Figure 1.

Core components of the ABA and light signaling systems. Long-term ABA treatment causes COP1 activation and phyB stimulates the ABA biosynthesis. ABA activates ABA receptors of the PYR/PYL/RCAR family that inhibits A-type protein phosphatases 2C (PP2Cs). PP2C inactivation activates class 3 sucrose nonfermenting-1-related protein kinases (SnRK2s) that phosphorylate ABA-responsive element binding factors AREB/ABF. Activated ABFs initiate the expression of responsive genes by binding to the cis-acting ABA response element (ABRE). In response to light, phytochromes inactivate COP1-SPA complexes and induce degradation of negative regulators of photomorphogenesis, PIFs. PhyB inhibits the regulatory activity of PIF1 and PIF3. These events promote photomorphogenesis by establishing the dynamic protein module PIF1-COP1/SPA1 and triggering HY5-mediated light signaling. Degradation of PIFs and stabilization of HY5 result in promotion of photomorphogenesis. HY5 physically interacts with transcription factors (TFs) and other proteins, and directly affects the expression of numerous genes. By promoting COP1 protein destabilization and turnover, DET1 positively regulates COP1 activity toward the degradation of HY5. Keeping HY5 levels tightly regulated is essential for its functioning during dark-to-light transition.