The circadian PRRs quintet orchestrates photoperiodic responsive hypocotyl growth by transcriptionally repressing PIF4/PIF5 in Arabidopsis
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ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE116381 | GEO | 2020/06/21
REPOSITORIES: GEO
Similar Datasets
Project description:The circadian PRRs quintet orchestrates photoperiodic responsive hypocotyl growth by transcriptionally repressing PIF4/PIF5 in Arabidopsis
| PRJNA478329 | ENA
Project description:We identified genome-wide PRR9 targets by conducting chromatin immunoprecipitation followed by high-throughput sequencing. Plants were grown in cycling 12 h light/12 h dark for two weeks before harvesting at ZT4. The four samples include the immunoprecipitated and input control for prr9-1 PRR9::HA-PRR9 CCR2::LUC #109 (HA9) and the prr9-1 (s9c) parental control. PRR5 PRR7 and TOC1 raw data available from the following Series: PRR5: GSE36361 TOC1: GSE35952 PRR7: GSE49282 (GSM1196649 and GSM1196650)
2015-12-03 | E-GEOD-71397 | biostudies-arrayexpress
Project description:Ambient temperature potentially affects all biological systems. However, the period length of circadian clocks is close to 24 h over a broad range of physiological temperatures, known as temperature compensation. The mechanism underpinning the temperature compensation remains largely unknown. Here, we show that inhibitors of time progression, TIMING OF CAB EXPRESSION 1 (TOC1) and PSEUDO-RESPONSE REGULATOR 5 (PRR5) proteins, are required for the temperature compensation in Arabidopsis thaliana (Arabidopsis). Compared to the wild-type, the prr5 toc1 double mutant shows a short period at high temperatures. TOC1 and PRR5 proteins are ubiquitinated and degraded at low temperatures, by a ubiquitin E3 ligase LOV KELCH PROTEIN 2 (LKP2) that was sought as a minor player in the clock. The lkp2 mutants show long periods only at lower temperatures. Collectively, the clock keeps its periodicity against ambient temperature by the temperature-dependent quantity control of inhibitors of time progression.
DOI:10.1126/sciadv.adq0187
2024-10-04 | PXD044813 | JPOST Repository
Project description:The hypocotyls of germinating seedlings elongate in a search for light to enable autotrophic sugar production. Upon exposure to light, photoreceptors that are activated by blue and red light halt elongation by preventing the degradation of the hypocotyl-elongation inhibitor HY5 and by inhibiting the activity of the elongation-promoting transcription factors PIFs. The question of how sugar affects hypocotyl elongation and which cell types stimulate and stop that elongation remains unresolved. We found that overexpression of a sugar sensor, Arabidopsis hexokinase 1 (HXK1), in guard cells promotes hypocotyl elongation under white and blue light through PIF4. Furthermore, expression of PIF4 in guard cells is sufficient to promote hypocotyl elongation in the light, while expression of HY5 in guard cells is sufficient to inhibit the elongation of the hy5 mutant and the elongation stimulated by HXK1. HY5 exits the guard cells and inhibits hypocotyl elongation, but is degraded in the dark. We also show that the inhibition of hypocotyl elongation by guard cells' HY5 involves auto-activation of HY5 expression in other tissues. It appears that guard cells are capable of coordinating hypocotyl elongation and that sugar and HXK1 have the opposite effect of light on hypocotyl elongation, converging at PIF4.
| S-EPMC8217561 | biostudies-literature
Project description:In many organisms, the circadian clock is composed of functionally coupled morning and evening oscillators that regulate the bouts of dawn and dusk activity. In Arabidopsis, oscillator coupling relies on a core loop in which the evening oscillator component TOC1 was proposed to activate a subset of morning-expressed oscillator genes. Our systems-biological approach overturns the current view of the Arabidopsis circadian clock showing that TOC1 does not function as an activator but as a timely-controlled general repressor of morning and evening oscillator components. Repression occurs through rhythmic binding to the promoters of all oscillator genes, suggesting a previously unexpected direct connection between the morning and evening loops. Examination of TOC1 genome-wide binding using TOC1 Minigene (TMG) seedlings expressing the genomic fragment of TOC1 fused to the Yellow Fluorescent Protein in a toc1-2 mutant background (TMG-YFP/toc1-2 seedlings) grown under LD cycles (12h light:12h dark).
2012-03-08 | E-GEOD-35952 | biostudies-arrayexpress
Project description:Light is an important environmental factor. Plants adapt to their light environment by developing the optimal phenotypes. Light-mediated hypocotyl growth is an ideal phenotype for studying how plants respond to light. Thus far, many signaling components in light-mediated hypocotyl growth have been reported. Here, we focused on identifying the transcription factors (TFs) involved in blue light-mediated hypocotyl growth. We analyzed the blue-light-mediated hypocotyl lengths of Arabidopsis TF-overexpressing lines and identified three NF-YC proteins, NF-YC7, NF-YC5, and NF-YC8 (NF-YCs being the short name), as the negative regulators in blue light-inhibited hypocotyl elongation. NF-YC-overexpressing lines developed longer hypocotyls than those of the wild type under blue light, while the deficient mutants nf-yc5nf-yc7 and nf-yc7nf-yc8 failed to exhibit hypocotyl elongation under blue light. NF-YCs physically interacted with CRY2 (cryptochrome 2) and PIF4/5 (phytochrome interacting factor 4 or 5), while the NF-YCs-PIF4/5 interactions were repressed by CRY2. Moreover, the overexpression of CRY2 or deficiency of PIF4/5 repressed NF-YC7-induced hypocotyl elongation under blue light. Further investigation revealed that NF-YC7 may increase CRY2 degradation and regulate PIF4/5 activities under blue light. Taken together, this study will provide new insight into the mechanism of how blue light inhibits hypocotyl elongation.
