Wounding results in the controlled cell death of a few rows of cells adjacent to disrupted cells resulting in physical wound closure, which combined with phenolic compound deposition, prevents water loss and pathogen entry. The control of these processes remains uncharacterized. Cell death in a mutant of Arabidopsis thaliana lacking BOTRYTIS SENSITIVE1/MYB108 (BOS1/MYB108) function was characterized utilizing physiological, cell biological and genetic methods. The bos1 mutant has a wound induced runaway cell death that includes enhanced reactive oxygen species (ROS) production that followed the extent of enhanced cell death. Exogenous abscisic acid (ABA) enhanced wound induced cell death in Col-0 plants and was sufficient to trigger cell death in bos1. Uncontrolled cell death was dependent of the production and perception of ABA. Furthermore, bos1 had altered sensitivity to and accumulation of ABA. Arabidopsis possesses a genetic program controlling the extent of wound inducible cell death. BOS1 acts as a negative regulator of ABA induced cell death, which functions in the control of this wound sealing program. This program is distinct from other known cell death programs in that it is ABA dependent, but independent of salicylate biosynthesis, ethylene, jasmonate, metacaspases and ROS derived from RBOHD and RBOHF.