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Differentiation plasticity regulated by TGF-β family proteins in development and disease

Nature Cell Biology volume 9, pages 1000–1004 (2007)Cite this article

During development, stem and progenitor cells gradually commit to differentiation pathways. Cell fate decisions are regulated by differentiation factors, which activate transcription programmes that specify lineage and differentiation status. Among these factors, the transforming growth factor (TGF)-β family is important in both lineage selection and progression of differentiation of most, if not all, cell and tissue types. There is now increasing evidence that TGF-β family proteins have the ability to redirect the differentiation of cells that either have fully differentiated or have engaged in differentiation along a particular lineage, and can thereby elicit 'transdifferentiation'. This capacity for cellular plasticity is critical for normal embryonic development, but when recapitulated in the adult it can give rise to, or contribute to, a variety of diseases. This is illustrated by the ability of TGF-β family members to redirect epithelial cells into mesenchymal differentiation and to cause switching of mesenchymal cells from one lineage to another. Hence, various pathologies in adults may be considered diseases of abnormal development and differentiation.

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Figure 1: Epithelial–mesenchymal transition (EMT) in development and disease.
Figure 2

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Authors and Affiliations

  1. Rik Derynck is in the Department of Cell and Tissue Biology, Programs in Cell and Developmental Biology, University of California – San Francisco, San Francisco, CA 94143-0512, USA. rik.derynck@ucsf.edu,

    Rik Derynck

  2. Department of Anatomy and Program in Human Genetics, Rosemary J. Akhurst is in the Cancer Research Institute, University of California – San Francisco, San Francisco, CA 94143-0875, USA rakhurst@cc.ucsf.edu,

    Rosemary J. Akhurst

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Derynck, R., Akhurst, R. Differentiation plasticity regulated by TGF-β family proteins in development and disease. Nat Cell Biol 9, 1000–1004 (2007). https://doi.org/10.1038/ncb434

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