Function of NOT9B and the CCR4-NOT complex in phytochrome A dependent light signalling

• Applicant: Professor Dr. Andreas Hiltbrunner
• Subject Area: Plant Physiology
• Term: from 2020 to 2023
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 453030721

Phytochromes (phys) are red/far-red photoreceptors in plants that play a critical role in adaptation of growth and development to changes in the environment. In most plants, phytochromes are represented by small gene families. PhyA and phyB are the main phytochromes in seed plants involved in regulation of growth and development, including seed germination, de-etiolation, induction of flowering, and responses to canopy shade. PhyB is the primary receptor for red light, while phyA is required for sensing far-red light and light of very low intensity.When activated by light, phytochromes translocate from the cytosol into the nucleus and regulate gene expression. There are two well-investigated signalling pathways downstream of phytochromes that inhibit light responses. The PHYTOCHROME INTERACTING FACTORs (PIFs), a subgroup of the bHLH transcription factors, negatively regulate light signalling. In parallel, the CONSTITUTIVELY PHOTOMORPHOGENIC 1/SUPPRESSOR OF PHYA-105 (COP1/SPA) E3 ubiquitin ligase complex targets positive regulators of light signalling for degradation by the proteasome. Light-activated phytochromes inhibit both PIFs and COP1/SPA and thereby induce responses to light.To identify novel signalling pathways downstream of phytochromes that are potentially independent of PIFs and COP1/SPA, we performed a yeast two hybrid screen for proteins that interact with light-activated phyA. In this screen we found NOT9B, a component of the CCR4-NOT complex. The CCR4-NOT complex is comparably well characterised in yeast, Drosophila, and mammals and plays a role in different aspects of RNA metabolism and regulation of gene expression. However, much less is known about the function of CCR4-NOT in plants. We show that NOT9B is a negative regulator of phyA-mediated light responses and we propose that NOT9B associated with CCR4-NOT represses light signalling. Preliminary data show that light-activated phyA binds NOT9B and thereby displaces NOT9B from CCR4-NOT to relieve repression of phyA-dependent light signalling. In the proposed project we want to further investigate the molecular mechanisms underlying regulation of CCR4-NOT by phyA and understand how CCR4-NOT modulates expression of light-controlled genes.

• DFG Programme: Research Grants