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Arabidopsis De-etiolated 1 Represses Photomorphogenesis by Positively Regulating Phytochrome Interacting Factors in the Dark

ABSTRACT: Arabidopsis seedlings undergo photomorphogenic development even in darkness when the function of De-etiolated 1 (DET1), a repressor of photomorphogenesis, is disrupted. Our results indicate that DET1 directly interacts with a group of transcription factors known as the phytochrome-interacting factors (PIFs). Furthermore, our results suggest that DET1 positively regulates PIF protein levels primarily by stabilizing PIF proteins in the dark. Genomic analysis also revealed that DET1 may control the expression of light-regulated genes to mediate photomorphogenesis partially through PIFs.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE60835 | GEO | 2015/03/19

SECONDARY ACCESSION(S): PRJNA259643

REPOSITORIES: GEO

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Arabidopsis De-etiolated 1 Represses Photomorphogenesis by Positively Regulating Phytochrome Interacting Factors in the Dark

Project description:Arabidopsis seedlings undergo photomorphogenic development even in darkness when the function of De-etiolated 1 (DET1), a repressor of photomorphogenesis, is disrupted. Our results indicate that DET1 directly interacts with a group of transcription factors known as the phytochrome-interacting factors (PIFs). Furthermore, our results suggest that DET1 positively regulates PIF protein levels primarily by stabilizing PIF proteins in the dark. Genomic analysis also revealed that DET1 may control the expression of light-regulated genes to mediate photomorphogenesis partially through PIFs. Total of twelve samples, two treatments and three genotypes, and each have three replicates.

2015-03-19 | E-GEOD-60835 | biostudies-arrayexpress

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Project description:Light-induced phosphorylation is necessary and essential for the degradation of phytochrome-interacting factors (PIFs), the central repressors of photomorphogenesis. Although the kinases responsible for PIF phosphorylation have been extensively studied, the phosphatases underlying PIF dephosphorylation are largely unknown. Here, we real that mutation of FyPP1 and FyPP3, two catalytic subunits of PP6 phosphatases, promoted photomorphogenesis of seedlings in the dark. PP6 and PIFs functioned synergistically to repress photomorphogenesis. FyPP1 and FyPP3 directly interacted with and dephosphorylated PIF3 and PIF4. The light-induced degradation of PIF4 and the PIF transcriptional activities were dependent on PP6 activity. These data demonstrate that PP6 phosphatases repress photomorphogenesis through regulation of PIF phosphorylation, protein stability and transcriptional activity.

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DET1-mediated COP1 regulation avoids HY5 activity over second-site targets to tune plant photomorphogenesis

Project description:DE-ETIOLATED1 (DET1) is a negative regulator of plant photomorphogenesis acting as a component of the C3D complex, which can further associate to CULLIN4 to form a CRL4C3D E3 ubiquitin ligase. CRL4C3D is thought to act together with CRL4COP1SPA ubiquitin ligase, to promote the ubiquitin-mediated degradation of the master regulatory transcription factor ELONGATED HYPOCOTYL5 (HY5), thereby controlling photomorphogenic gene regulatory networks. Yet, functional links between COP1 and DET1 have long remained elusive. Here, upon mass spectrometry identification of DET1 and COP1-associated proteins, we provide in vivo evidence that DET1 associates with COP1 to promote its destabilization, a process necessary to dampen HY5 protein abundance. By regulating HY5 over-accumulation, DET1 is critical to avoid its association to second-site loci, including many PIF3 target genes. Accordingly, excessive HY5 levels result in an increased HY5 repressive activity and are sufficient to trigger fusca-like phenotypes otherwise observed typically in COP1 and COP9 signalosome mutant seedlings. This study therefore identifies that DET1-mediated regulation of COP1 stability tunes down HY5 cistrome and avoids hyper-photomorphogenic responses that might compromise plant viability.

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Project description:Analysis of etiolated seedlings exposed for 1hr to red light. Phytochromes are red/far-red light receptors, palying important roles in photomorphogenesis. Results suggest that red light and phytochromes regulate a set of genes' expression in seedlings.

