Plants sense the presence of potentially competing nearby individuals as a reduction in the red to far‐red ratio of the incoming light. In anticipation of eventual shading, a set of plant responses known as the shade avoidance syndrome (SAS) is initiated soon after detection of this signal by the phytochrome photoreceptors. Here we analyze the function of P HYTOCHROME R A PIDLY R EGULATED 1 ( PAR1) and PAR2 , two Arabidopsis thaliana genes rapidly upregulated after simulated shade perception. These genes encode two closely related atypical basic helix–loop–helix proteins with no previously assigned function in plant development. Using reverse genetic approaches, we show that PAR1 and PAR2 act in the nucleus to broadly control plant development, acting as negative regulators of a variety of SAS responses, including seedling elongation and photosynthetic pigment accumulation. Molecularly, PAR1 and PAR2 act as direct transcriptional repressors of two auxin‐responsive genes, S MALL A UXIN U P R EGULATED 15 ( SAUR15 ) and SAUR68 . Additional results support that PAR1 and PAR2 function in integrating shade and hormone transcriptional networks, rapidly connecting phytochrome‐sensed light changes with auxin responsiveness.

Circadian rhythms are daily biological oscillations driven by an endogenous mechanism known as circadian clock. The protein kinase CK2 is one of the few clock components that is evolutionary conserved among different taxonomic groups. CK2 regulates the stability and nuclear localization of essential clock proteins in mammals, fungi, and insects. Two CK2 regulatory subunits, CKB3 and CKB4, have been also linked with the Arabidopsis thaliana circadian system. However, the biological relevance and the precise mechanisms of CK2 function within the plant clockwork are not known. By using ChIP and Double–ChIP experiments together with in vivo luminescence assays at different temperatures, we were able to identify a temperature-dependent function for CK2 modulating circadian period length. Our study uncovers a previously unpredicted mechanism for CK2 antagonizing the key clock regulator CIRCADIAN CLOCK-ASSOCIATED 1 (CCA1). CK2 activity does not alter protein accumulation or subcellular localization but interferes with CCA1 binding affinity to the promoters of the oscillator genes. High temperatures enhance the CCA1 binding activity, which is precisely counterbalanced by the CK2 opposing function. Altering this balance by over-expression, mutation, or pharmacological inhibition affects the temperature compensation profile, providing a mechanism by which plants regulate circadian period at changing temperatures. Therefore, our study establishes a new model demonstrating that two opposing and temperature-dependent activities (CCA1-CK2) are essential for clock temperature compensation in Arabidopsis. Most organisms are able to rhythmically coordinate their physiology and metabolism in consonance with the day-night cycle. The cellular mechanism responsible for generating the biological rhythms is known as circadian clock. In contrast to many other biochemical reactions, the pace of the clock does not change with temperature (i.e. the clock does not run faster at high temperatures). This is a property known as clock temperature compensation, and despite its importance for circadian function, we know few details about the mechanisms responsible for the temperature-dependent regulation of circadian period length. Plants, as sessile organisms, are particularly sensible to maintaining the clock running at the proper pace, regardless the external temperature. In our study, we have identified that the activity of two key plant clock components (CK2 and CCA1) is regulated by temperature. Notably, these temperature-dependent activities are antagonistic, and they counterbalance each other at increasing temperatures so that the clock does not run faster at these high temperatures. When we alter the expression and activity of CK2 and CCA1, we observe that the clock is not longer able to maintain the proper pace, thus demonstrating that the balance between these two activities is essential for clock temperature compensation in plants.

A dominant suppressor of the ABAR overexpressor, soar1-1D, from CHLH/ABAR [coding for Mg-chelatase H subunit/putative abscisic acid (ABA) receptor (ABAR)] overexpression lines was screened to explore the mechanism of the ABAR-mediated ABA signalling. The SOAR1 gene encodes a pentatricopeptide repeat (PPR) protein which localizes to both the cytosol and nucleus. Down-regulation of SOAR1 strongly enhances, but up-regulation of SOAR1 almost completely impairs, ABA responses, revealing that SOAR1 is a critical, negative, regulator of ABA signalling. Further genetic evidence supports that SOAR1 functions downstream of ABAR and probably upstream of an ABA-responsive transcription factor ABI5. Changes in the SOAR1 expression alter expression of a subset of ABA-responsive genes including ABI5. These findings provide important information to elucidate further the functional mechanism of PPR proteins and the complicated ABA signalling network.

The hormone abscisic acid (ABA) regulates the stress signals crucial for plant tolerance to adverse environmental conditions. The circadian clock also uses environmental cues for appropriate timing of plant physiology and metabolism. Despite previous studies showing the connections between ABA and clock signalling pathways, the molecular nodes underlying these connections remained unknown. In a recent study, we have shown that the essential clock component TOC1 (Timing of CAB expression 1) regulates the diurnal expression of the ABA-related gene ABAR/CHLH/GUN5 by direct binding to its promoter. Treatment with ABA specifically induces TOC1 at midday and this induction controls both the phase of TOC1 binding and the expression of ABAR. TOC1 induction by ABA is abolished in ABAR RNAi plants revealing a new feedback loop that reciprocally links ABAR and TOC1 expression. This regulation is essential for ABA function as TOC1 and ABAR over-expressing and mutant plants display altered ABA-mediated tolerance to drought conditions. Notably, TOC1 is also implicated in ABA-mediated inhibition of seed germination but in an opposite direction to that observed for dehydration responses. These opposing functions open interesting questions about the spatial and temporal networks connecting ABA and clock signalling pathways.