Murine somatic cell nuclear transfer using reprogrammed donor cells expressing male germ cell-specific genes

J Vet Med Sci. 2016 Jan;78(1):149-52. doi: 10.1292/jvms.14-0596. Epub 2015 Sep 14.

Abstract

In vivo-matured mouse oocytes were enucleated, and a single murine embryonic fibroblast (control or reprogrammed by introducing extracts from murine testis tissue, which showed expression of male germ cell-specific genes) was injected into the cytoplasm of the oocytes. The rate of blastocyst development and expression levels of Oct-4, Eomes and Cdx-2 were not significantly different in both experimental groups. However, the expression levels of Nanog, Sox9 and Glut-1 were significantly increased when reprogrammed cells were used as donor nuclei. Increased expression of Nanog can be supportive of complete reprogramming of somatic cell nuclear transfer murine embryos. The present study suggested that donor cells expressing male germ cell-specific genes can be reconstructed and can develop into embryos with normal high expression of developmentally essential genes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult Stem Cells
  • Animals
  • Blastocyst / physiology
  • CDX2 Transcription Factor
  • Female
  • Fibroblasts
  • Glucose Transporter Type 1 / metabolism
  • Homeodomain Proteins / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Nanog Homeobox Protein
  • Nuclear Transfer Techniques / veterinary*
  • Octamer Transcription Factor-3 / metabolism
  • Oocytes
  • Polymerase Chain Reaction / veterinary
  • SOX9 Transcription Factor / metabolism
  • T-Box Domain Proteins / metabolism
  • Testis / cytology
  • Transcription Factors / metabolism

Substances

  • CDX2 Transcription Factor
  • Cdx2 protein, mouse
  • Eomes protein, mouse
  • Glucose Transporter Type 1
  • Homeodomain Proteins
  • Nanog Homeobox Protein
  • Nanog protein, mouse
  • Octamer Transcription Factor-3
  • SOX9 Transcription Factor
  • Slc2a1 protein, mouse
  • Sox9 protein, mouse
  • T-Box Domain Proteins
  • Transcription Factors