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Bisphenol A causes melatonin biosynthesis epigenetic reprogramming of melatonin biosynthesis genes in arabidopsis
Yu Zheng1,2, Chun Bao1,2, Jingxian Fang2
1Hubei Key Laboratory of Environmental and Health Effects of Persistent Toxic Substances, School of Environment and Health, Jianghan University, Wuhan, China.
Abstract:
Bisphenol A (BPA) is a widely used chemical that is commonly found in soils and surface waters worldwide and acts as an oxidative stressor on plants. Our understanding of how BPA exposure affects cellular redox homeostasis remains limited. We discovered that the epigenetic reprogramming of melatonin biosynthesis helps defend against oxidative stress induced by BPA in Arabidopsis. Five key BPA-responsive genes were identified, with AT1G26220 (encoding SNAT2) showing exceptional specificity to BPA and its analogs in various tissues. BPA binding to consecutive M1-M2 elements in the AT1G26220 promoter led to decreased H3K9ac and H3K14ac levels, subsequently significantly reducing AT1G26220's expression. It alters the melatonin biosynthesis pathway in order to maintain the redox homeostasis in plants by increasing the cellular antioxidative capacity and alleviating specific BPA-induced cellular damage. This epigenetic reprogramming changes the melatonin biosynthesis pathway, enhancing the dynamic redox homeostasis in plants. Additionally, this specific oxidative response in plants reduces the harmful effects of BPA to some extent. Our study finds a sophisticated and structure-specific epigenetic response to BPA in plants, providing a solid molecular mechanism that enhances our understanding of plant resistance to BPA at the cellular level and contributes to assessing BPA risks globally.
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