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. 2017 May 18;12(5):e0177400. doi: 10.1371/journal.pone.0177400

Fig 3. flg22-induced ROS burst is regulated by BRL3 and AtRGS1.

Fig 3

(A) ROS burst in response to 1 μM flg22 in leaf discs of brl3 mutants are slightly higher than wild type (n = 16 to 24). 1 μM flg22 triggers a rapid (within 2–4 minutes) and transient oxidative burst in leaf discs obtained from 6- to 8-week-old Col-0 (wt) but not in fls2 mutants, where the receptor for flg22, FLS2, is genetically ablated. The ROS burst in brl3 mutant plants were elevated slightly but not significantly. (B) ROS burst is fine tuned by BRL3 and AtRGS1. Max ROS burst peak (18th min) in response to 1 μM flg22 in leaf discs of brl3-2/rgs1-2 mutants are significantly higher than wild type (n = 16 to 24). (C) ROS burst is negatively regulated by another member of the BRI1 family, BRL1. brl1 mutants show significantly higher ROS burst than wild type (n = 16 to 24). The point mutation in flg22 co-receptor, BAK1, leads to dimished ROS burst in bak1-5 mutants thus these plants serve as negative control for ROS assay. Measurement of the ROS burst was carried out using the luminol-based luminescence protocol described in Materials and Methods.