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Gene expression in hemera mutants in red light condition

ABSTRACT: The hemera (hmr) mutant was identified as the first photomorphogenetic mutant with the combination of long hypocotyl and albino phenotypes in the light. Phytochrome-Interacting bHLH transcription Factors (PIFs), which are repressors of photomorphogenesis accumulate in darkness and are degraded in the light in a phytochrome-dependent manner. Two PIFs, PIF1 and PIF3 accumulated in the light in hmr mutants. In order to determine the gene expression of PIF-dependent genes in hmr mutants in the light, we have performed whole-genome expression analysis on two hmr mutants: a null allele, hmr-5; and a weak allele, hmr-22.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE43311 | GEO | 2014/06/01

SECONDARY ACCESSION(S): PRJNA185409

REPOSITORIES: GEO

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Gene expression in hemera mutants in red light condition

Project description:The hemera (hmr) mutant was identified as the first photomorphogenetic mutant with the combination of long hypocotyl and albino phenotypes in the light. Phytochrome-Interacting bHLH transcription Factors (PIFs), which are repressors of photomorphogenesis accumulate in darkness and are degraded in the light in a phytochrome-dependent manner. Two PIFs, PIF1 and PIF3 accumulated in the light in hmr mutants. In order to determine the gene expression of PIF-dependent genes in hmr mutants in the light, we have performed whole-genome expression analysis on two hmr mutants: a null allele, hmr-5; and a weak allele, hmr-22. Wild-type (Col-0) and hmr mutant seeds were surface-sterilized and plated on half-strength Murashige and Skoog (MS) growth medium without sucrose. The seeds were stratified in the dark at 4ºC for 4d. Seedlings were grown in constant red light (Rc, 10?mol/m2/s) at 21°C for 4d.

2014-06-01 | E-GEOD-43311 | biostudies-arrayexpress

Arabidopsis PP6 phosphatases dephosphorylate PIF proteins to repress photomorphogenesis.

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.

2019-09-04 | GSE128498 | GEO

Gene expression in the rcb (regulator for chloroplast biogenesis) mutant in red light conditions

Project description:The regulator for chloroplast biogenesis (rcb) mutant was identified as a mutant defective in phytochrome-mediated chloroplast biogenesis. The rcb mutant has long hypocotyl and albino phenotypes. RCB initiates chloroplast biogenesis in the nucleus by promoting the degradation of the master repressors for chloroplast biogenesis, the PIFs (Phytochrome Interacting Factors). To understand how RCB regulates the expression of PIF-regulated genes, we performed genome-wide expression analysis of RCB-dependent genes using a rcb-10 null allele.

2019-06-20 | GSE122351 | GEO

Mechanism of early light signaling by the carboxy-terminal output module of Arabidopsis phytochrome B

Project description:Phytochromes are evolutionarily conserved photoreceptors in bacteria, fungi, and plants. The prototypical phytochrome comprises an N-terminal photosensory module and a C-terminal histidine kinase signaling-output module. However, the plant phytochrome has been postulated to transduce light signals by interacting with a group of nodal Phytochrome-Interacting transcription Factors (PIFs) and triggering their degradation via the N-terminal photosensory module, while its C-terminal output module, including a Histidine Kinase-Related Domain (HKRD), is thought not to participate directly in signaling. Here, we show that the C-terminal module of Arabidopsis phytochrome B (PHYB) is unexpectedly sufficient to mediate the degradation of PIF3 and to induce a distinct set of PIF-regulated photosynthetic genes. These signaling functions require the HKRD and particularly its dimerization. A D1040V mutation, which disrupts the dimerization of HKRD and the interaction between the C-terminal module and PIF3, abrogates the early light signaling functions of PHYB in nuclear accumulation, photobody biogenesis, and PIF3 degradation. In contrast, disruption of the interaction between PIF3 and PHYB’s N-terminal photosensory module has little effect on PIF3 degradation. Together, this study provides novel insight into the central mechanism of early phytochrome signaling that the C-terminal signaling-output module of PHYB interacts with PIF3 in the nucleus to mediate PIF3 degradation by light.

