Abstract
In Arabidopsis, the seedling hypocotyl has emerged as an exemplar model system to study light and temperature control of cell expansion. Light sensitivity of this organ is epitomized in the fluence rate response where suppression of hypocotyl elongation increases incrementally with light intensity. This finely calibrated response is controlled by the photoreceptor, phytochrome B, through the deactivation and proteolytic destruction of phytochrome-interacting factors (PIFs). Here we show that this classical light response is strictly temperature dependent: a shift in temperature induces a dramatic reversal of response from inhibition to promotion of hypocotyl elongation by light. Applying an integrated experimental and mathematical modelling approach, we show how light and temperature coaction in the circuitry drives a molecular switch in PIF activity and control of cell expansion. This work provides a paradigm to understand the importance of signal convergence in evoking different or non-intuitive alterations in molecular signalling.
Highlights
In Arabidopsis, the seedling hypocotyl has emerged as an exemplar model system to study light and temperature control of cell expansion
As PIF4 and PIF5 have been implicated in temperaturedependent hypocotyl elongation, they presented good candidate regulators of the photothermal switch[6,10,20,31]
We used the simple hypocotyl system to interrogate the interaction between light and temperature through the phytochrome B (phyB)– phytochromeinteracting factors (PIFs) signalling module. phyB inhibits while PIFs promote hypocotyl extension and control is achieved through reciprocal phyB–PIF cross-regulation
Summary
In Arabidopsis, the seedling hypocotyl has emerged as an exemplar model system to study light and temperature control of cell expansion. The previous decades of research have identified multiple photoreceptors, downstream factors and hormonal pathways regulating and fine tuning this process[2,3,4,5], often utilizing seedling hypocotyl length to measure the extent of de-etiolation As elongation of this simple organ is regulated by ambient temperature, the hypocotyl provides a tractable system to study the intersection of light and temperature[6,7,8,9,10,11]. An earlier report showed that light is required for the auxin-induced hypocotyl cell elongation at high temperatures[8] This observation is in apparent conflict with current understanding that light, acting through photoreceptors such as phyB, is a strong suppressor of hypocotyl extension
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