Tobacco Leaf Trichomes Navigate Hypersensitive Cell Death Elicited By The Elicitin ParA1

ParAl produced by Phytophthora parasitica belongs to elicitins that induce hypersensitive cell death (HCD) in tobacco. Leaf trichomes growing on leaf surfaces while exposed to the air may function to sense signals from the environment. Here I studied whether ParAl induces HCD in the trichome cells and whether the trichome navigates the death signal into leaf tissues.Micro-HR was observed in leaf trichome cells following the application of ParAl to the plant. Several responses associated with HCD were induced by the elicitin. In ParAl-treated tricomes, DNA seemed to be fragmentized, showing as smear in gel; chromatins condensed; the cell membrane became more permeable; oxidative burst occurred; and expression of the HCD marker gene hinl was induced. These results suggest that ParAl activates the HCD pathway in leaf trichomes. Particularly, oxidative burst and micro-HR appeared first in the top cell of trichome.Micro-HR developed in mesophylls following treatment of leaves with ParAl. Comparison of the time course of micro-HR and relevant responses occurring in the trichome and leaf tissue indicates a role that the trichome plays in navigating the death signal into leaf tissues. Three hours after ParAl was applied, hinl expression, increase in the membrane permeability, oxidative burst, and chromatin condensation were evident in trichome cells. Comparatively, these events were not observed until 6 hour after treatment. Moreover, micro-HR appeared in trichomes 6 hours posttreatment, whereas it did in mesophyll cells 15 hours. DNA degradation was detected for trichome cells 15 hours, 3 hours earlier than in mesophylls. These results suggest that the HCD process starts first in trichome cells and is progressive into mesophyll cells. Thus, leaf trichome plays a role in navigating the death signal from the top toward mesophylls.