Complementation of methylation deficiency in embryonic stem cells by a DNA methyltransferase minigene

Research output: Contribution to journalResearch articleContributedpeer-review

Contributors

  • Kerry Lee Tucker - , Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology (MIT) (Author)
  • Dale Talbot - , Whitehead Institute for Biomedical Research (Author)
  • Min Ae Lee - , Harvard University, Max Delbrück Center for Molecular Medicine (MDC) (Author)
  • Heinrich Leonhardt - , Franz Volhard Clinic (Author)
  • Rudolf Jaenisch - , Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology (MIT) (Author)

Abstract

Previous attempts to express functional DNA cytosine methyltransferase (EC 2.1.1.37) in cells transfected with the available Dnmt cDNAs have met with little or no success. We show that the published Dnmt sequence encodes an amino terminal-truncated protein that is tolerated only at very low levels when stably expressed in embryonic stem cells. Normal expression levels were, however, obtained with constructs containing a continuation of an ORF with a coding capacity of up to 171 amino acids upstream of the previously defined start site. The protein encoded by these constructs comigrated in SDS/PAGE with the endogenous enzyme and restored methylation activity in transfected cells. This was shown by functional rescue of Dnmt mutant embryonic stem cells that contain highly demethylated genomic DNA and fail to differentiate normally. When transfected with the minigene construct, the genomic DNA became remethylated and the cells regained the capacity to form teratomas that displayed a wide variety of differentiated cell types. Our results define an amino-terminal domain of the mammalian MTase that is crucial for stable expression and function in vivo.

Details

Original languageEnglish
Pages (from-to)12920-12925
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume93
Issue number23
Publication statusPublished - 12 Nov 1996
Peer-reviewedYes
Externally publishedYes

External IDs

PubMed 8917520

Keywords

ASJC Scopus subject areas