|YU, KESHUN - University Of Kentucky|
|SOARES, JULIANA - University Of Kentucky|
|MANDAL, MIHIR - University Of Kentucky|
|WANG, CAIXIA - University Of Kentucky|
|CHANDA, BIDISHA - University Of Kentucky|
|GIFFORD, ANDREW - Brookhaven National Laboratory|
|FOWLER, JOANNA - Brookhaven National Laboratory|
|Navarre, Duroy - Roy|
|KACHROO, AARDRA - University Of Kentucky|
|KACHROO, PRADEEP - University Of Kentucky|
Submitted to: Plant Cell Reports
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/20/2013
Publication Date: 4/25/2013
Citation: Yu, K., Soares, J., Mandal, M., Wang, C., Chanda, B., Gifford, A., Fowler, J., Navarre, D.A., Kachroo, A., Kachroo, P. 2013. A feed-back regulatory loop between glycerol-3-phosphate and lipid transfer proteins DIR1 and AZI1 mediates azelaic acid-induced systemic immunity. Plant Cell Reports. 3:1266-1278.
Interpretive Summary: In plants, recognition of a pathogen by specific resistance proteins often results in the generation of signals that travel to distal parts of the plant and activate broad spectrum resistance, not just at the site of infection but throughout the plant. This work shows how a regulatory loop regulates this broad spectrum disease resistance and advances our understanding of how plants resist disease. Increasing knowledge of plant resistance mechanisms will make it increasingly possible to develop plants with improved disease resistance, which can increase food security and decrease pesticide use.
Technical Abstract: Systemic acquired resistance (SAR), a highly desirable form of plant defense, provides broad-spectrum immunity against diverse pathogens. The recent identification of seemingly unrelated chemical inducers of SAR warrants an investigation of their mutual interrelationships. We show that SAR induced by the dicarboxylic acid, azelaic acid (AA) requires the phosphorylated sugar derivative, glycerol-3-phosphate (G3P). Pathogen inoculation induced the release of free unsaturated fatty acids (FAs) and thereby triggered AA accumulation because these FAs serve as precursors for AA. AA accumulation in turn increased the levels of G3P, which was required for AA-conferred SAR. The lipid transfer proteins, DIR1 and AZI1, both of which are required for G3P and AA-induced SAR, were essential for G3P accumulation. Conversely, reduced G3P resulted in decreased AZI1 and DIR1 13 transcription. Our results demonstrate that an intricate feed-back regulatory loop 14 between G3P, DIR1, and AZI1 regulates SAR and that AA functions upstream of G3P in 15 this pathway.