Ontology highlight
ABSTRACT:
PROVIDER: PRJNA746679 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15144410_1.fastq.gz | Fastqsanger.gz | |||
| SRR15144410_2.fastq.gz | Fastqsanger.gz | |||
| SRR15144411_1.fastq.gz | Fastqsanger.gz | |||
| SRR15144411_2.fastq.gz | Fastqsanger.gz | |||
| SRR15144412_1.fastq.gz | Fastqsanger.gz |
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Project description:After perception of vegetation proximity by the phytochrome photoreceptors, shade-avoider plants initiate a set of responses known as the Shade Avoidance Syndrome (SAS). Shade perception by the phytochrome B (phyB) photoreceptor unleashes the PHYTOCHROME INTERACTING FACTORs (PIFs) and initiates SAS responses. In Arabidopsis thaliana seedlings, shade perception involves rapid and massive changes in gene expression, increases auxin production and promotes hypocotyl elongation. Other components, such as phyA and ELONGATED HYPOCOTYL 5 (HY5), also participate in the shade regulation of the hypocotyl elongation response by repressing it. However, it remains unclear why and how so many regulators with either positive or negative activities modulate the same response. Our physiological, genetic, cellular and transcriptomic analyses showed that (1) these components are organized in two main branches or modules (phyA/HY5 and PIFs/HFR1/SAV3) and (2) the connection between them is dynamic and changes with the time of shade exposure. We propose a model for the regulation of shade-induced hypocotyl elongation in which the temporal and spatial functional importance of the various SAS regulators analyzed in here helps to explain the co-existence of differentiated regulatory branches with overlapping activities. Despite the temporal differences observed between phyA, HY5 and PIFs/HFR1/SAV3, their activities overlap and eventually converge in controlling hypocotyl elongation. Hence, we aimed to further investigate possible convergence points between these two groups of regulators.To expand our understanding of the role and interaction of HY5 and PIF4, PIF5 and PIF7 (PIF457) activities, we carried out RNA sequencing (RNA-seq) of seedlings exposed to different times of shade exposure of four genotypes: wild-type (Col-0), the single mutant hy5, the triple pif457 and the quadruple hy5 pif457.
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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.
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Project description:An RNA-seq was conducted to investigate how REF6 and PIF7 participate in shade avoidance memory.
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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 investigate the function of bZIP59 during SAS, we performed RNA-Seq of wild type Col-0 and a T-DNA insertion line bzip59 (SALK_024459) in while light and shade.
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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.
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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.
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Project description:The ATHB2 microProtein affects plant development and the shade avoidance response (RNA-Seq)
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Project description:For shade-intolerant plants, changes in light quality indicative of competition from neighboring plants trigger shade avoidance syndrome (SAS). PYHTOCHROME-INTERACTING FACTOR 7 is the major transcriptional regulator of SAS in Arabidopsis. However, the epigenetic reprogramming under shade is poorly understood. To identify the histone chaperone ASF1 and HIRA function during SAS, we performed transcriptome deep sequencing (RNA-seq) to search for differentially expressed genes (DEGs) by comparing transcript levels between Col-0 and pif7-1, asf1ab, or hira-1 seedlings during white light and shade conditions. Our data shown that histone chaperone ASF1, through interacting with PIF7 and helping of HIRA, positively regulates shade-induced genes expression.
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