Programmed cell death (PCD) in plants refers to rapid and localized cell death that occurs as a result of regular biological processes, or in response to infection or injury. Understanding the molecular mechanisms of PCD will fill key knowledge gaps in regard to plant development or resistance mechanisms. Upon pathogen invasion salicylic acid and reactive oxygen intermediate (ROI) signaling responses are triggered that contribute to the PCD outcome. Substantial research efforts have been conducted to identify genes involved in these PCD pathways including the generation and characterization of disease lesion mimic mutants (DLMMs) that spontaneously express PCD and necrotic lesions that resemble necrotrophic diseases in the absence of infection by a pathogen. The constitutive expression of PCD may be a result of the deletion of gene/s that directly or indirectly suppress PCD when it is not needed. Five fast neutron generated DLMMs in the cultivar (cv) Steptoe background (FN360, FN361, FN365, FN370 and FN396) were crossed with the cv Morex and 400 F2 individuals of each population were screened for the mutant phenotype. Allele frequency mapping was used to map the mutation in each population to different chromosomal locations showing that each was caused by a different gene. Thus, each phenotype is the result of different mutated gene(s) in the PCD pathway that needs to be functionally validated.