Fig. 7
A model for the regulatory network integrating BR and H2O2 signals in cell elongation. Binding of BR to receptor kinase BRI1 not only inhibits the kinase activity of BIN2 to promote dephosphorylation of BZR1, but also increases cellular level of H2O2, which causes oxidation of BZR1 at a conserved cysteine residue. This oxidation enhances BZR1 transcriptional activity by promoting its interaction with partners, such as ARF6 and PIF4. The oxidized BZR1 is reduced by thioredoxin TRXh5. As the level of H2O2 and TRXh5 activity can be altered by many signals, such redox regulation of BZR1 plays an important role in fine-tuning BR responses by additional signals
