Long-term haematopoietic reconstitution by Trp53-/-p16Ink4a-/-p19Arf-/- multipotent progenitors

Omobolaji O. Akala, In-Kyung Park, Dalong Qian, Michael Pihalja, Michael W. Becker and Michael F. Clarke ()
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Omobolaji O. Akala: Cellular and Molecular Biology Graduate Program, University of Michigan, 2966 Taubman Medical Library, Ann Arbor, Michigan 48109-0619, USA
In-Kyung Park: Internal Medicine, University of Michigan, 1500 East Medical Center Drive, Ann Arbor, Michigan 48109, USA
Dalong Qian: Internal Medicine, Stanford University, 1050 Arastradero Road, Palo Alto, California 93404, USA
Michael Pihalja: Internal Medicine, University of Michigan, 1500 East Medical Center Drive, Ann Arbor, Michigan 48109, USA
Michael W. Becker: University of Rochester, Rochester, New York 14642, USA
Michael F. Clarke: Internal Medicine, Stanford University, 1050 Arastradero Road, Palo Alto, California 93404, USA

Nature, 2008, vol. 453, issue 7192, 228-232

Abstract: Self-renewal in stem cells Stem cells maintain themselves over the life-time of an organism by their ability to self-renew. Multipotent progenitor cells are like stem cells in their ability to form many kinds of differentiated cells, but they do not self-renew and have a limited lifespan. Gene knock-out experiments in mice now show that by deleting just three genes, multipotent progenitor cells can be converted into long-term renewing cells. The normal role of the genes — p16Ink4a , p19Arf , and Tp53 — is to prevent progenitors from self-renewing. They are involved in pathways commonly repressed in cancer, pointing to a possible mechanism for tumorigenic mutation in progenitor cells.

Date: 2008
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DOI: 10.1038/nature06869

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