Abstract
High temperature promotes guard cell expansion, which opens stomatal pores to facilitate leaf cooling. How the high-temperature signal is perceived and transmitted to regulate stomatal aperture is, however, unknown. Here, we used a reverse-genetics approach to understand high temperature-mediated stomatal opening in Arabidopsis (Arabidopsis thaliana). Our findings reveal that high temperature-induced guard cell movement requires components involved in blue light-mediated stomatal opening, suggesting cross talk between light and temperature signaling pathways. The molecular players involved include phototropin photoreceptors, plasma membrane H+-ATPases, and multiple members of the 14-3-3 protein family. We further show that phototropin-deficient mutants display impaired rosette evapotranspiration and leaf cooling at high temperatures. Blocking the interaction of 14-3-3 proteins with their client proteins severely impairs high temperature-induced stomatal opening but has no effect on the induction of heat-sensitive guard cell transcripts, supporting the existence of an additional intracellular high-temperature response pathway in plants.
Highlights
47 Plants experience constant fluctuations in temperature and are increasingly exposed to global heatwaves (Perkins et al 2012)
We report the existence of a high-temperature signalling pathway controlling Arabidopsis guard cell movement that requires phototropins and plasma membrane (PM) H+-ATPase activity for full stomatal opening, yet operates independently from known high temperature-signalling components
Isolated guard cells respond to high temperature in the light and the dark Stomatal responses to high temperature were investigated using epidermal peel bioassays to ensure that temperature effects could be analysed in isolation, without confounding alterations in humidity
Summary
47 Plants experience constant fluctuations in temperature and are increasingly exposed to global heatwaves (Perkins et al 2012). High temperature-induced hypocotyl elongation has been attributed, in part, to accelerated reversion of the plant photoreceptor phytochrome B (phyB) to its inactive Pr form during long nights and at low light levels (Jung et al, 2016; Legris et al, 2016). PhyB inactivation elevates abundance of the bHLH transcription factor PHYTOCHROME INTERACTING FACTOR 4 (PIF4), driving auxin biosynthesis and stem elongation (Koini et al, 2009; Franklin et al., 2011; Jung et al, 2016). PIF4 promotes the accumulation of FLOWERING LOCUS T (FT) transcript to accelerate flowering in short photoperiods (Kumar et al, 2012). High temperature-mediated upregulation of FT and HEAT SHOCK PROTEIN 70 (HSP70) transcripts involves eviction of the alternative histone, H2A.Z, from nucleosomes. Induction of HSPs by heat shock in Arabidopsis protoplasts has further been shown to involve the heat-activated calcium channel CYCLIC NUCLEOTIDE-GATED ION CHANNEL 6 (CNGC6) (Gao et al, 2012)
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