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Dev Cell. 2011 Oct 18;21(4):655-68. doi: 10.1016/j.devcel.2011.08.009. Epub 2011 Sep 22.

Cyclin E constrains Cdk5 activity to regulate synaptic plasticity and memory formation.

Author information

1
Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA.

Abstract

Cyclin E is a component of the core cell cycle machinery, and it drives cell proliferation by regulating entry and progression of cells through the DNA synthesis phase. Cyclin E expression is normally restricted to proliferating cells. However, high levels of cyclin E are expressed in the adult brain. The function of cyclin E in quiescent, postmitotic nervous system remains unknown. Here we use a combination of in vivo quantitative proteomics and analyses of cyclin E knockout mice to demonstrate that in terminally differentiated neurons cyclin E forms complexes with Cdk5 and controls synapse function by restraining Cdk5 activity. Ablation of cyclin E led to a decreased number of synapses, reduced number and volume of dendritic spines, and resulted in impaired synaptic plasticity and memory formation in cyclin E-deficient animals. These results reveal a cell cycle-independent role for a core cell cycle protein, cyclin E, in synapse function and memory.

PMID:
21944720
PMCID:
PMC3199337
DOI:
10.1016/j.devcel.2011.08.009
[Indexed for MEDLINE]
Free PMC Article

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