DNA methylation-mediated silencing of neuronatin (NNAT) in pig parthenogenetic fetuses

Gene. 2014 Nov 15;552(1):204-8. doi: 10.1016/j.gene.2014.09.035. Epub 2014 Sep 19.

Abstract

It is generally believed that aberrant expression of imprinted genes participates in growth retardation of mammalian parthenogenesis. Neuronatin (NNAT), a paternally expressed gene, plays important roles in neuronal growth and metabolic regulation. Here we have compared the gene expression and promoter methylation pattern of NNAT between pig normally fertilized (Con) and parthenogenetic (PA) embryos. The results showed loss of NNAT expression (p<0.001) and hypermethylation of NNAT promoter in PA samples. Additionally, partial methylation was observed in Con fetuses, while almost full methylation and unmethylation of NNAT promoter were apparent in Metaphase II (MII) oocytes and mature sperms, respectively, which identified the CpG promoter region as a putative differentially methylated region (DMR) of NNAT. The data demonstrate that promoter hypermethylation is associated with the silencing of NNAT in pig PA fetuses, which may be related to developmental failure of pig parthenogenesis at early stages.

Keywords: Imprinted gene; Methylation; NNAT; PA fetuses; Promoter region.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cells, Cultured
  • CpG Islands / genetics
  • DNA Methylation / genetics*
  • Fetus / metabolism*
  • Gene Expression / genetics
  • Male
  • Nerve Tissue Proteins / genetics*
  • Oocytes / metabolism
  • Promoter Regions, Genetic / genetics*
  • Spermatozoa / metabolism
  • Swine / genetics*

Substances

  • Nerve Tissue Proteins