Interplay between genotoxic factors formaldehyde and UV-B exacerbates genome instability in Arabidopsis

Abstract

Maintenance of genome stability is quintessential feature for all living\norganisms. The simplest aldehyde formaldehyde and UV-B radiation, two\nenvironmental toxic factors, cause DNA damage, affect genome stability,\nsubsequently growth and development across kingdoms. However, the\ninterrelationship of genotoxicity caused by formaldehyde and UV-B\nremains fragmented in plants. Here, we show that mutants lacking one\naldehyde detoxifying enzyme, alcohol dehydrogenase 2 (ADH2, also named\nGSNOR/FALDH), are hypersensitive to low dosage UV-B radiation or UV-B\nradiation-mimetic chemical in seedling and root growth. The defects are\nnot caused by the alteration of UV-B sensing, secondary metabolites\nflavonoid accumulation, or ROS accumulation, rather are UV-B-induced\ngenotoxicity. Increased DNA damage response genes and comet assay tail,\ncell cycle arrest upon exposure to UV-B provide direct evidence for DNA\ndamage in gsnor mutant. Pharmacological analyses show that the\nsusceptibility to genotoxic stresses is caused by the increased DNA\ncrosslink which results from the enhanced endogenous formaldehyde in\ngsnor while UV-B promotes the production of formaldehyde. This implies\nformaldehyde clearance through GSNOR plays a critical role in response\nto environmental genotoxic stress and interplay between formaldehyde and\nUV-B exacerbates genome instability.