Project description:It is evident that epigenetic factors, especially DNA methylation, play essential roles in obesity development. To learn systematic association of DNA methylation to obesity, we used pig as a model, and sampled eight diverse adipose tissues and two distinct skeletal muscle tissues from three pig breeds with distinguished fat levels: the lean Landrace, the fatty Rongchang, and the feral Tibetan pig. We sequenced 180 methylated DNA immunoprecipitation (MeDIP) libraries, generated 1,381 Gbp sequence data, and provided a genome-wide DNA methylation map for pig adipose and muscle studies. The analysis showed global similarities and differences between breeds, genders and tissues, and identified the differentially methylated regions (DMRs) that are preferentially located in intermediate CpG promoters and CpG island shores. The DMRs in promoters are highly associated to obesity development. We also analyzed methylation and regulation of the known obesity-related genes and predicted novel candidate genes. The comprehensive map here provides a solid base for exploring epigenetic mechanisms of adipose deposition and muscle growth. We collected eight diverse adipose tissues and two phenotypically distinct skeletal muscle tissues from three well-defined pig models with distinct fat rates, and studied genome-wide DNA methylation differences among breeds, males and females, and tissues.
Project description:Genomic DNA is isolated from C57BL6/J mice at E17.5 and postnatal d21, and we used MCAM to identify genes undergoing methylation change during late fetal to early postnatal mouse liver development.
Project description:Genomic DNA is isolated from C57BL6/J mice at E17.5 and postnatal d21, and we used MCAM to identify genes undergoing methylation change during late fetal to early postnatal mouse liver development. Two-condition experiment, P21 vs. E17.5. Biological replicates: 2 for each condition.
Project description:DNA methylation marks are thought to be set up during early development and to remain static thereafter in healthy tissues. Here, we characterize the liver DNA methylation patterns of mice before birth, during early postnatal development (from birth until weaning) and in adulthood. Our analyses show extensive epigenetic reprogramming in the liver occurring during postnatal development. 118,877 of 261,317 CpGs analyzed throughout the genome significantly changed their methylation level by more than 5% from birth to nine weeks of age, with some changing by up to 86%. Interestingly, changes in DNA methylation occur primarily in intergenic enhancer regions while gene promoters seem little affected. Analysis of 166 CpGs at multiple time points by locus-specific bisulfite sequencing reveals that this reprogramming primarily occurs between postnatal day 1 and day 20. This time period coincides with two major cellular changes in the liver: the differentiation of hepatocytes and extensive cell division. While cell multiplication leaves a distinct footprint on the DNA methylation patterns, we show that the extensive epigenetic reprogramming likely results from differentiation of hepatoblasts into hepatocytes. Overall, our data suggest that epigenetic remodeling is an important aspect of normal liver maturation and involves a large number of gene enhancers.
Project description:DNA methylation marks are thought to be set up during early development and to remain static thereafter in healthy tissues. Here, we characterize the liver DNA methylation patterns of mice before birth, during early postnatal development (from birth until weaning) and in adulthood. Our analyses show extensive epigenetic reprogramming in the liver occurring during postnatal development. 118,877 of 261,317 CpGs analyzed throughout the genome significantly changed their methylation level by more than 5% from birth to nine weeks of age, with some changing by up to 86%. Interestingly, changes in DNA methylation occur primarily in intergenic enhancer regions while gene promoters seem little affected. Analysis of 166 CpGs at multiple time points by locus-specific bisulfite sequencing reveals that this reprogramming primarily occurs between postnatal day 1 and day 20. This time period coincides with two major cellular changes in the liver: the differentiation of hepatocytes and extensive cell division. While cell multiplication leaves a distinct footprint on the DNA methylation patterns, we show that the extensive epigenetic reprogramming likely results from differentiation of hepatoblasts into hepatocytes. Overall, our data suggest that epigenetic remodeling is an important aspect of normal liver maturation and involves a large number of gene enhancers.