Give a brief note on the control of the Cell Cycle

The cell cycle is a highly regulated process that ensures cells grow, replicate their DNA and divide accurately. Its control is crucial for normal development, tissue repair and prevention of diseases like cancer. This control is achieved mainly through a combination of regulatory proteins, checkpoints, inhibitory pathways and external signaling factors, all of which coordinate to monitor and regulate the progression of the cycle at every stage.

1. Cyclins and CDKs – The Core Regulators

Cyclin-dependent kinases (CDKs) are special enzymes that become active only when they bind to a protein called cyclin, to form a cyclin-CDK complex. Different cyclins appear and disappear at specific times in the cell cycle, and this timing controls CDK activity. Each cyclin-CDK complex triggers important events of a particular phase of cell cycle.
  • In the G1 phase, Cyclin D binds to CDK4 or CDK6 to push the cell toward the S phase.
  • During the S phase, Cyclin E and later Cyclin A bind to CDK2 to promote DNA synthesis.
  • In the G2 and M phases, Cyclin B joins with CDK1 to drive the cell into mitosis.
These complexes phosphorylate (add phosphate) to key proteins, switching them on or off to move the cycle forward.

2. Cell Cycle Checkpoints – Surveillance System

Checkpoints act like security checks. They make sure everything is correct before the cycle continues.
  • G1/S checkpoint: Checks for DNA damage and ensures the cell is ready for replication. If damaged DNA is detected, the cycle is paused.
  • G2/M checkpoint: Ensures DNA has been copied completely and correctly before entering mitosis.
  • Spindle checkpoint: During metaphase, it confirms that all chromosomes are attached to spindle fibres properly.
If problems are found, the cycle stops temporarily so the cell can repair the issue. If not repairable, the cell may self-destruct (apoptosis).

3. Inhibitors and Tumour Suppressor Genes

Proteins like p21, p27 and p16 act as natural brakes. They stop CDKs from working when the cell needs time to fix errors. The p53 tumour suppressor gene is very important here. When DNA damage occurs, p53 becomes active and tells the cell to produce p21, which then blocks CDK activity, halting the cycle in G1 phase. This gives time for repair or leads to apoptosis if the damage is serious.

4. External Signals and Growth Factors

Cells also respond to signals from outside. Growth factors like epidermal growth factor (EGF) and platelet-derived growth factor (PDGF) encourage the cell to start the cycle by increasing cyclin levels. On the other hand, signals like TGF-beta promote CDK inhibitors to stop unwanted growth.





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