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Characterisation of the epidermal diurnal transcriptome of mice with K14-Cre-driven Bmal1 knockout

ABSTRACT: Characterisation of the epidermal diurnal transcriptome of mice with K14-Cre-driven Bmal1 knockout

PROVIDER: PRJNA1075084 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27928437.fastq.gz	Fastqsanger.gz
	SRR27928438.fastq.gz	Fastqsanger.gz
	SRR27928439.fastq.gz	Fastqsanger.gz
	SRR27928440.fastq.gz	Fastqsanger.gz
	SRR27928441.fastq.gz	Fastqsanger.gz

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Characterisation of the epidermal diurnal transcriptome of mice with K14-Cre-driven Bmal1 knockout

Project description:To preserve a state of health, mammals employ an integrated network of molecular oscillators to drive daily rhythms of tissue-specific homeostatic processes. Importantly, the output, structure and coherence of this network is compromised by physiological ageing, disease and lifestyle changes. Yet, the key signalling nodes in this network, their underlying mechanisms of communication, and potential for therapeutic intervention, remain undefined. To dissect this system, we construct a minimal clock network consisting of two communicating nodes: the peripheral epidermal clock and central brain clock. We show that communication between the brain and epidermal clocks is sufficient for wild-type core clock activity and specific homeostatic processes, but inputs from other clock nodes are essential for full daily physiology. Unexpectedly, we find evidence that the epidermal clock selectively suppresses or interprets systemic signals to ensure coherence of specific homeostatic processes, identifying an unrecognised gatekeeper role for peripheral clocks. Together, we introduce a novel approach for dissecting a tissues daily physiology, and in turn identify key signalling nodes required to maintain epidermal homeostasis.

2024-05-02 | GSE255474 | GEO

Diurnal profiling of mouse liver of hepatocyte specific BMAL1 KO mice (Bmal1 HepKO)

Project description:Diurnal profiling of mouse liver of hepatocyte specific BMAL1 KO mice (Bmal1 HepKO)

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Diurnal profiling of mouse liver of hepatocyte specific BMAL1 KO mice (Bmal1 HepKO)

Project description:Obesity and liver diseases are associated with the disruption of the circadian clock that orchestrates mammalian physiology to optimize nutrient metabolism and storage. We show here that the activity of the circadian clock regulator BMAL1 is perturbed during liver fibrosis in humans. To understand the impact of BMAL1 perturbation in obesity and liver diseases, we assessed the impact of a high fat diet or leptin deficiency on Bmal1 knockout mice. While Bmal1 knockout mice were prone to obesity, they were protected against insulin resistance, hepatic steatosis, inflammation, and fibrosis. In addition to direct transcriptional regulation of metabolic programs by BMAL1, we show that adaptation of the growth hormone and sex hormone pathways plays a critical role in this protection. Similar endocrine perturbations correlate with the development of liver fibrosis in humans, suggesting that endocrine perturbation associated with circadian disruption is critical for the pathogenesis of metabolic and liver diseases.

2022-01-26 | GSE190221 | GEO

Cell-specific regulation of the circadian clock by BMAL1 in the paraventricular nucleus: Implications for regulation of systemic biological rhythms

Project description:Circadian rhythms are internal biological rhythms driving temporal tissue-specific, metabolic programs. Loss of the circadian transcription factor BMAL1 in the paraventricular nucleus (PVN) of the hypothalamus reveals its importance in metabolic rhythms, but its functions in individual PVN cells are poorly understood. Here, loss of BMAL1 in the PVN results in arrhythmicity of processes controlling energy balance and alters peripheral diurnal gene expression. BMAL1 chromatin immunoprecipitation sequencing (ChIP-seq) and single-nucleus RNA sequencing (snRNA-seq) reveal its temporal regulation of target genes, including oxytocin (OXT), and restoring circulating OXT peaks in BMAL1-PVN knockout (KO) mice rescues absent activity rhythms. While glutamatergic neurons undergo day/night changes in expression of genes involved in cell morphogenesis, astrocytes and oligodendrocytes show gene expression changes in cytoskeletal organization and oxidative phosphorylation. Collectively, our findings show diurnal gene regulation in neuronal and non-neuronal PVN cells and that BMAL1 contributes to diurnal OXT secretion, which is important for systemic diurnal rhythms.