2017-12-31 | GSE90925 | GEO

Gene expression in pif1pif3pif4pif5 mutant under dark or red light conditions

Project description:Light initiates the seedling deetiolation transition by promoting major changes in gene expression mainly regulated by phytochrome (phy) photoreceptors. During the initial dark-to-light transition, phy photoactivation induces rapid changes in gene expression that eventually lead to the photomorphogenic development. Recent reports indicate that this process is achieved by phy-induced degradation of Phy-Interacting bHLH transcription Factors (PIFs) PIF1, PIF3 PIF4 and PIF5, which are partly redundant constitutive repressors of photomorphogenesis that accumulate in darkness. In order to test whether light/phy-regulated gene expression occurs through these PIFs, we have performed whole-genome expression analysis in the pif1pif3pif4pif5 quadruple mutant (pifq).

2009-11-01 | GSE17159 | GEO

Genome-wide identification of PIF3-binding sites and direct-target genes of PIF3 transcriptional regulation in skotomorphogenesis [ChIP-Seq]

Project description:Dark-grown seedlings exhibit skotomorphogenic development. Genetic and molecular evidence indicates that a quartet of Arabidopsis Phytochrome (phy)-Interacting bHLH Factors (PIF1, 3, 4 and 5) are critically necessary to maintaining this developmental state, and that light activation of phy induces a switch to photomorphogenic development by inducing rapid degradation of the PIFs. Here, using combined ChIP-seq and RNA-seq analyses, we have identified genes that are direct targets of PIF3 transcriptional regulation, and we provide evidence that the quartet collectively regulate these genes by shared, direct binding to the target promoters in promoting skotomorphogenesis. Four biological replicates data of PIF3-binding sites were collected by comparing the parallel ChIP samples from transgenic seedlings overexpressing Myc-epitope-tagged PIF3 (35S:PIF3-5xMyc, P3M) in pif3-3 null mutant background and the wild-type (WT) control.

2013-02-01 | E-GEOD-39215 | biostudies-arrayexpress

Phytochrome Interacting Factors 4 and 5 redundantly limit seedling de-etiolation in continuous far-red light.

Project description:Phytochromes are red/far red photosensors regulating numerous developmental programs in plants. Among them phytochrome A (phyA) is essential to enable seedling de-etiolation in continuous far-red (FR) light a condition mimicking the environment under a dense canopy. The ecological relevance of this response is demonstrated by the high mortality rate of phyA mutants germinating in deep vegetational shade. phyA signaling involves a direct interaction of the photoreceptor with members of the bHLH transcription factor family, PIF1 and PIF3 (Phytochrome Interacting Factor). Here we investigated the involvement of PIF4 and PIF5 in phyA signaling and found that they redundantly control de-etiolation in FR light. The pif4pif5 double mutant is hypersensitive to low fluence rates of FR light. This phenotype is dependent on FR light perception by phyA but does not rely on alterations of the phyA level. Our microarrays analysis shows that PIF4 and PIF5 are part of an inhibitory mechanism repressing the expression of some light-responsive genes in the dark and are also needed for full expression of several growth-related genes in the light. Unlike PIF1 and PIF3, PIF4 and PIF5 are not degraded in response to FR light indicating that they are light-regulated by a different mechanism. Our genetic analysis suggests that this is achieved through the sequestration of these PIFs by the closely related bHLH transcription factor HFR1 (long Hypocotyl in FR light).

2009-08-19 | GSE16333 | GEO

Transcription profiling of Arabidopsis thaliana phytochrome interacting factors 4 and 5 redundantly limit seedling de-etiolation in continuous far-red light.

2009-09-17 | E-GEOD-16333 | biostudies-arrayexpress

Transcriptome-wide analysis of gene expression in dark-grown WT and pif mutant seedlings

Project description:We sequenced mRNA from WT and PhytochromeInteractingFactor (pif) mutant seedlings grown for 2d in darkness. Transcriptome profiles of the wild-type (WT), pif1, pif3, pif, pif5 monogenic mutants, pif3pif4pif5 (pif345), pif1pif4pif5(pif145), pif1pif3pif5 (pif135) and pif1pif3pif4 (pif134) triple mutants and pif1pif3pif4pif5 (pifq) quadruple mutant seedlings. Biological triplicate samples were analyzed from libraries constructed using a 3'-capture, 5' to 3' directional method.

2014-10-02 | E-GEOD-42665 | biostudies-arrayexpress

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

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