A proliferating cell must not merely perform cell-cycle events; it must perform them in the correct order. Eukaryotic cells enforce that order using regulatory networks built around cyclins, cyclin-dependent kinases (CDKs) and checkpoints.

A CDK is a protein kinase whose activity depends on binding a regulatory protein called a cyclin. CDK abundance can remain relatively stable while cyclin abundance rises and falls. As particular cyclins accumulate, they activate particular CDKs; the resulting cyclin-CDK complexes phosphorylate target proteins that drive the cell into a new phase.

Oscillating cyclins create directional transitions

A simplified logic is

cyclin accumulates
      ↓
cyclin-CDK becomes active
      ↓
target proteins are phosphorylated
      ↓
cell-cycle transition occurs
      ↓
cyclin is degraded

Cyclin destruction helps make transitions directional: once the regulatory state has changed, the cell does not simply oscillate backward into the previous phase.

Checkpoints couple progression to completion of prerequisites

A checkpoint is a control system that can delay a later cell-cycle event until required conditions are satisfied.

Three important checkpoints illustrate different responsibilities.

G1/S control

Before committing to DNA replication, cells can integrate signals such as growth conditions, cell size and DNA integrity. If severe problems are detected, entry into S phase can be delayed.

G2/M control

Before mitosis, cells verify that DNA replication is complete and that major DNA damage has been resolved sufficiently for chromosome segregation to proceed.

Spindle-assembly checkpoint

During mitosis, the cell delays irreversible sister-chromatid separation until chromosomes have established appropriate attachments to the spindle.

A checkpoint is not a phase

The phases G1, S, G2 and M describe cellular states and processes. A checkpoint is a regulatory decision system acting at a transition or within a phase.

The deeper idea is therefore not that cells contain three literal 'inspection stations'. Cell-cycle progression emerges from molecular networks in which cyclin-CDK phosphorylation promotes transitions and inhibitory signals restrain those regulators when prerequisite events are incomplete.

Cyclin-CDK control provides timing; checkpoints connect that timing machinery to the actual state of DNA replication, genome integrity and chromosome segregation.