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. 2017 Sep 5;114(38):10280–10285. doi: 10.1073/pnas.1706593114

Fig. S3.

Fig. S3.

ABA-dependent activation of ABA signaling by RCAR4. (A) Protoplasts of the aba2-1 mutant were transfected with HAI2 effector (0.1 µg) to achieve ∼90% inhibition of ABA signaling at 10 µM exogenous ABA. Cotransfection of RCAR4 effector (5 µg, filled circle) restored ABA signaling, expressed as a fold increase of reporter activity. Cells transfected with the empty vector construct (EV, open circle) served as the control. Protoplasts were exposed to exogenous ABA levels as indicated for ∼16 h before analysis. The ABA response is given as fold induction relative to the control without ABA and RCAR4 expression and was set to 1. (B) Titration of the RCAR4 effector. The analysis was performed as described in A except that the effector DNA varied as indicated in the presence of 100 nM exogenous ABA (+ABA) or without (−ABA). The reporter expression in protoplasts without effector and exogenous ABA was set to 1. Each data point represents the mean of three independent transfections (mean ± SD).