Increasing p16INK4a expression decreases forebrain progenitors and neurogenesis during ageing

Anna V. Molofsky, Shalom G. Slutsky, Nancy M. Joseph, Shenghui He, Ricardo Pardal, Janakiraman Krishnamurthy, Norman E. Sharpless and Sean J. Morrison ()
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Anna V. Molofsky: University of Michigan
Shalom G. Slutsky: University of Michigan
Nancy M. Joseph: University of Michigan
Shenghui He: University of Michigan
Ricardo Pardal: University of Michigan
Janakiraman Krishnamurthy: The Lineberger Comprehensive Cancer Center, The University of North Carolina School of Medicine
Norman E. Sharpless: The Lineberger Comprehensive Cancer Center, The University of North Carolina School of Medicine
Sean J. Morrison: University of Michigan

Nature, 2006, vol. 443, issue 7110, 448-452

Abstract: Stem cell ageing In this issue, three separate labs report the discovery of a protein that regulates ageing specifically in stem cells. This helps answer a fundamental question: why do mammalian progenitor cells gradually lose their ability to divide and generate new cells as they grow old? Norman Sharpless and colleagues generated a knockout mouse lacking tumour suppressor p16INK4a, a protein involved in cell cycle control and known to be expressed in an age-dependent manner. Studying its role in regeneration of the blood, pancreas and brain, the three groups separately found that p16INK4a is not only a biomarker, but an effector of ageing. By comparing the effect of elevated or reduced p16INK4a expression in mice, they found that p16INK4a halts proliferation of stem cells, but only in older mice. Taken together, the work suggests that p16INK4a reduces cancer incidence via its tumour suppressor action, at the same time contributing to ageing by reducing stem cell function. The work also suggests that type 2 diabetes might be linked to the failure of the pancreatic islets to renew, and that blocking this protein in certain tissues might combat some effects of ageing.

Date: 2006
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DOI: 10.1038/nature05091

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