NITRIC OXIDE ASSOCIATED PROTEIN1 (AtNOA1) is necessary for copper-induced lateral root elongation in Arabidopsis thaliana.

• Stimulation of lateral root formation in response to excess Cu2+ exposure is one of an important strategies to avoid Cu2+-induced damage in plant. • We reported that NITRIC OXIDE ASSOCIATED PROTEIN1 (AtNOA1) participated in Cu2+-induced lateral root (LR) formation by affecting Cu2+ homeostasis and Cu2+-induced auxin relocation. • In addition, Cu2+-induced H 2 O 2 level was higher in Atnoa1 than WT, but the accumulation of H 2 O 2 have no effect on Cu2+-induced LR formation. Copper (Cu2+) is an essential metal micronutrients required for normal plant growth and development, but is highly toxic when in excess. Inhibition of primary root elongation and stimulation of lateral root (LR) formation are usual reported symptoms when exposure to high concentrations of Cu2+. The mechanism underlying Cu2+-induced LR formation remains to be further elucidated. Here, we reported that Cu2+-induced LR formation is regulated by NITRIC OXIDE ASSOCIATED PROTEIN1 (AtNOA1), mainly through mediating Cu2+-induced LR elongation growth, but not LR primordium initiation. The initiation of LR primordium is inhibited by the mutation of AtNOA1. Transcriptional analysis displayed that the expression of genes involved in Cu2+ homeostasis and tolerance showed significant difference between Atnoa1 and WT. Cu2+-induced auxin redistribution was inhibited in Atnoa1 , indicated by auxin response reporter plants (DR5:GUS and DR5:GFP). Furthermore, Cu2+-induced LR formation were more sensitive to exogenous auxin transport inhibitors NOA and NPA in Atnoa1 than in WT. Interestingly, Cu2+-induced H 2 O 2 level was higher in Atnoa1 than WT, but Cu2+-induced LR formation was normal in H 2 O 2 -related mutants. These results showed that AtNOA1 regulated the initiation of LR primordium and mediates Cu2+-induced LR elongation in Arabidopsis thaliana. AtNOA1 mediates Cu2+-induced LR elongation maybe through affecting Cu2+ homeostasis and Cu2+-induced auxin redistribution, but not depending on Cu2+-induced H 2 O 2 accumulation. [ABSTRACT FROM AUTHOR]