The Cell Cycle and Regulation

Study Notes

The cell cycle is a series of events that cause a cell to divide into two daughter cells.
In eukaryotic cells, the cell cycle is divided into interphase and the mitotic phase.
Interphase is divided into G1, S, and G2 phases.
During S phase, DNA replication occurs.
Mitotic phase consists of mitosis and cytokinesis.
Mitosis is the process of separating chromosomes into two identical sets.
Cytokinesis is the separation of all cell components.
The cell cycle is regulated by cell cycle checkpoints.
Cells can enter a quiescent state called G0.
Errors in mitosis can cause mutations that lead to cancer.
Regulation of the cell cycle is crucial for cell survival and involves detection and repair of genetic damage and prevention of uncontrolled cell division.
Cyclins and cyclin-dependent kinases (CDKs) are key regulatory molecules that determine a cell's progress through the cell cycle.
Cyclins form regulatory subunits and CDKs form catalytic subunits of an activated heterodimer.
Different cyclin-CDK combinations determine the downstream proteins targeted.
Cyclin D is the first cyclin produced in cells that enter the cell cycle in response to extracellular signals.
Cyclin D-CDK4/6 complexes mono-phosphorylate the retinoblastoma susceptibility protein (Rb) to pRb, which induces G1/S cell cycle gene expression and progression into S phase.
Hyperphosphorylated Rb dissociates from the E2F/DP1/Rb complex, activating E2F and resulting in transcription of various genes.
Cyclin E produced binds to CDK2, forming the cyclin E-CDK2 complex, which pushes the cell from G1 to S phase.
Mitotic cyclin-CDK complexes promote the initiation of mitosis by stimulating downstream proteins involved in chromosome condensation and mitotic spindle assembly.
G1 cyclin-CDK activities primarily tune the timing rather than the commitment of cell cycle entry.
The cell cycle is regulated by cyclin-dependent kinases (CDKs) and cyclins.
CDKs are activated by binding to cyclins and phosphorylate target proteins.
The progression of the cell cycle is regulated by inhibitors such as the cip/kip and INK4a/ARF families.
Synthetic inhibitors of Cdc25 can be used as antineoplastic and anticancer agents.
Cdk4/6 inhibitors have been developed as a therapeutic target for anti-tumor effectiveness.
A semi-autonomous transcriptional network works with the CDK-cyclin machinery to regulate the cell cycle.
Cell cycle checkpoints prevent cell cycle progression until necessary phase processes are completed and DNA damage is repaired.
Checkpoints include the G1/S checkpoint, G2/M checkpoint, and metaphase checkpoint.
Mutations that allow cells to speed through checkpoints or skip them altogether can lead to cancer.
Loss of Rb can lead to primary resistance to Cdk4/6 inhibitors.
Cells can leave the cell cycle and stay in G0 until their death, removing the need for cellular checkpoints.
Checkpoint regulation plays an important role in an organism's development and sexual reproduction.
p53 plays a crucial role in triggering control mechanisms at both G1/S and G2/M checkpoints.
Fluorescence imaging of the cell cycle is possible with the fluorescent ubiquitination-based cell cycle indicator (FUCCI).
A disregulation of the cell cycle components may lead to tumor formation.
The proportion of cells in active cell division in tumors is much higher than in normal tissue.
The cells actively undergoing cell cycle are targeted in cancer therapy.
The fastest cycling mammalian cells in culture have a cycle time as short as 9 to 10 hours.
Cells are most radiosensitive in late M and G2 phases and most resistant in late S phase.
Homologous recombination is an accurate process for repairing DNA double-strand breaks.