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Both phototropins (phot1 and phot2) and cryptochromes (cry1 and cry2) were proven as the Arabidopsis thaliana blue light receptors. Phototropins predominately function in photomovement, and cryptochromes play a role in photomorphogenesis. Although cryptochromes have been proposed to serve as positive modulators of phototropic responses, the underlying mechanism remains unknown. Here, we report that depleting sucrose from the medium or adding gibberellic acids (GAs) can partially restore the defects in phototropic curvature of the phot1 phot2 double mutants under high‐intensity blue light; this restoration does not occur in phot1 phot2 cry1 cry2 quadruple mutants and nph3 (nonphototropic hypocotyl 3) mutants which were impaired phototropic response in sucrose‐containing medium. These results indicate that GAs and sucrose antagonistically regulate hypocotyl phototropism in a cryptochromes dependent manner, but it showed a crosstalk with phototropin signaling on NPH3. Furthermore, cryptochromes activation by blue light inhibit GAs synthesis, thus stabilizing DELLAs to block hypocotyl growth, which result in the higher GAs content in the shade side than the lit side of hypocotyl to support the asymmetric growth of hypocotyl. Through modulation of the abundance of DELLAs by sucrose depletion or added GAs, it revealed that cryptochromes have a function in mediating phototropic curvature. [ABSTRACT FROM AUTHOR]

• 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]

• Root waving responses have been attributed to both environmental and genetics factors, but the potential inducers and transducers of root waving remain elusive. Thus, the identification of novel signal elements related to root waving is an intriguing field of research. • Genetic, physiological, cytological, live cell imaging, and pharmacological approaches provide strong evidence for the involvement of Arabidopsis thaliana NITRIC OXIDE-ASSOCIATED PROTEIN1 (AtNOA1) in salicylic acid (SA)-induced root waving. • SA specially induced root waving, with an overall decrease in root elongation in A. thaliana, and this SA-induced response was disrupted in the Atnoa1 mutant, as well as in nonexpresser of pathogenesis-related genes 1 (npr1), which is defective in SA-mediated plant defense signal transduction, but not in npr3/4 single and double mutants. The expression assays revealed that the abundance of AtNOA1 was significantly increased by application of SA. Genetic and pharmacological analyses showed that SA-induced root waving involved an AtNOA1-dependent Ca2+ signal transduction pathway, and PIN-FORMED2 (PIN2) -based polar auxin transport possibly plays a crucial role in this process. • Our work suggests that SA signaling through NPR1 and AtNOA1 is involved in the control of root waving, which provides new insights into the mechanisms that control root growth behavior on a hard agar surface. [ABSTRACT FROM AUTHOR]