Temperature-dependent shade avoidance involves the receptor-like kinase ERECTA

Plants detect the presence of neighbouring vegetation by monitoring changes in the ratio of red (R) to farred (FR) wavelengths (R:FR) in ambient light. Reductions in R:FR are perceived by the phytochrome family of plant photoreceptors and initiate a suite of developmental responses termed the shade avoidance syndrome. These include increased elongation growth of stems and petioles, enabling plants to overtop competing vegetation. The majority of shade avoidance experiments are performed at standard laboratory growing temperatures (>20°C). In these conditions, elongation responses to low R:FR are often accompanied by reductions in leaf development and accumulation of plant biomass. Here we investigated shade avoidance responses at a cooler temperature (16°C). In these conditions, Arabidopsis thaliana displays considerable low R:FR-mediated increases in leaf area, with reduced low R:FR-mediated petiole elongation and leaf hyponasty responses. In Landsberg erecta, these strikingly different shade avoidance phenotypes are accompanied by increased leaf thickness, increased biomass and an altered metabolite profile. At 16°C, low R:FR treatment results in the accumulation of soluble sugars and metabolites associated with cold acclimation. Analyses of natural genetic variation in shade avoidance responses at 16°C have revealed a regulatory role for the receptor-like kinase ERECTA

Phytochrome interacting factors 4 and 5 control seedling growth in changing light conditions by directly controlling auxin signaling.

Plant growth is strongly influenced by the presence of neighbors that compete for light resources. In response to vegetational shading shade-intolerant plants such as Arabidopsis display a suite of developmental responses known as the shade-avoidance syndrome (SAS). The phytochrome B (phyB) photoreceptor is the major light sensor to mediate this adaptive response. Control of the SAS occurs in part with phyB, which controls protein abundance of phytochrome-interacting factors 4 and 5 (PIF4 and PIF5) directly. The shade-avoidance response also requires rapid biosynthesis of auxin and its transport to promote elongation growth. The identification of genome-wide PIF5-binding sites during shade avoidance revealed that this bHLH transcription factor regulates the expression of a subset of previously identified SAS genes. Moreover our study suggests that PIF4 and PIF5 regulate elongation growth by controlling directly the expression of genes that code for auxin biosynthesis and auxin signaling components

SHADE AVOIDANCE 4 is required for proper auxin distribution in the hypocotyl

The phytohormone auxin is involved in virtually every aspect of plant growth and development. Through polar auxin transport, auxin gradients can be established, which then direct plant differentiation and growth. Shade avoidance responses are well- known processes that require polar auxin transport. In this study, we have identified a mutant, shade avoidance 4 (sav4), defective in shade-induced hypocotyl elongation and basipetal auxin transport. SAV4 encodes an unknown protein with armadillo repeat- and tetratricopeptide repeat-like domains known to provide protein-protein interaction surfaces. C terminally yellow fluorescent protein-tagged SAV4 localizes to both the plasma membrane and the nucleus. Membrane-localized SAV4 displays a polar association with the shootward plasma membrane domain in hypocotyl and root cells, which appears to be necessary for its function in hypocotyl elongation. Cotransfection of SAV4 and ATP-binding cassette B1 (ABCB1) auxin transporter in tobacco (Nicotiana benthamiana) revealed that SAV4 blocks ABCB1-mediated auxin efflux. We thus propose that polarly localized SAV4 acts to inhibit ABCB-mediated auxin efflux toward shoots and facilitates the establishment of proper auxin gradients

Quantitative Trait Loci Associated with the "Shade Avoidance" Type Response in A. thaliana when Grown under Oscillating Daily Summer Temperatures

A poster discussing "shade avoidance" in A. thaliana plants

3D modelling of branching in plants

Shoot branching is a key determinant of overall aboveground plant form. During plant development, the number of branches formed strongly influences the amount of light absorbed by the plant, and thus the plant’s competitive strength in terms of light capture in relation to neighbouring plants. Branching is regulated by multiple internal factors which are modulated by different environmental signals. A key environmental signal in the context of a plant population is a low red / far-red intensity ratio (R:FR) of the light reflected by neighbouring plants. For instance, low R:FR results in suppression of branching in favour of elongation growth, which is a key aspect of shade avoidance. Shade avoidance enables plants to anticipate future competition by preventing being shaded, rather than to react to prevailing shade conditions. Internally, branching is regulated by a finely tuned plant hormone network. The interactions within this network are modified by environmental cues such as R:FR which is perceived by specific photoreceptors. Combined, internal and external signals enable regulation of branch formation under the influence of environmental conditions. The different aspects of branching control act at different levels of biological organization (organ, whole plant, plant community). These aspects can be integrated in one modelling approach, called functional-structural plant modelling (FSPM), explicitly considering spatial 3D plant development. An FSP model typically contains detailed information at any moment in development of the plant on the number, size, location and orientation of all organs that make up the plant. In FSP models, physiological and physical processes occur within the plant (e.g. photosynthesis and transport of assimilates), and interaction with the environment occurs at the interface of organ and environment (e.g. light absorption by a leaf). Explicit simulation of absorption and scattering of light at the level of the plant organ is an important aspect of FSPM. In combination with dedicated experiments, this modelling tool can be used to analyse the response of plants to (imminent) competition, simulate the competitive advantage of shade avoidance for plants of different architecture, and predict plant form in various light environments. To assess the effect of plant population density through R:FR signalling on tillering (branching) in spring wheat (Triticum aestivum L.), an FSPM study was conducted (Figure 1). A simple descriptive relationship was used to link R:FR as perceived by the plant to extension growth of tiller buds and probability of a bud to form a tiller. A further study included a complete sub-model of branching regulation, aiming at simulating branching as an emergent property in Arabidopsis (Arabidopsis thaliana) under the influence of R:FR. These and other studies show that FSPM is a promising tool to simulate aspects of plant development, such as branching, under the influence of environmental factors. In close combination with dedicated experiments, FSPM can shape our ideas of the mechanisms controlling plant development, can integrate existing knowledge on plant development, and can predict plant development in untested conditions

Inhibition of the shade avoidance response by formation of non-DNA binding bHLH heterodimers.

In shade-intolerant plants such as Arabidopsis, a reduction in the red/far-red (R/FR) ratio, indicative of competition from other plants, triggers a suite of responses known as the shade avoidance syndrome (SAS). The phytochrome photoreceptors measure the R/FR ratio and control the SAS. The phytochrome-interacting factors 4 and 5 (PIF4 and PIF5) are stabilized in the shade and are required for a full SAS, whereas the related bHLH factor HFR1 (long hypocotyl in FR light) is transcriptionally induced by shade and inhibits this response. Here we show that HFR1 interacts with PIF4 and PIF5 and limits their capacity to induce the expression of shade marker genes and to promote elongation growth. HFR1 directly inhibits these PIFs by forming non-DNA-binding heterodimers with PIF4 and PIF5. Our data indicate that PIF4 and PIF5 promote SAS by directly binding to G-boxes present in the promoter of shade marker genes, but their action is limited later in the shade when HFR1 accumulates and forms non-DNA-binding heterodimers. This negative feedback loop is important to limit the response of plants to shade