Abstract
DNA methylation and the alternative splicing of precursor messenger RNAs (pre-mRNAs) are two important genetic modification mechanisms. However, both are currently uncharacterized in the muscle metabolism of rabbits. Thus, we constructed the Tianfu black rabbit obesity model (obese rabbits fed with a 10% high-fat diet and control rabbits from 35 days to 70 days) and collected the skeletal muscle samples from the two groups for Genome methylation sequencing and RNA sequencing. DNA methylation data showed that the promoter regions of 599 genes and gene body region of 2522 genes had significantly differential methylation rates between the two groups, of which 288 genes had differential methylation rates in promoter and gene body regions. Analysis of alternative splicing showed 555 genes involved in exon skipping (ES) patterns, and 15 genes existed in differential methylation regions. Network analysis showed that 20 hub genes were associated with ubiquitinated protein degradation, muscle development pathways, and skeletal muscle energy metabolism. Our findings suggest that the two types of genetic modification have potential regulatory effects on skeletal muscle development and provide a basis for further mechanistic studies in the rabbit.
Highlights
The growth and development of muscle are closely related to nutrition, heredity, gender, and age and involve a variety of metabolic mechanisms
80% of the reads of the whole-methylome bisulfite sequencing data from skeletal muscle were uniquely mapped to the rabbit reference genome (Table 1)
We analyzed the deep sequencing distribution to check the validity of the methylome data of skeletal muscle samples from control group (CON−G) and high-fat diet-induced group (HFD−G) (Figure S1)
Summary
The growth and development of muscle are closely related to nutrition, heredity, gender, and age and involve a variety of metabolic mechanisms. Studies have shown that the excessive accumulation of fat in obese humans can damage the AMPK signal pathway [1] and cause disorders in the microvascular function of skeletal muscle, leading to decreased insulin sensitivity [2]. Compared with those in normal mice, the excessive accumulations of visceral fat in obese mice cause the disordered secretion of adipokines, inflammatory reactions, abnormal distributions of skeletal muscle bundles, and muscle atrophy [3]. The molecular mechanisms involved in the development and metabolism of the rabbit skeletal muscle are unclear
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