LHY2 Integrates Night-Length Information to Determine Timing of Poplar Photoperiodic Growth

For boreal and temperate regions, one of the most important adaptations of the trees is to cease growth to prepare for the winter, mainly to protect the shoot apical meristems which will resume the tree growth in the following vegetative season. In those latitudes, photoperiod (hours of daylight) is considered as the most important external cue, being short days the growth-repressing signal.

In a similar way, flowering plants integrate this photoperiodic information to trigger flowering. In the model plant Arabidopsis thaliana, which is a facultative long-day plant, the decision to flower was explained by an external coincidence model. This means that the protein which leads to flower (FT) is produced when the synthesis of its activator carries out during the day. This model was also proposed to explain the growth cessation in trees. However, due to some data suggest an additional repressive mechanism, in this work we focused on unraveling the importance of the night instead of the day regarding the growth cessation, obtaining original and interesting results.

Ramos-Sánchez et al. (2019) show that the circadian clock gene LHY2 rises its expression increasing the night hours, only by extending the night but not advancing it. We also show that this increase seems to be quantitative and it is abolished by a night break with red light. Regarding FT2 expression, we observe a quantitative decrease in its mRNA accumulation whenever we extend the night and that the SD-repressing effects disappeared after a night break with red light.

Through molecular and genetic experiments using cutting edge plant molecular biology methodologies, we demonstrate that LHY2 necessary and sufficient to repressed FT2 gene in response to night-length by direct binding to its 3’ cis regulatory region. Then, we propose a molecular and genetic repressive model by which the tree is able to integrate in a quantitative way the hours of night, using this information for regulating the growth cessation.