A 'shade-avoidance syndrome' in humans could be extremely dangerous, but such a 'syndrome' is essential for plant survival. Plants that grow under dense canopies or that are closely packed can sense a decrease in the ratio of red to far-red incoming light, and this induces responses (such as stem elongation and flowering acceleration) that help them beat the competition. In Arabidopsis, phytochrome (phy) B — a red/far-red light photoreceptor — is known to have an important role in shade avoidance, but how does it function? In Nature, Cerdán and Chory now provide insights.

It has been widely accepted that there is a signalling pathway that induces flowering as part of the shade-avoidance syndrome. However, it has not been clear whether this is an independent signalling pathway or part of another control pathway, such as the photoperiod pathway, which allows plants to respond to changes in day length. CONSTANS (CO) is an important component of the photoperiod pathway and, in Arabidopsis, the photoreceptors phyA and cryptochrome 2 can act through CO to activate FLOWERING LOCUS T (FT), which induces flowering. phyA and phyB regulate flowering in opposite ways — phyA, which discriminates short days (SDs) from long days (LDs), weakly promotes flowering under LD conditions, whereas phyB, which does not, delays flowering under both SD and LD conditions.

In their study, Cerdán and Chory first identified Arabidopsis seedlings that were defective in phyB signalling, and they scored the defective seedlings for faults in flowering time. This allowed them to identify PFT1 (PHYTOCHROME AND FLOWERING TIME 1), a protein that might function specifically in phy signalling downstream of phyA and phyB.

Next, Cerdán and Chory monitored the flowering time of various mutant plants (pft1, phyA and phyB combinations) under SD and LD conditions. Under both sets of conditions, they found that pft1 plants were late flowering and that pft1 could block the early-flowering phenotype of phyB plants. They also found that pft1 plants responded strongly to photoperiod. They therefore proposed that “...the main role of PFT1 in phytochrome signalling is to regulate flowering time downstream of phyB in a photoperiod-independent pathway”.

When the authors cloned PFT1, they found that it encodes a protein that has features similar to some transcriptional activators. Furthermore, by tagging PFT1 with green fluorescent protein, they showed that it is present in the nucleus. In addition, they found that phyB probably regulates PFT1 post-transcriptionally, because the phyB mutation barely affects PFT1 messenger RNA levels.

So, how does pft1 block the phyB early-flowering phenotype? FT integrates several flowering-time pathways, so Cerdán and Chory analysed FT mRNA levels in wild-type, pft1, phyB and pft1 phyB plants. They found that FT mRNA levels are higher in phyB than in wild-type plants, and that FT mRNA levels were low in the pft1 and pft1 phyB plants. These results indicate that phyB could have an inhibitory effect on PFT1, which would otherwise activate its downstream target FT.

The authors confirmed that the phyB/PFT1/FT pathway functions independently of the photoperiod pathway by showing that there is no significant correlation between CO mRNA levels and the flowering time of pft1 or phyB plants. In addition, they verified that PFT1 has a specific role in a phyB pathway that regulates flowering time in response to light-quality changes by showing that pft1 plants are unable to accelerate flowering in response to shade conditions.

Cerdán and Chory therefore propose that the phyB/PFT1/FT pathway is a photoperiod-independent light-quality sensing pathway that triggers flowering in response to a low ratio of red to far-red incoming light. This work has clarified this role of phyB in shade avoidance, and, if plants could be made to delay flowering even when they are shaded by their neighbours, it might also have implications for increasing crop yields.