Transcription factor AtNAC002 positively regulates Cu toxicity tolerance in Arabidopsis thaliana

Copper (Cu) is an essential micronutrient for plant growth and development, but environmental Cu pollution has become increasingly severe, adversely affecting both ecosystems and crop productivity. In this study, we identified the AtNAC002 gene as a positive regulator of Cu toxicity in Arabidopsis thaliana. We found that AtNAC002 expression was induced by Cu excess, and the atnac002 mutant was Cu-sensitive, accumulating more Cu than the wild-type. Additionally, atnac002 mutants exhibit reduced activities of antioxidant enzymes (SOD, POD, and CAT), leading to increased levels of reactive oxygen species and malondialdehyde, which decrease Cu resistance. AtNAC002 might play a role in vacuolar and mitochondrial Cu compartmentalization by regulating genes involved in Cu detoxification, specifically COX11 and HCC1. Furthermore, AtNAC002 was implicated in flavone and flavanol biosynthesis, with the atnac002 mutant showing reduced flavonoid content. Our findings suggest that AtNAC002 is integral to the regulation of Cu toxicity tolerance in A. thaliana. This knowledge is critical for advancing our understanding and offers potential molecular breeding targets to enhance plant performance under Cu excess, which is significant for improving global food security and forest restoration. ●AtNAC002 was identified as a positive Cu toxicity regulator in Arabidopsis thaliana, advancing our understanding of plant Cu stress tolerance.●Under Cu stress, AtNAC002 is induced, and the atnac002 mutant shows heightened Cu sensitivity with higher Cu2+ accumulation than WT.●AtNAC002 regulates genes involved in Cu sequestration and storage for detoxification such as COX11 and HCC1, aiding plants in minimizing Cu toxicity.