Abstract
In most tissues, anchorage-dependent growth and cell cycle progression are dependent on cells engaging extracellular matrices (ECM) via integrin receptor adhesion complexes. In a highly conserved manner, cells disassemble adhesion complexes, round up, and retract from their surroundings prior to division, suggestive of a primordial link between the cell cycle machinery and the regulation of cell adhesion to the ECM. Here, we demonstrate that CDK1
mediates this link. CDK1, in complex with cyclin A2, promotes adhesion complex and actin cytoskeleton organisation during interphase, and mediates a large increase in adhesion complex area as cells transition from G1 into S. Adhesion complex area decreases in G2 and disassembly occurs several hours prior to mitosis. This loss requires elevated cyclin B1 levels and is caused by inhibitory phosphorylation of CDK1-cyclin complexes. The inactivation of CDK1 is therefore the trigger that initiates remodelling of adhesion complexes and the actin cytoskeleton in preparation for rapid entry into mitosis.
mediates this link. CDK1, in complex with cyclin A2, promotes adhesion complex and actin cytoskeleton organisation during interphase, and mediates a large increase in adhesion complex area as cells transition from G1 into S. Adhesion complex area decreases in G2 and disassembly occurs several hours prior to mitosis. This loss requires elevated cyclin B1 levels and is caused by inhibitory phosphorylation of CDK1-cyclin complexes. The inactivation of CDK1 is therefore the trigger that initiates remodelling of adhesion complexes and the actin cytoskeleton in preparation for rapid entry into mitosis.
Original language | English |
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Pages (from-to) | 3203-3218 |
Number of pages | 15 |
Journal | The Journal of cell biology |
Volume | 217 |
Issue number | 9 |
Early online date | 21 Jun 2018 |
DOIs | |
Publication status | Published - 2018 |