Gene Expression Profiling of Embryo-Derived Stem Cells Reveals Candidate Genes Associated With Pluripotency and Lineage Specificity

  1. Tetsuya S. Tanaka1,
  2. Tilo Kunath2,
  3. Wendy L. Kimber1,
  4. Saied A. Jaradat1,
  5. Carole A. Stagg1,
  6. Masayuki Usuda3,
  7. Takashi Yokota3,
  8. Hitoshi Niwa4,
  9. Janet Rossant2, and
  10. Minoru S.H. Ko1,5
  1. 1Laboratory of Genetics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, 21224-6820, USA; 2Samuel Lunenfeld Research Institute, Mount Sinai Hospital, University of Toronto, Toronto, Ontario, Canada; 3Department of Stem Cell Regulation, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan; 4Laboratory for Pluripotent Cell Studies, RIKEN Center for Developmental Biology, Kobe, Hyogo, Japan

Abstract

Large-scale gene expression profiling was performed on embryo-derived stem cell lines to identify molecular signatures of pluripotency and lineage specificity. Analysis of pluripotent embryonic stem (ES) cells, extraembryonic-restricted trophoblast stem (TS) cells, and terminally-differentiated mouse embryo fibroblast (MEF) cells identified expression profiles unique to each cell type, as well as genes common only to ES and TS cells. Whereas most of the MEF-specific genes had been characterized previously, the majority (67%) of the ES-specific genes were novel and did not include known differentiated cell markers. Comparison with microarray data from embryonic material demonstrated that ES-specific genes were underrepresented in all stages sampled, whereas TS-specific genes included known placental markers. Investigation of four novel TS-specific genes showed trophoblast-restricted expression in cell lines and in vivo, whereas one uncharacterized ES-specific gene, Esg-1, was found to be exclusively associated with pluripotency. We suggest that pluripotency requires a set of genes not expressed in other cell types, whereas lineage-restricted stem cells, like TS cells, express genes predictive of their differentiated lineage.

[Supplemental material is available online at www.genome.org andhttp://lgsun.grc.nia.nih.gov/microarray/data.html]

Footnotes

  • ↵5 Corresponding author.

  • E-MAIL KoM{at}grc.nia.nih.gov; FAX (410) 558-8331.

  • Article and publication are at http://www.genome.org/cgi/doi/10.1101/gr.670002.

    • Received July 30, 2002.
    • Accepted October 7, 2002.
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  1. doi: 10.1101/gr.670002 Genome Res. 12: 1921-1928 Cold Spring Harbor Laboratory Press

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