Hypothetical model for controlling NPH3 phosphorylation status. (a) Regarding the first positive phototropism, pulse BL-activated phot1 causes the forward reaction from the NPH3 dark form (in which pS223 is predominant and pS744 is minor) to the NPH3 BL form (in which pS223 is minor and pS744 is predominant), reaching saturation on the irradiated and shaded sides of the hypocotyl, resulting in the refractory state in the fluence-response curve. (b) Regarding the second positive phototropism, PP2C19 promotes the reverse reaction from the NPH3 BL form to the NPH3 dark form, whereas phot1 promotes the forward reaction, leading to an equilibrium state between the NPH3 dark and BL forms under continuous BL conditions. RL preirradiation suppresses the phot1 autophosphorylation activity through the RPT2 induction, enhancing the reverse reaction from the NPH3 BL form to the NPH3 dark form. In pp2c19 and rpt2 mutants, the equilibrium shifts toward the NPH3 BL form, leading to their abnormalities in the second positive phototropism.