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P-body mediated translational control in photomorphogenesis

Project description:Light, an important environmental factor regulates most of plant physiology and development. In the photomorphogenic stage, light globally enhances translation status in de-etiolating Arabidopsis seedlings. More than 1500 genes showed increased translation but not transcription in this developmental process. This implies these mRNAs are translationally repressed in dark-grown seedlings. Through transcriptome and translatome comparisons, we revealed that p-bodies attenuate the translation of mRNAs in the etiolated seedlings. We found hundreds of mRNAs accumulated and also increased translation for thousands of genes in dark-grown dcp5-1, including genes known to regulate the transition from skotomorphogenesis to photomorphogenesis. Our data reports p-bodies regulate both RNA stability and attenuation of translation for specific mRNAs in the dark.

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Expression data from epidermis specific phytochrome B or global phytochrome B line comparing to phyB-9 mutant.

Project description:Seedling hypocotyls display negative gravitropism in the dark but agravitropism in the light. The Arabidopsis thaliana pif quadruple mutant (pifQ), which lacks four PHYTOCHROME-INTERACTING FACTORS (PIFs), is agravitropic in the dark. Endodermis-specific expression of PIF1 rescues gravitropism in pifQ mutant seedlings. Since phytochromes induce light responses by inhibiting PIFs and the COP1-SPA ubiquitin E3 ligase complex in the nucleus, we asked whether phyB can cell autonomously inhibit hypocotyl negative gravitropism in the endodermis. We found that while epidermis-specific expression of PHYB rescues hypocotyl negative gravitropism and all other phyB mutant phenotypes, endodermis-specific expression of PHYB does not. Epidermal phyB induces the phosphorylation and degradation of endodermal PIFs in response to red light. This induces a global gene expression pattern similar to that induced by red light treatment of seedlings expressing PHYB under the control of its own endogenous promoter. Our results imply that epidermal phyB generates an unidentified mobile signal that travels to the endodermis where it promotes PIF degradation and inhibits hypocotyl negative gravitropism.

2017-02-08 | GSE87591 | GEO

PHYTOCHROME INTERACTING FACTORs trigger environmentally responsive chromatin dynamics

Project description:The pivotal interplay between light receptors and PHYTOCHROME-INTERACTING FACTORs (PIFs) serves as an essential regulatory hub that perceives and integrates environmental cues into the plant’s transcriptional networks. A critical control component of environmentally-responsive gene networks is the histone variant H2A.Z which provides transcriptional plasticity and prevents undesired gene activation. However, the functional relationship between PIF transcription factors (TFs) and H2A.Z is despite their outstanding importance, only poorly understood. Here, we describe a photo-genomic approach that utilizes the rapid and reversible light-mediated manipulation of PIF7 activity to visualize PIF7 DNA binding and H2A.Z occupancy kinetics on a genome-wide scale. Strikingly, we discovered that PIF shape the H2A.Z landscape in a light quality-dependent manner. We found that DNA binding of PIF7 is not regulated by H2A.Z but most importantly, PIFs initiate H2A.Z eviction and through the direct interaction with EIN6 ENHANCER (EEN), a crucial subunit of INO80 chromatin remodeling complex. Collectively, we describe a PIF-INO80 regulatory module that controls plant growth in response to environmental changes.

2021-04-30 | GSE139296 | GEO

Interaction between gibberellins and brassinosteroids during etiolated growth in Arabidopsis.

Project description:The proper transition between the skotomorphogenic and photomorphogenic developmental programs is key for seedling survival and it is therefore tightly regulated. Besides light, which is the major cue that triggers this transition, several hormone pathways participate in this control, mainly antagonizing the light effect. Two of these hormones are gibberellins (GA) and brassinosteroids (BR). Both hormones promote the skotomorphogenesis and prevent photomorphogenesis, as evidenced by the partially de-etiolated phenotype caused by GA or BR deficiency, or by a blockage in the respective signaling pathways. We have previously shown that BR mediate GA activity in the control of this transition. For instance, treatment of dark-grown, GA-deficient seedlings with BRs was able to partially restore morphological phenotypes such as hypocotyl growth, and importantly to restore completely the molecular phenotype of CAB2 and RbcS gene expression. On the contrary, GA-treatment did not alter the same phenotypes in the BR deficient det2 mutant. Thus, the aim of this study was to investigate to what extent BRs mediate GA activity in dark-grown seedlings, and for that purpose we have the examined global changes in gene expression caused by treatment with GA and BRs in BR- and GA-deficient seedlings, respectively.

2012-08-02 | GSE32889 | GEO

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