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Mus musculus

ABSTRACT: A Transcriptomic Dataset of Liver Tissues from Global and Liver-Specific Bmal1 Knockout Mice

PROVIDER: PRJNA1172598 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31044246_1.fastq.gz	Fastqsanger.gz
	SRR31044246_2.fastq.gz	Fastqsanger.gz
	SRR31044247_1.fastq.gz	Fastqsanger.gz
	SRR31044247_2.fastq.gz	Fastqsanger.gz
	SRR31044248_1.fastq.gz	Fastqsanger.gz

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Proteomics analysis of regulation by Bmal1 and physiological time-restricted feeding

Project description:To define regulation of tissue proteomes by Bmal1, daily feeding rhythm, and the interaction, we employed Bmal1-stopFL mice, which do not express the main transcriptional activator of the molecular clock, Bmal1, except in cre recombinase-expressing cells1,2 (Figure 1A). Bmal1-stopFL mice lacking cre (Bmal1 knockout, KO) are analogous to Bmal1-null mice and display severely impaired behavioral and molecular rhythms1-3. Hepatocyte-specific Alfp-cre and skeletal muscle-specific Hsa-cre genes were introduced to generate a single line wherein both hepatocyte and skeletal muscle Bmal1 were reconstituted (Liver+Muscle-RE), i.e., rescued (Smith, Koronowski et al. 2023). This approach had the benefit of analyzing liver and muscle from the same mice but comes with the qualification that the abundance of some proteins may be influenced by Bmal1 function in the other tissue, or by a synergistic effect of Bmal1 in both tissues, rather than through rescue of local Bmal1 function alone. Proteomic anlaysis was performed in liver and skeletal muscle.

2024-01-26 | PXD040362 | Pride

Mus musculus

Project description:Gene expression profiles in the heart tissues of heart-specific Bmal1 knockout mice

| PRJNA262134 | ENA

Gene expression profiles in the heart tissues of heart-specific Bmal1 knockout mice

Project description:Mice without cardiac Bmal1 function develop severe progressive heart failure with age. To examine the mechanism underlying the failing heart phenotype observed in heart-specific Bmal1 knockout mice, microarray analyses were performed. The analyses revealed that broad classes of genes regulating cellular energy metabolism were upregulated or downregulated in the heart tissues of heart-specific Bmal1 knockout mice compared with those of control animals. Heart total RNA extracted from six animals per genotype (control and heart-specific Bmal1 knockout) was pooled and then used for a microarray analysis.

2014-09-27 | E-GEOD-61787 | biostudies-arrayexpress

Reprogramming of rhythmic liver metabolism by intestine clock

Project description:To assess potential impact of intestine clock on the rhythmicity of peripheral tissues (liver, kidney and WAT), mice with Bmal1 specifically deleted in the intestine (Bmal1-iKO mice, showing loss of clock function in the intestine) were generated. We collected liver, kidney and WAT samples from Bmal1-iKO and control (Bmal1-flox) mice every 4 hours throughout a light/dark cycle, and subsequently performed transcriptomic analyses.

2023-06-01 | GSE220864 | GEO

Liver Circadian RNA-Seq from WT and Bmal1 muscle-specific KO (mKO) mice

Project description:Transcriptomic analysis to reveal the impact of muscle-specific Bmal1 knockout on daily cycles of gene expression in the liver

2023-04-05 | GSE171432 | GEO

Effect of leptin deficiency in Bmal1 knockout mice across different tissues

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 disruption 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, but were absent in hepatocyte specific Bmal1 knockout mice. This suggestsing that systemic endocrine perturbation associated with circadian disruptionthe disruption of BMAL1 activity is critical for the pathogenesis of metabolic and liver diseases.

2022-01-26 | GSE150102 | GEO

Gene expression profiles in the heart tissues of heart-specific Bmal1 knockout mice

2014-09-27 | GSE61787 | GEO

HNF4A defines tissue-specific circadian rhythms by beaconing BMAL1::CLOCK chromatin binding and shaping rhythmic chromatin landscape

Project description:ChIP-seqs of BMAL1, HNF4A, FOXA2, H3K4me1, and H3K27ac were profiled in mouse liver tissues upon Hnf4a or Bmal1 knockout. BMAL1, H3K4me1, and H3K27ac ChIP-seq were profiled in U2OS cells ectopically expressing HNF4A.

2021-09-23 | GSE157452 | GEO

Hepatic transcriptome phenotypes after mTORC1 activation through Tsc1 and Depdc5 mutations

Project description:We report RNA-seq results from liver tissues of control mice, liver-specific Tsc1 knockout mice, liver-specific Depdc5 knockout mice and liver-specific Tsc1/Depdc5 double knockout mice.

2020-04-14 | GSE136684 | GEO

Twenty-four hour rhythms in the absence of the clock gene Bmal1

Project description:Circadian (~24 hour) clocks exist in almost all types of living organism and play a fundamental role in regulating daily physiological and behavioural processes. The transcription factor BMAL1 (ARNTL) is thought to be one of the principal drivers of the molecular clock in mammals since its deletion abolishes 24-hour activity patterning, an important physiological output of the clockwork. However, whether or not Bmal1-/- mice can nevertheless display molecular 24-hour rhythms is unknown. Here, we determined whether Bmal1 function is necessary for daily molecular oscillations in two tissues – skin fibroblasts and liver. Unexpectedly, both tissues exhibited robust 24-hour oscillations over 2-3 days in the absence of any exogenous synchronizers such as daily light or temperature cycles. This demonstrates a competent 24-hour molecular pacemaker in Bmal1 knockouts. Indeed, molecular oscillations were pervasive throughout the transcriptome, proteome and phosphoproteome of Bmal1-/- mice. In particular, several proteins exhibited rhythmic phosphorylation in both Bmal1-proficient and -deficient cells, highlighting an unanticipated role for post-translational regulators in 24-hour rhythms in the absence of any known clock mechanisms.

2020-02-17 | PXD009243 | Pride

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