VND genes redundantly regulate cell wall thickening during parasitic nematode infection.

ABSTRACT

Plant-parasitic root knot nematodes are major agricultural pests worldwide, as they infect plant roots and cause substantial damages to crop plants. Root-knot nematodes induce specialized feeding cells known as giant cells in the root vasculature, which serve as nutrient reservoirs for the infecting nematodes. Here we show that the cell walls of giant cells thicken to form pitted patterns that superficially resemble to metaxylem cells. Interestingly, VASCULAR-RELATED NAC-DOMAIN1 (VND1) was found to be up-regulated, while the xylem-type programmed cell death marker XYLEM CYSTEINE PEPTIDASE 1 (XCP1) was down-regulated upon nematode infection. The vnd2 and vnd3 mutants showed reduced secondary cell wall pore size, while the vnd1 vnd2 vnd3 triple mutant produced significantly fewer nematode egg masses when compared with the wild type. These results suggest that giant cell development pathway likely share common signaling modules with the metaxylem differentiation pathway, and VND1, VND2, and VND3 redundantly regulate plant-nematode interaction through secondary cell wall formation.