Project description:Shade can trigger the shade avoidance syndrome (SAS) in shade-intolerant species, which cause exaggerated growth and affect crop yield. We report that Arabidopsis transcription factors bZIP59 negatively regulate SAS. To identify direct targets of bZIP59 at the genome-wide level, we performed ChIP-Seq using ProbZIP59::bZIP59-GFP/bzip59 transgenic plants under white light or transferred to shade conditions for 2 hours. Our results indicated shade light dramatically increased the DNA binding ability of bZIP59, and shade-enhanced binding of bZIP59 majorly located around transcriptional start site (TSS) of genes.
Project description:The transcriptome of a light sensitive tea cultivar ‘Huangjinya’ plants exposed to sunlight and shade were analyzed by high-throughput sequencing followed by de novo assembly.
Project description:Shade avoidance helps plants maximize their access to light for growth under crowding. It is unknown, however, whether a priming shade avoidance mechanism exists that allows plants to respond more effectively to successive shade conditions. Here, we show that the shade-intolerant plant Arabidopsis can remember a first experienced shade event and respond more efficiently to the next event on hypocotyl elongation. The transcriptional regulator PHYTOCHROME-INTERACTING FACTOR 7 (PIF7) and the histone H3K27-demethylase RELATIVE OF EARLY FLOWERING 6 (REF6) were identified as being required for this shade avoidance memory. RNA-sequencing analysis revealed that shade induction of shade memory-related genes was impaired in the pif7 and ref6 mutants. Based on the enrichments of H3K27me3, REF6 and PIF7, we found that priming shade treatment induced PIF7 accumulation, which further recruited REF6 to demethylate H3K27me3 on the chromatin of certain memory-related genes, leading to a state poised for their transcription. Upon the second shade treatment, enhanced shade-mediated induction of these genes resulted in stronger hypocotyl growth responses. We conclude that the transcriptional memory mediated by epigenetic modification plays a key role in the ability of primed plants to remember previously experienced shade and acquire enhanced responses to recurring shade conditions.
Project description:Coping of evergreen conifers of boreal forests with freezing temperatures on bright winter days puts the photosynthetic machinery in great risk of oxidative damage. To survive harsh winter conditions, conifers have evolved a unique but poorly characterised photoprotection mechanism, a sustained form of non-photochemical quenching (sustained NPQ). Here we focused on functional properties and underlying molecular mechanisms related to the development of sustained NPQ in Norway spruce (Picea abies). Data was collected during four consecutive years (2016-19) from trees growing in sun and shade habitats. When day temperatures dropped below -4°C, specific N-terminally triply phosphorylated LHCB1 isoform (3p-LHCII) and phosphorylated PSBS (p-PSBS) were detected in the thylakoid membrane. Development of sustained NPQ coincided with the highest level of 3p-LHCII and p-PSBS, occurring after prolonged combination of bright winter days and temperature close to -10°C. Artificial induction of both the sustained NPQ and recovery from naturally induced sustained NPQ provided information on differential dynamics and light-dependence of 3p-LHCII and p-PSBS accumulation and dephosphorylation as essential prerequisites of sustained NPQ. Data obtained collectively suggest three novel components related to sustained NPQ in spruce. (i) Freezing temperatures induce 3p-LHCII accumulation independently of light, which is suggested to initiate de-stacking of appressed thylakoid membranes due to increased electrostatic repulsion of adjacent membranes. (ii) p-PSBS accumulation is both light- and temperature-dependent and closely linked to the initiation of sustained NPQ, which (iii) in concert with PSII photoinhibition is likely to trigger sustained NPQ in spruce.
Project description:Arabidopsis is a shade avioding plant. Under simulated shade light with reduced red-to-far red (R:FR) ratio around 0.7, hypocotyls of Arabidopsis seedlings elongate, which is one of the typical shade avoidance responses.We discovered that when the R:FR ratio further decreases to around 0.1 (strong shade), the shade-induced elongation of hypocotyl is abolished and phytochrome A (phyA) mediates this response.In this study, we aim to examine the difference between shade and strong shade treatment and uncover the role of phyA in regulating the shade avoidance responses.
Project description:As sessile organisms plants developed a veriety of adaptive responses to the ever changing environment. One of these responses is the shade avoidance syndrome which is composed of different responses like elongation growth, hyponastic leafs or early flowering to shade (low R/FR). Phytochrcome Interacting Factor 4 and 5 are bHLH transcription factors reported to activate gene expression upon perception of low R/FR. Using this miroarray experiment we identified new genes regulated by PIF4 and PIF5 in response to shade and investigated their genome wide role.