DNA Damage and Chromatin Conformation Changes Confer Nonhost Resistance: A Hypothesis Based on Effects of Anti-cancer Agents on Plant Defense Responses

Over the last decades, medical research has utilized DNA altering procedures in cancer treatments with the objective of killing cells or suppressing cell proliferation. Simultaneous research related to enhancing disease resistance in plants reported that alterations in DNA can enhance defense responses. These two opposite perspectives have in common their effects on the center for gene transcription, the nuclear chromatin. A review of selected research from both anticancer- and plant defense-related research provides examples of some specific DNA altering actions: DNA helical distortion, DNA intercalation, DNA base substitution, DNA single cleavage by DNases, DNA alkylation/methylation, and DNA binding/exclusion. The actions of the pertinent agents are compared, and their proposed modes of action are described in this study. Many of the DNA specific agents affecting resistance responses in plants, e.g., the model system using pea endocarp tissue, are indeed anticancer agents. The tumor cell death or growth suppression in cancer cells following high level treatments may be accompanied with chromatin distortions. Likewise, in plants, DNA-specific agents activate enhanced expression of many genes including defense genes, probably due to the chromatin alterations resulting from the agents. Here, we propose a hypothesis that DNA damage and chromatin structural changes are central mechanisms in initiating defense gene transcription during the nonhost resistance response in plants.