De novo methylation, expression, and infectivity of retroviral genomes introduced into embryonal carcinoma cells. Academic Article uri icon

Overview

MeSH

  • Animals
  • Cell Line
  • Cells, Cultured
  • Clone Cells
  • DNA Replication
  • Mice
  • Virus Replication

MeSH Major

  • Cell Transformation, Neoplastic
  • Genes, Viral
  • Leukemia, Experimental
  • Moloney murine leukemia virus

abstract

  • We have investigated the block to expression of Moloney murine leukemia virus in murine embryonal carcinoma (EC) cells. Infected EC cells were found to contain up to 100 integrated proviral genomes. However, expression of virus as measured by XC plaque and virus-specific RNA synthesis did not occur at significant levels, in contrast to productively infected differentiated cells. Analysis of the DNA in the infected EC cells revealed that the proviral genomes were highly methylated, as shown by their resistance to cleavage by Sma I. Integrated proviral genomes in infected differentiated cells were readily cut by Sma I and thus were not methylated at these sites. Transfection of DNA from infected EC cells to cells permissive for virus expression failed to induce virus expression. The proviral genomes, however, were potentially infectious because they induced XC plaques when the recipient cells for transfection were treated with 5-azacytidine. This drug is believed to interfere with DNA methylation. We conclude that expression of proviral genomes introduced into EC cells is suppressed and that this inactivation can be correlated with the de novo methylation of the viral DNA. De novo methylation activity thus may be a characteristic of early embryonic cells.

publication date

  • July 1982

has subject area

  • Animals
  • Cell Line
  • Cell Transformation, Neoplastic
  • Cells, Cultured
  • Clone Cells
  • DNA Replication
  • Genes, Viral
  • Leukemia, Experimental
  • Mice
  • Moloney murine leukemia virus
  • Virus Replication

Research

keywords

  • Journal Article

Identity

Language

  • eng

PubMed Central ID

  • PMC346584

PubMed ID

  • 6955793

Additional Document Info

start page

  • 4098

end page

  • 4102

volume

  • 79

number

  • 13