UDP-D-Glucuronate 4-Epimerases 1 (GAE1) and GAE6 are Critical for Pectin Abundance and Immunity in Arabidopsis thaliana
G. BETHKE (1), A. Thao (1), G. Xiong (2), B. Li (3), N. Soltis (3), N. Hatsugai (1), R. Hillmer (1), F. Katagiri (1), D. Kliebenstein (4), M. Pauly (4), J. Glazebrook (1) (1) University of Minnesota, U.S.A.; (2) Energy Biosciences Institute, University of California, U.S.A.; (3) University of California, U.S.A.; (4) University of California, U.S.A.; (5) University of California, U.S.A.

Plant cell walls are important early barriers to infection by pathogens and sources of immunity-inducing signals. Cell walls of Arabidopsis thaliana leaves contain about 50% pectin. Pectin is synthesized from the activated sugar precursor UDP-GalA produced by UDP-D-glucuronate 4-epimerases (GAE). The expression of GAE1 and GAE6 was repressed upon treatment with the bacterial pathogen Pseudomonas syringae pv. maculicola (Pma ES4326) in a manner that depended on central regulators of immunity including PAD4 and EDS1. Mutant gae1 gae6 plants showed increased susceptibility to Pma ES4326 and to specific isolates of the fungal pathogen Botrytis cinerea. Leaves of gae1 gae6 plants are brittle and reduced in the pectin homogalacturonan. Oligogalacturonides (OGs), are released from pectin through the action of pathogen pectinases, and serve as inducers of immune responses. B. cinerea or a commercial pectinase, macerozyme, released less soluble, likely low molecular weight, pectin from gae1 gae6 cell walls than from wild-type Col-0 walls. Immune signaling in response to treatment with a commercial pectinase, macerozyme, but not OGs, is reduced in gae1 gae6 plants. Macerozyme induced Pattern Triggered Immunity to B. cinerea isolate Gallo1 in wild-type Col-0 but not in gae1 gae6, suggesting that generation of an inducing signal was reduced in gae1 gae6. Our data suggest that pectin abundance is an important contributor to physical properties of cell walls and to plant immunity.

Abstract Number: C18-5, P15-435
Session Type: Concurrent