| S-EPMC10419918 | biostudies-literature
Project description:Diurnal variation in nitrogen homeostasis is observed across phylogeny. But whether these are endogenous rhythms, and if so, molecular mechanisms that link nitrogen homeostasis to the circadian clock remain unknown. Here, we provide evidence that a clock-dependent peripheral oscillator, Krüppel-like factor 15 transcriptionally coordinates rhythmic expression of multiple enzymes involved in mammalian nitrogen homeostasis. In particular, Krüppel-like factor 15-deficient mice exhibit no discernable amino acid rhythm, and the rhythmicity of ammonia to urea detoxification is impaired. Of the external cues, feeding plays a dominant role in modulating Krüppel-like factor 15 rhythm and nitrogen homeostasis. Further, when all behavioral, environmental and dietary cues were controlled in humans, nitrogen homeostasis exhibited an endogenous circadian rhythmicity. Thus, in mammals, nitrogen homeostasis exhibits circadian rhythmicity, and is orchestrated by Krüppel-like factor 15.
| S-EPMC3299986 | biostudies-literature
Project description:UnlabelledThe excessive metastatic propensity of melanoma makes it the most deadly form of skin cancer, yet the underlying mechanism of metastasis remains elusive. Here, mining of cancer genome datasets discovered a frequent loss of chromosome 19p13.3 and associated downregulation of the zinc finger transcription factor ZBTB7A in metastatic melanoma. Functional assessment of ZBTB7A-regulated genes identified MCAM, which encodes an adhesion protein key to melanoma metastasis. Using an integrated approach, it is demonstrated that ZBTB7A directly binds to the promoter and transcriptionally represses the expression of MCAM, establishing ZBTB7A as a bona fide transcriptional repressor of MCAM. Consistently, downregulation of ZBTB7A results in marked upregulation of MCAM and enhanced melanoma cell invasion and metastasis. An inverse correlation of ZBTB7A and MCAM expression in association with melanoma metastasis is further validated with data from analysis of human melanoma specimens.ImplicationsTogether, these results uncover a previously unrecognized role of ZBTB7A in negative regulation of melanoma metastasis and have important clinical implications.
| S-EPMC4543565 | biostudies-literature
Project description:Our aim is to identify circadian transcripts that are co-regulated with [Ca2+]cyt, with the eventual goal of identifying genetic regulators and targets for circadian oscillations of [Ca2+]cyt. We have identified two conditions in which [Ca2+]cyt behaves differently to other circadian outputs. 1. Treatment of plants with nicotinamide, a metabolic inhibitor of ADPR cyclase, abolishes the circadian oscillations of [Ca 2+]cyt. However, leaf movement, CCA1, LHY, TOC1 and CAB transcript abundance and CAB promoter activity are all rhythmic albeit with a longer period (Dodd et al., 2007). 2. The toc1-1 mutant, which shortens the circadian period of all other rhythms tested, has no effect on the period of [Ca2+]cyt oscillations (Xu et al., 2007). We will measure the circadian regulation of transcript abundance in wild type (C24), toc1-1 and nicotinamide (C24)-treated plants. Method: Wild type (C24) and toc1-1 seeds were sown on 1/2MS 0.8% agar plates and imbibed at 4 C for 48 hours. Seedlings were grown in LD cycles of 12hL:12hD at 19 C for 11 days to entrain the oscillator. Following transfer to LL at dawn on the 12th day, 50% of the wild type seedlings were dosed with 50 mM nicotinamide every 2 hours over the entire course of the experiment. Wild type, toc1-1 and nicotinamide-treated seedlings (approx. 100 for each sample, excluding roots) were harvested at 4 hour intervals from 49 to 93 hours in LL (12 time points covering the entire third and fourth circadian cycles). Two independent replicates of the whole experiment will be hybridised.
2009-12-10 | GSE19271 | GEO
Project description:Higher plants adapt their growth to high temperature by a dramatic change in plant architecture. It has been shown that the transcriptional regulator phytochrome-interacting factor 4 (PIF4) and the phytohormone auxin are involved in the regulation of high temperature-induced hypocotyl elongation in Arabidopsis. Here we report that PIF4 regulates high temperature-induced hypocotyl elongation through direct activation of the auxin biosynthetic gene YUCCA8 (YUC8). We show that high temperature co-upregulates the transcript abundance of PIF4 and YUC8. PIF4-dependency of high temperature-mediated induction of YUC8 expression as well as auxin biosynthesis, together with the finding that overexpression of PIF4 leads to increased expression of YUC8 and elevated free IAA levels in planta, suggests a possibility that PIF4 directly activates YUC8 expression. Indeed, gel shift and chromatin immunoprecipitation experiments demonstrate that PIF4 associates with the G-box-containing promoter region of YUC8. Transient expression assay in Nicotiana benthamiana leaves support that PIF4 directly activates YUC8 expression in vivo. Significantly, we show that the yuc8 mutation can largely suppress the long-hypocotyl phenotype of PIF4-overexpression plants and also can reduce high temperature-induced hypocotyl elongation. Genetic analyses reveal that the shy2-2 mutation, which harbors a stabilized mutant form of the IAA3 protein and therefore is defective in high temperature-induced hypocotyl elongation, largely suppresses the long-hypocotyl phenotype of PIF4-overexpression plants. Taken together, our results illuminate a molecular framework by which the PIF4 transcriptional regulator integrates its action into the auxin pathway through activating the expression of specific auxin biosynthetic gene. These studies advance our understanding on the molecular mechanism underlying high temperature-induced adaptation in plant architecture.
| S-EPMC3315464 | biostudies-literature