A Thermosensory ePIFphany!

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Published on: January 25, 2017

Often times in the scientific literature you will find that a topic suddenly becomes trendy. This might follow a technological advancement that opens up a new subject area, a serendipitous co-discovery or after an important publication opens a Pandoras box of questions. Over the past few months the Arabidopsis research literature has seen a number of exciting papers that have tackled different aspects of the plants response to heat, otherwise known as thermosensing.

These papers focus on two aspects of this response, either in heat perception or at the convergence point for the downstream cascade of signals. At the level of perception back-to-back papers published at the end of 2016 showed that phytochromeB, already a well known light receptor, also acts as a temperature sensor [1,2]. At the phenotypic level this involves the regulation of growth, as phyB mutants that have a single point mutation and are stuck in the Pfr form have longer hypocotyls. At the level of gene expression the mutant phyB protein constitutively binds to the promotors of warm-responsive genes. Temperature does not cause changes to PhyB mRNA or protein indicating that the protein directly act as a thermosensor. One of these papers show that PHYB negatively regulates the temperature-dependent expression of the PIF4 transcription factor [2] so in phyB mutants the longer hypocotyl can be traced, at least in part, due to extra PIF4 expression. This regulation is relevant to three more recent papers in which regulation of PIF4 activity is a central and recurring theme.

In the first of these papers Scott Hayes and colleagues investigate the response stimulated by UV light, which is perceived by the UVR8 receptor [3]. They show that whereas PIF4 is stimulated by increasing temperature, this is off-set by the activity of UVR8 which, when subject to high levels of UV-B, reduces PIF4 expression. A possible in vivo explanation for this response is provided in an associated comment piece [4] that postulates that in direct sunlight (where there is plentiful UV-B) there is no need for a hypocotyl elongation. However at high temperature without UV-B, the plant may interpret that it is growing in the shade so it might require a burst of hypocotyl elongation, which is mediated via PIF4.

The final two papers are from the lab of Vinod Kumar and focus on the activity of the PIF4 protein. Firstly they show that two well-studied signaling modules acting via either HY5 or DET1 differently impact PIF4 activity. Whereas DET1 directly interacts with PIF4, HY5 binds to the PIF4 recognition motif on its known DNA targets. At high temperature the HY5 protein is removed by the activity of the E3 ligase COP1, freeing up PIF4 expression. A previous study has shown UVR8 can sequester the COP1 protein so in high UV-B the activity of COP1 may be removed thus allowing HY5 to compete with PIF4 for its binding sites. Although the recent ‘UV-focused study’ [3] showed that HY5 gene expression was increased by UV-B, the role of HY5 in their experiments was slightly confused. The subtle and overlapping roles of these multiple proteins makes it challenging to obtain a complete picture of each of their roles independently of each other, which in any case would be an unrealistic in vivo situation.

As growth increases at higher temperature so does the plants suspectibility to pathogens, processes that are linked via PIF4. pif4 mutants are more resistant to infection and natural variation of the PIF4 gene provides a range of circumstances whereby plants become unresponsive to temperature change yet have higher levels of immunity. These findings have great significance for future crop improvement strategies that are extremely relevant for our warming world.

As with the integration of white light, UV-B and temperature signals, the link between temperature and disease is finely modulated to ensure that the plant maximizes its environmental situation and is able to rapidly adapt to its current conditions (such as on a windy day when the levels of shade and UV-B are highly variable).

This recent set of papers show that the PIF4 protein plays a central role through each adaptive molecular decision.

Vinod Kumar kindly provides an audio overview of this recent set of papers. Also on the GARNet YouTube Channel.

1- Jung et al (2016) Phytochromes function as thermosensors in Arabidopsis Science 354 doi: 10.1126/science.aaf6005

2- Legris et al (2016) Phytochrome B integrates light and temperature signals in Arabidopsis Science 354 http://dx.doi.org/10.1126/science.aaf5656

3- Hayes et al (2016) UV-B Perceived by the UVR8 Photoreceptor Inhibits Plant Thermomorphogenesis Current Biology http://dx.doi.org/10.1016/j.cub.2016.11.004

4- Ezer and Wigge (2017) Current Biology 27, R19–R41

5- Huang et al (2013) Conversion from CUL4-based COP1-SPA E3 apparatus to UVR8-COP1-SPA complexes underlies a distinct biochemical function of COP1 under UV-B PNAS http://dx.doi.org/10.1073/pnas.1316622110

6- Gangappa and Kumar (2017) DET1 and HY5 Control PIF4-Mediated Thermosensory Elongation Growth through Distinct Mechanisms Cell Reports 18, 344–351 January 10, 2017 a 2017 The Author(s). http://dx.doi.org/10.1016/j.celrep.2016.12.046

7- Gangappa et al. (2017) PIF4 Coordinates Thermosensory Growth and Immunity in Arabidopsis Current Biology http://dx.doi.org/10.1016/j.cub.2016.11.012

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  1. […] Over the past few weeks work from either Phil Wigge, Kerry Franklin and Vinod Kumar have moved on our understanding of how PIF4 integrates environmental signals, demonstrating the strength of UK science in this key area of fundamental plant developmental biology. This work is summarised in a post on the GARNet blog. […]

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