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Stem Cell Reviews

, Volume 2, Issue 1, pp 1–4 | Cite as

The funGenES consortium

Functional genomics in engineered embryonic stem cells
  • Jürgen Hescheler
  • Agapios Sachinidis
  • Shuhua Chen
  • Johannes WinklerEmail author
Original Article
  • 75 Downloads

Abstract

Although the complete sequence of a mammalian genome defines the information content of each cell, understanding the selective usage of this information during the development of specific cell types is limited. The fundamental questions that remain to be answered includes, which are the gene subsets that define the pluripotential self-renewing state of embryonic stem (ES) cells, partially and terminally differentiated developmental states, and how are transitions between these states regulated (lineage commitment)? The FunGenES consortium has been formed to address this challenge by mapping the gene subsets involved in pluripotent, lineage committed, and selected differentiated cell types using gene expression profiling and functional screens. They create an atlas of mammalian genome participating in early and late developmental processes. To fulfil the aim, mouse ES cells were used as an in vitro developmental model system that is very close to the human as they are pluripotent. They can be differentiated through the three major developmental pathways ecto-, meso-, and endoderm into many committed cell types and can be genetically engineered with relative ease. Knowledge of genetic pathways in mouse ES cell differentiation and development might be translated to human ES cells and the potential development of stem cell-based therapies.

Index Entries

Differentiation ES cells functional genomics lineage selection 

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References

  1. 1.
    Robertson E, Bradley A, Kuehn M, Evans M. Nature 1986); 323;445–448.PubMedCrossRefGoogle Scholar
  2. 2.
    Gossler A, Doetschman T, Korn R, Serfling E, Kemler R. Proc Natl Acad Sci USA 1986;83:9065–9069.PubMedCrossRefGoogle Scholar
  3. 3.
    Gadue P, Huber TL, Nostro MC, Kattman S, Keller GM. Exp Hematol 2005;33:955–964.PubMedCrossRefGoogle Scholar
  4. 4.
    Thomson JA, Itskovitz-Eldor J, Shapiro SS, et al. Science 1998;282:1145–1147.PubMedCrossRefGoogle Scholar
  5. 5.
    Brook FA, Gardner RL. Proc Natl Acad Sci USA 1997;94: 5709–5712.PubMedCrossRefGoogle Scholar
  6. 6.
    Li M, Pevny L, Lovell-Badge R, Smith A. Curr Biol 1998;8: 971–974.PubMedCrossRefGoogle Scholar

Copyright information

© Humana Press Inc 2006

Authors and Affiliations

  • Jürgen Hescheler
    • 1
  • Agapios Sachinidis
    • 1
  • Shuhua Chen
    • 1
  • Johannes Winkler
    • 1
    Email author
  1. 1.Centre of Physiology and PathophysiologyInstitute of NeurophysiologyKölnGermany

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