Cyclin C/cdk3 promotes Rb-dependent G0 exit

Cell. 2004 Apr 16;117(2):239-51. doi: 10.1016/s0092-8674(04)00300-9.

Abstract

G0 is a physiological state occupied by resting or terminally differentiated cells that have exited the cell cycle. In contrast to the well-characterized cyclin/cdk-mediated inactivation of pRb that controls the G1/S transition, little is known about regulation of the G0/G1 transition. However, pRb is likely to participate in this process because its acute somatic inactivation is sufficient for G0-arrested cells to re-enter the cell cycle. One physiological regulator of this event may be cyclin C because its highest mRNA levels occur during G0 exit. Here we show that a non-cdk8-associated cellular pool of cyclin C combines with cdk3 to stimulate pRb phosphorylation at S807/811 during the G0/G1 transition, and that this phosphorylation is required for cells to exit G0 efficiently. Thus, G1 entry is regulated in an analogous fashion to S phase entry, but involves a distinct cyclin/cdk combination.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Cell Cycle / genetics
  • Cell Cycle / physiology
  • Cyclin C
  • Cyclin-Dependent Kinase 3
  • Cyclin-Dependent Kinases / genetics
  • Cyclin-Dependent Kinases / metabolism*
  • Cyclins / genetics
  • Cyclins / metabolism*
  • G1 Phase / genetics
  • G1 Phase / physiology
  • Humans
  • Phosphorylation
  • RNA, Messenger / metabolism
  • Resting Phase, Cell Cycle / genetics
  • Resting Phase, Cell Cycle / physiology*
  • Retinoblastoma Protein / genetics
  • Retinoblastoma Protein / metabolism*
  • Serine / metabolism
  • Tumor Cells, Cultured

Substances

  • CCNC protein, human
  • Cyclin C
  • Cyclins
  • RNA, Messenger
  • Retinoblastoma Protein
  • Serine
  • CDK3 protein, human
  • Cyclin-Dependent Kinase 3
  • Cyclin-Dependent Kinases