Phytochrome signaling mechanisms and the control of plant development

Abstract

As they emerge from the ground, seedlings adopt a photosynthetic lifestyle, which is accompanied by dramatic changes in morphology and global alterations in gene expression that optimizes the plant body plan for light capture. Phytochromes are red and far-red photoreceptors that play a major role during photomorphogenesis, a complex developmental program that seedlings initiate when they first encounter light. The earliest phytochrome signaling events after excitation by red light include their rapid translocation from the cytoplasm to subnuclear bodies (photobodies) that contain other proteins involved in photomorphogenesis, including a number of transcription factors and E3 ligases. In the light, phytochromes and negatively acting transcriptional regulators that interact directly with phytochromes are destabilized, whereas positively acting transcriptional regulators are stabilized. Here, we discuss recent advances in our knowledge of the mechanisms linking phytochrome photoactivation in the cytoplasm and transcriptional regulation in the nucleus.

Figure 1. Two classes of photomorphogenetic mutants

The left panel shows 4-day old wild-type Col-0 and det1-1 seedlings grown in the dark; the right panel shows 4-day old Col-0, phyB-9, and hmr-2 seedlings grown under 8 μmol m^-2 s^-1 of R light.

Figure 2. Regulatory mechanisms of phyA nuclear accumulation

The nuclear accumulation of phyA is facilitated by FHY1 and FHL. FHY1/FHL are down-regulated by phyA signaling both at the transcriptional and post-translational levels.

Figure 3. Phy signaling pathways to turn on photomorphogenesis

There are two major signaling pathways: first, in the “blue” pathway, phys de-repress the positively acting transcriptional regulators, including HY5, LAF1 and HFR1, by inhibiting the COP1 and DET1 containing CUL4 E3 ubiquitin ligases; Second, in the “orange” pathway, phys trigger the degradation of the negatively acting transcriptional regulators PIFs. The activity of PIFs could be enhanced by the COP1/DET1 through HFR1 repression; the protein stability of at least PIF3 is promoted by COP1 through an unknown mechanism. The recently identified HMR acts early in the pathways and is involved in the degradation of PIFs and phyA as well as the inhibition of DET1.