signaling pathways in animals. An important unanswered question in plant innate immunity is how PAMP-activated pathways relate to signaling pathways that respond to pathogen-specific signals.
The specific aims are designed to further investigate Arabidopsis OG signaling pathway(s) and to identify Pseudomonas syringae Type III effectors that disrupt these pathways. We also hypothesize those Og-activated genes that encode cytochrome P450s function in the biosynthesis of antimicrobial compounds. We have found that some P. syringae strains elicit the exudation of antimicrobial secondary products from Arabidopsis roots, but that P. syringae strain DC3000 blocks this exudation in a process that involves Type III secretion. This is a novel system to study how PAMP-elicited innate immune responses confer basal resistance and how pathogens overcome this resistance. There are five aims. We propose to use a variety of molecular genetic and genomic methods to determine how the OG signaling pathway intersects with other defense response signaling pathways. We will use forward genetic and genomic analyses to identify components of OG signaling pathway(s). We will identify P. syringae type III effectors that block OG-activated signaling pathways and/or the synthesis/exudation of antimicrobial compounds by roots. We will identify signaling pathways that lead to the biosynthesis of antimicrobial compounds. Finally, we will enter the data from this project into IMDS, a public, web-accessible relational database.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Method to Extend Research in Time (MERIT) Award (R37)
Project #
5R37GM048707-17
Application #
7541751
Study Section
Genetics Study Section (GEN)
Program Officer
Anderson, James J
Project Start
1993-01-01
Project End
2009-12-31
Budget Start
2009-01-01
Budget End
2009-12-31
Support Year
17
Fiscal Year
2009
Total Cost
$465,993
Indirect Cost
Name
Massachusetts General Hospital
Department
Type
DUNS #
073130411
City
Boston
State
MA
Country
United States
Zip Code
02199
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