Phytochrome B Nuclear Bodies Respond to the Low Red to Far-Red Ratio and to the Reduced Irradiance of Canopy Shade in Arabidopsis.

The current consensus is that plant responses to canopy shade involve the perception of low red to far-red ratios (R:FRs) by phytochrome B (phyB), which leads to the direct activation of auxin synthesis genes by PHYTOCHROME INTERACTING FACTORs (PIFs). In addition to its effect on R:FRs, shade also reduces irradiance, but whether shade-induced drops in irradiance affect phyB activity has not been demonstrated. To address this issue, we investigated whether irradiance and R:FRs have similar effects on the nuclear distribution of phyB in petiole cells of light-grown plants. Under high-irradiance white light, phyB formed large nuclear bodies. Lowering irradiance without changing R:FRs or lowering R:FRs by adding far-red light led to the appearance of small nuclear bodies containing phyB. Large nuclear bodies remained but with some concomitant reduction in diameter. The appearance of small nuclear bodies was rapid, stable, and reversible upon the return to high irradiance and high R:FRs. High levels of red light but not of blue light were enough to restrain the formation of small phyB nuclear bodies. Irradiance was effective within the range found in natural canopies and even under relatively low R:FRs. The promotion of leaf hyponasty by lowering irradiance was impaired in phyB and pif mutants, as previously reported for the response to R:FRs. The expression of auxin-related genes showed a similar hierarchy of response to low R:FRs and low irradiance. We propose that phyB is able to perceive not only the low R:FRs, but also the low irradiance of shade.

Cryptochrome as a sensor of the blue/green ratio of natural radiation in Arabidopsis.

Green light added to blue light has been proposed to shift cryptochromes from their semireduced active form to the reduced, inactive state. Whether the increased proportion of green light observed under leaf canopies compared to open places reduces cryptochrome-mediated effects remained to be elucidated. Here we report that the length of the hypocotyl of Arabidopsis (Arabidopsis thaliana) seedlings grown under controlled conditions decreased linearly with increasing blue/green ratios of the light within the range of ratios found in natural environments. This effect was stronger under higher irradiances. We developed a model, parameterized on the basis of field experiments including photoreceptor mutants, where hypocotyl growth of seedlings exposed to different natural radiation environments was related to the action and interaction of phytochromes and cryptochromes. Adding the blue/green ratio of the light in the term involving cryptochrome activity improved the goodness of fit of the model, thus supporting a role of the blue/green ratio under natural radiation. The blue/green ratio decreased sharply with increasing shade by green grass leaves to one-half of the values observed in open places. The impact of blue/green ratio on cryptochrome-mediated inhibition of hypocotyl growth was at least as large as that of irradiance. We conclude that cryptochrome is a sensor of blue irradiance and blue/green ratio.

Suppression of pleiotropic effects of functional cryptochrome genes by Terminal Flower 1.

TERMINAL FLOWER 1 (TFL1) encodes a protein with similarity to animal phosphatidylethanolamine-binding proteins and is required for normal trafficking to the protein storage vacuole. In Arabidopsis thaliana the tfl1 mutation produces severe developmental abnormalities. Here we show that most aspects of the tfl1 phenotype are lost in the cry1 cry2 double-mutant background lacking cryptochromes 1 and 2. The inhibition of hypocotyl growth by light is reduced in the tfl1 mutant but this effect is absent in the cry1 or cry2 mutant background. Although the promotion of flowering under long rather than short days is a key function of cryptochromes, in the tfl1 background, cryptochromes promoted flowering under short days. Thus, normal CRY control of photoperiod-dependent flowering and hypocotyl growth inhibition requires a functional TFL1 gene.