(A) and (B) Relative seedling growth inhibition of 10-day-old (A) Col-0, bri1-301 and bin2-1 or (B) Col-0 and BZR1Δ seedlings induced by increasing concentrations of flg22 in either light or dark. (C) Relative seedling growth inhibition of 10-day-old Col-0 seedlings grown on medium supplemented or not with BL (1 μM), GA (1 μM), BL+GA (1 μM + 1 μM) or mock solution in light or dark. (D) Relative seedling growth inhibition of Col-0 or wrky40 seedlings induced by increasing concentrations of flg22 in either light or dark. Bars represent SE of n = 16 (A, B and D) or n = 8 (C) Asterisks indicate a statistically significant difference compared to Col-0 in the same condition (light or dark and same concentration of flg22), according to a Student’s t-test (p<0.05); ‘a’ indicates a statistically significant difference compared to the same genotype/treatment and concentration of flg22 in light, according to a Student’s t-test (p<0.05). All experiments were repeated at least three times with similar results. Values are relative to Col-0 (A, B and D) or mock-treated seedlings (C) (set to 100). Absolute values of these experiments are shown in Figure 4—figure supplement 3. (E) Schematic model depicting the BZR1-mediated inhibition of PTI. Upon BR- and DELLA-dependent activation, BZR1 induces the expression of negative regulators of PTI, such as WRKY11, WRKY15, WRKY18, or HBI1. In addition, BZR1 also inhibits the expression of immune genes, acting cooperatively with WRKY40 and possibly other WRKYs. Ultimately, the BZR1-mediated changes in transcription would lead to the suppression of PTI signaling. The PTI signaling pathway is shadowed in violet; the BR signaling pathway is shadowed in green.