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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Microarray of hippocampus from 5mo wt, Bmal1 KO and Nr1d1 (Rev-Erb-alpha) KO mice at a single timepoint

ABSTRACT: Deletion of the circadian clock proteins Bmal1 or Nr1d1 (also known as Rev-Erb-alpha) can not only cause circadian dysfunction, but also neuroinflammation in the hippocampus. In this array, 3 wt, 2 Bmal1 KO, and 2 Nr1d1 KO mice, all 5mo, were kept in standard 12h:12h light:dark condition, then anesthetized and perfused with PBS+heparin. Mice were harvest in between noon and 3pm. Whole hippocampus was removed and flash frozen, then RNA was extracted using Trizol reagent and PureLink RNA columns, per manufacturers instructions. RNA microarray analysis was performed by the Washington Univ. Genome Technology Access Center using Agilent Mouse 4x44K mouse V2 array.

ORGANISM(S): Mus musculus

SUBMITTER: Erik Musiek

PROVIDER: E-MTAB-7590 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Microarray analysis of mouse cerebral cortex from brain-specific Bmal1 knockout and Per1;Per2 double mutant mice at 2 timepoints

Project description:The aim of this study was to examine the effect of genetic disruption of the circadian clock on gene expression in the cortex across timepoints. Circadian clock protein regulate many critical aspects of cellular function, and Bmal1 knockout mice develop severe neuroinflammation, suggesting a role for circadian clock gene in brain homeostatic function. We compared brain-specific Bmal1 KO mice (Nestin-Cre;Bmal1(flox/flox) with Per1/2 double mutant mice, in order to assess the effects of deletion of the positive and negative limbs of the core clock. 11mo Cre-, NestinCre+/-;Bmal1(fx/fx), or Per1brdm,Per2brdm mice were entrained to 12h light:dark conditions with lights on at 6am for one month, then placed in constant darkness for 24 hours, after which mice were harvested at 6am (CT6) or 6pm (CT18), still in the dark. Mice were anesthetized in the dark, then perfused briefly with PBS+heparin. The brain was then quickly dissected on a cold surface, and the cerebral cortex flash frozen in liquid nitrogen. Cortex samples were mechanically dissociated with a Qiashredder device, then extracted with chloroform and diluted in 70% ethanol. RNA was extracted using Qiagen RNEasy kit according to manufacturers specifications. cDNAs were chemically labeled with Kreatech ULS RNA labeling kit (Kreatech Diagnostics) and Cy5-labeled cDNAs were hybridized to Agilent Mouse v2 4x44K microarrays (G4846A-026655).

2018-09-11 | E-MTAB-7151 | biostudies-arrayexpress

Transcriptome changes in mouse livers upon Bmal1 or Nr1d1 knock out and interactome of lnc-Crot by 4C-seq

Project description:To explore the circadian regulations of Bmal1, we examined the transcriptome changes in mouse livers upon Bmal1 knock out at two circadian time points, CT0 and CT12. To explore the circadian regulations of Nr1d1, we examined the transcriptome changes in mouse livers upon Nr1d1 knock out at two circadian time points, CT0 and CT12. To explore interactome of lnc-Crot, 4C-seq was performed with lnc-Crot as bait region at CT6 and CT18.

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Transcriptional Repressor Gm129 Modulates the Circadian Gene Expression by Inhibiting CLOCK:BMAL1 Activity

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2014-01-07 | E-GEOD-53828 | biostudies-arrayexpress

Gene Model 129 (Gm129) Encodes a Novel Transcriptional Repressor that Modulates Circadian Gene Expression

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Long-range chromosome interactions mediated by cohesin shape circadian gene expression [4C]

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2016-04-04 | E-GEOD-68830 | biostudies-arrayexpress

Long-range chromosome interactions mediated by cohesin shape circadian gene expression [ChIP-Seq]

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Transcriptomic analysis of cortex tissue from neuron-specific Bmal1 KO mice

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Bmal1 controls circadian cell proliferation and susceptibility to UVB-induced DNA damage in the epidermis [Bmal1 KO]

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2012-08-01 | E-GEOD-38624 | biostudies-arrayexpress

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2014-01-01 | GSE43071 | GEO

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.

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