Abstract
In the current study, we characterized the expression and histone modification profiles of the alternative promoters found within imprinted Igf2r, Mest, Zac1, Peg3, Snrpn and non-imprinted Myc loci. In terms of expression pattern, the alternative promoters are highly tissue-specific, which is in a stark contrast to the ubiquitous expression of the corresponding main promoters. The alternative promoters are associated with the histone modification mark H3K4me1, but not with H3K4me3, which is frequently associated with the main promoters. Phylogenetic analyses also indicated that the majority of the alternative promoters are unique to the mammalian lineage, further suggesting the recent formation of these promoters during mammalian evolution. Overall, this study suggests that the alternative promoters of imprinted loci may have been derived from enhancers in recent evolutionary times and co-evolved with the genomic imprinting mechanism.
Highlights
In mammalian genomes, a subset of genes are expressed mainly from one allele due to an epigenetic mechanism termed genomic imprinting, by which one allele is repressed by DNA methylation and histone modifications [1, 2]
The isolated total RNA was subsequently reverse-transcribed with the gene-specific primers that were derived from the 2nd exon of imprinted genes, including Snrpn, Zac1, Gtl2, Dlk1, Igf2r and non-imprinted Myc, which served as a control
These cDNAs were further modified with G-tailing, which were amplified for Next Generation Sequencing (NGS) runs
Summary
A subset of genes are expressed mainly from one allele due to an epigenetic mechanism termed genomic imprinting, by which one allele is repressed by DNA methylation and histone modifications [1, 2]. It has been predicted that imprinted genes may play significant roles in fetal development and animal behaviors. Consistent with this, mutations in these imprinted genes have very similar functional outcomes, such as changes in fetal growth rates and in animal nurturing behaviors [1, 2]. It has been hypothesized that genomic imprinting may have coevolved with the reproduction scheme of placental mammals to control the dosage of the genes that play important roles in the reproduction-related physiology and behaviors [4,5,6,7]
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