ABSTRACT
After localized invasion by bacterial pathogens, systemic acquired resistance (SAR) is induced in uninfected plant tissues, resulting in enhanced defense against a broad range of pathogens. Although SAR requires mobilization of signaling molecules via the plant vasculature, the specific molecular mechanisms remain elusive. The lipid transfer protein-defective in induced resistance 1-1 (DIR1-1) was identified in Arabidopsis thaliana by screening for mutants that were defective in SAR. Here we demonstrate that stomatal response to pathogens is altered in systemic leaves by SAR, and this guard cell SAR defense requires DIR1. Using a multi-omics approach, we have determined potential SAR signaling mechanisms specific for guard cells in systemic leaves by profiling metabolite, lipid, and protein differences between guard cells in wild type and dir1-1 mutant during SAR. We identified two 18C fatty acids and two 16C wax esters as putative SAR-related molecules dependent on DIR1. Proteins and metabolites related to amino acid biosynthesis and response to stimulus were also changed in guard cells of dir1-1 compared to wild type. Identification of guard cell-specific SAR-related molecules may lead to new avenues of genetic modification/molecular breeding for disease resistant plants.
One-sentence summary DIR1 affects many biological processes in stomatal guard cells during systemic acquired resistance (SAR), as revealed by multi-omics, and it may function through transporting two 18C fatty acids during SAR.
Footnotes
1 This material is based upon work supported by the National Science Foundation under Grant No. 1920420.
↵2 Author for contact: schen{at}ufl.edu
↵3 Senior author.
The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Sixue Chen (schen{at}ufl.edu).
S.C., and L.D. conceived and designed the research; L.D., J.K., J.N., and C.D. carried out all experimental work; L.D conducted data analysis, and L.D. and S.C. prepared manuscript.