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p57 controls adult neural stem cell quiescence and modulates the pace of lifelong neurogenesis
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p57 controls adult neural stem cell quiescence and modulates the pace of lifelong neurogenesis
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Journal Article
p57 controls adult neural stem cell quiescence and modulates the pace of lifelong neurogenesis
2013
Overview
Throughout life, neural stem cells (NSCs) in the adult hippocampus persistently generate new neurons that modify the neural circuitry. Adult NSCs constitute a relatively quiescent cell population but can be activated by extrinsic neurogenic stimuli. However, the molecular mechanism that controls such reversible quiescence and its physiological significance have remained unknown. Here, we show that the cyclin‐dependent kinase inhibitor p57
kip2
(p57) is required for NSC quiescence. In addition, our results suggest that reduction of p57 protein in NSCs contributes to the abrogation of NSC quiescence triggered by extrinsic neurogenic stimuli such as running. Moreover, deletion of
p57
in NSCs initially resulted in increased neurogenesis in young adult and aged mice. Long‐term
p57
deletion, on the contrary, led to NSC exhaustion and impaired neurogenesis in aged mice. The regulation of NSC quiescence by p57 might thus have important implications for the short‐term (extrinsic stimuli‐dependent) and long‐term (age‐related) modulation of neurogenesis.
The cyclin‐dependent kinase inhibitor p57 maintains adult neural stem cells in a quiescent state to preserve their proliferative and neurogenic potential throughout life.
Publisher
John Wiley & Sons, Ltd,Nature Publishing Group UK,Springer Nature B.V,Nature Publishing Group
Subject
/ Adult Stem Cells - metabolism
/ Animals
/ Brain
/ Cyclin-Dependent Kinase Inhibitor p57 - genetics
/ Cyclin-Dependent Kinase Inhibitor p57 - metabolism
/ EMBO11
/ EMBO27
/ Mice
/ Nerve Tissue Proteins - genetics
/ Nerve Tissue Proteins - metabolism
/ Neural Stem Cells - cytology
/ Neural Stem Cells - metabolism
/ Neurons
/ p57
/ Proteins
