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Genome-wide expression analysis of mouse chromosome 2 in gonadal fat and liver tissues reveals a complex architecture of obesity

ABSTRACT: Transcript abundance in adipose and liver tissues was used to map expression quantitative trait loci (eQTL) underlying fat accretion, weight gain and liver weight. Gonadal fat and liver tissues were used from 48 individuals F2 selected from a cohort (1,200 mice) originated from a cross between M16i and MB2 mice. A complex polygenic architecture within the MB2 locus was observed which was comprised of several locally regulated eQTL (cis-eQTL) with significant correlations to obesity traits. Total RNA obtained from isolated gonadal fat and liver tissues were used to mesured transcript abundance in order to detect expression QTLs.

ORGANISM(S): Mus musculus

SUBMITTER: Gloria Muñoz

PROVIDER: E-GEOD-20724 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide expression analysis of mouse chromosome 2 in gonadal fat and liver tissues reveals a complex architecture of obesity

Project description:Transcript abundance in adipose and liver tissues was used to map expression quantitative trait loci (eQTL) underlying fat accretion, weight gain and liver weight. Gonadal fat and liver tissues were used from 48 individuals F2 selected from a cohort (1,200 mice) originated from a cross between M16i and MB2 mice. A complex polygenic architecture within the MB2 locus was observed which was comprised of several locally regulated eQTL (cis-eQTL) with significant correlations to obesity traits.

2010-09-15 | GSE20724 | GEO

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2022-01-26 | PXD021046 | Pride

Multi-tissue expression profiling of TALLYHO/Jng and C57BL/6J Mice under high-fat and chow diets

Project description:In order to identify gene expression patterns that vary with diet, genetics, and their interaction, we performed expression profiling by RNA-Seq across four different tissues (liver, gonadal fat, soleus muscle, and pancreas) of TALLYHO/Jng (TH) and C57BL/6J (B6) male (M) and female (F) mice, fed either a chow or high fat (HF) diet at 5 weeks and 20 weeks of age.

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2010-04-13 | E-GEOD-15822 | biostudies-arrayexpress

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Project description:Exposure of mammalian fetuses to endocrine disruptors can increase the risk of adult-onset diseases. For example, we previously showed that exposure of mouse fetuses to bisphenol A (BPA) caused adult-onset obesity. To obtain insights into roles of epigenetic changes in the delayed toxic effects of endocrine disruption, we determined effects of fetal mouse exposure to BPA on genome-wide DNA methylation and mRNA expression in gonadal white adipose tissues by deep sequencing (MBD-seq and RNA-seq), bisulfite pyrosequencing, and real-time qPCR. Pregnant CD-1 mice (F0) were dosed daily with 0, 5, or 500 ug/kg/day BPA during 9-18 dpc, and the weaned F1 animals were fed ad libitum with standard chow until they were sacrificed at 19 weeks old. In the vehicle-exposed F1 animals, fggy promoter showed a clear bimodal pattern of very strong (55-95%) or very weak (5-30%) DNA methylation occurring at nearly equal incidence with no intermediate strength, and promoter hypermethylation completely suppressed mRNA expression. BPA exposure eliminated this naturally occurring dichotomy, shifting fggy promoter towards the hypomethylation state to release transcriptional suppression. Strength of Fggy mRNA expression significantly correlated with increased whole-body weight and gonadal fat weight of males but not females. Bioinformatics studies showed that expression of Fggy mRNA is stronger in mouse white adipose tissues than brown adipose tissues and enhanced in gonadal fat by diet-induced obesity. These observations suggest that prenatal exposure to BPA may disrupt the physiological bimodal nature of epigenetic regulation of fggy in mouse white adipose tissues, possibly contributing to the adult-onset obesity phenotype.

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