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Characterisation of the epidermal diurnal transcriptome of mice with tissue-specific circadian clock activity [LD]

Project description:Characterisation of the epidermal diurnal transcriptome of mice with tissue-specific circadian clock activity [LD]

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Mammary tumors from K14-cre; ApcCKO/+ mice vs control mammary glands

Project description:Many components of Wnt/β-catenin signaling pathway also play critical roles in mammary tumor development. To study the role of Apc in mammary tumorigensis, we introduced conditional Apc mutations specifically into two different mammary epithelial populations using K14-Cre (progenitor) and WAP-cre (lactaing luminal) transgenic mice. Only the K14-cre mediated Apc heterozygosity developed mammary adenocarcinomas demonstrating histological and molecular heterogeneity, suggesting the progenitor cell origin of these tumors. These tumors harbored truncation mutation in a very defined region in the remaining wild-type allele of Apc that would retain some down-regulating activity of β-catenin signaling. Our results suggest that not only the epithelial origin but also a certain Apc mutations are selected to achieve a specific level of β-catenin signaling optimal for mammary tumor development.

2009-02-10 | GSE14753 | GEO

Characterisation of the epidermal diurnal and circadian transcriptomes of mice with tissue-specific circadian clock activity

Project description:Characterisation of the epidermal diurnal and circadian transcriptomes of mice with tissue-specific circadian clock activity

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The BMAL1/HIF2A heterodimer modulates circadian variations of myocardial injury

Project description:Cardiac injury following myocardial infarction exhibits a circadian pattern, yet the underlying mechanism remains unclear. To elucidate genes governing circadian variation of myocardial injury, we conducted transcriptomic profiling of left-ventricular tissues from mice or humans experiencing myocardial injury at different daytimes. Through comprehensive analyses, including transgenic mouse models and functional studies, we identified BMAL1 as a pivotal transcription factor modulating diurnal variation of myocardial injury. Remarkably, we discovered that BMAL1 regulates circadian-dependent cardiac injury by forming a transcriptionally active heterodimer with HIF2A. Substantiating this finding, we determined the cryo-EM structure of the BMAL1/HIF2F/DNA complex, revealing a previously unknown capacity for structural rearrangement within BMAL1. Furthermore, we confirmed amphiregulin (AREG) as a transcriptional target of the BMAL1/HIF2A heterodimer, critical for modulating circadian variation of myocardial injury. Finally, targeting the BMAL1/HIF2A-AREG pathway via timed AREG administration or enhancing circadian rhythm pharmacologically offered significant cardioprotection, implicating this pathway in treating ischemic heart disease.

2024-03-20 | GSE255307 | GEO

Transcription profiling of mouse mammary tumors from K14-cre; ApcCKO/+ vs control mammary glands

Project description:Many components of Wnt/Î²-catenin signaling pathway also play critical roles in mammary tumor development. To study the role of Apc in mammary tumorigensis, we introduced conditional Apc mutations specifically into two different mammary epithelial populations using K14-Cre (progenitor) and WAP-cre (lactaing luminal) transgenic mice. Only the K14-cre mediated Apc heterozygosity developed mammary adenocarcinomas demonstrating histological and molecular heterogeneity, suggesting the progenitor cell origin of these tumors. These tumors harbored truncation mutation in a very defined region in the remaining wild-type allele of Apc that would retain some down-regulating activity of Î²-catenin signaling. Our results suggest that not only the epithelial origin but also a certain Apc mutations are selected to achieve a specific level of Î²-catenin signaling optimal for mammary tumor development. Experiment Overall Design: We have compared 3 mammary tumors from K14-cre; ApcCKO/+ mice with 3 control mammary glands.

2009-02-21 | E-GEOD-14753 | biostudies-arrayexpress

RNA-seq data for skin tissues from 3-days-old wildtype and RNF31fl/fl-K14-cre mice.

Project description:mRNA expression profile for skin tissues from 3-days-old wildtype and RNF31fl/fl-K14-cre mice.

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