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4.6Cell Communication and Cell Cycle

Regulation of Cell Cycle — AP BIOLOGY Revision Notes & Topical Questions

5 min read 9 parts Lesson 6 of 6 2 quizzes

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Lesson summary

4.6 Regulation of Cell Cycle — AP Biology notes: Describe checkpoints, cyclin and CDK control, and how disruption of the cell cycle causes cancer or apoptosis.Purpose — cells must pass checkpoints so that they are large enough, DNA is replicated correctly and nutrients are availa…

  • G1 checkpoint
  • G2 checkpoint
  • M (spindle) checkpoint
  • Drug effect
  • Cyclin-dependent kinases (CDKs)
  • Cyclin–CDK complexes

Section 1 of 9Checkpoints

Purpose
  • Purpose cells must pass checkpoints so that they are large enough, DNA is replicated correctly and nutrients are available.
Control
  • Control internal and external signals act at checkpoints.
G1 checkpoint
  • G1 checkpoint checks cell size, nutrients, growth factors and DNA damage; a cell that fails may enter G0.
G2 checkpoint
  • G2 checkpoint checks that DNA replication is complete and DNA is undamaged.
M (spindle) checkpoint
  • M (spindle) checkpoint checks that all chromosomes are attached to spindle microtubules before anaphase.
Drug effect
  • Drug effect a drug that stops cells at the G2 or M checkpoint raises the proportion of cells in that stage

Section 2 of 9Cyclins and cyclin-dependent kinases

Cyclins and cyclin-dependent kinases
Cyclins
  • Cyclins proteins whose levels rise and fall through the cell cycle and which bind CDKs to trigger the next stage.
Cyclin-dependent kinases (CDKs)
  • Cyclin-dependent kinases (CDKs) enzymes present at constant concentration, inactive until bound to cyclin, that phosphorylate other molecules to activate them.
Cyclin–CDK complexes
  • Cyclin–CDK complexes e.g. MPF; they phosphorylate target proteins to drive the cell past a checkpoint, then cyclin is degraded.
    • (mitosis-promoting factor)

Section 3 of 9Passing the G1 checkpoint

1
Growth factor binds a receptor on the cell surface.
2
A signal transduction pathway stimulates synthesis of G1 cyclin.
3
Cyclin binds and activates CDK.
4
Cyclin–CDK phosphorylates target proteins, releasing the brake on S-phase genes.
5
If DNA is undamaged the cell enters S phase; if damaged, p53 halts the cycle.

Section 4 of 9External controls

1Growth factors
  • Growth factors such as PDGF stimulate division.
2Density-dependent inhibition
  • Density-dependent inhibition normal cells stop dividing when crowded.
3Anchorage dependence
  • Anchorage dependence normal cells divide only when attached to a surface.
4Cancer cells
  • Cancer cells ignore these controls.

Section 5 of 9Disruption of the cell cycle

1
Proto-oncogenes
  • Proto-oncogenes promote division; mutation to oncogenes causes overstimulation.
    • (accelerator stuck on)
2
Tumour suppressor genes
  • Tumour suppressor genes e.g. p53 inhibit division and detect replication errors;
    • loss of function removes the brakes.
3
p53
  • p53 halts the cycle when DNA is damaged and can trigger repair or apoptosis.
4
Cancer
  • Cancer uncontrolled cell division from accumulated mutations in cell-cycle regulators.
5
Apoptosis
Apoptosis programmed cell death by an orderly caspase process,
  • which destroys cells with dangerous mutations and removes unneeded cells in development, e.g. skin webbing between developing fingers.
6
Apoptosis process
  • Apoptosis process the cell shrinks and is broken into fragments that neighbouring cells engulf, unlike necrosis,
    • where a damaged cell bursts and causes inflammation
7
Damage
  • Damage if damage cannot be repaired, the cell may be sent into apoptosis

Section 6 of 9Checkpoints compared

CheckpointPositionChecksKey protein
G1End of G1Size, nutrients, growth factors, DNA damagep53, cyclin D
G2End of G2DNA fully replicated and undamagedMPF
M (spindle)MetaphaseAll chromosomes attachedSpindle checkpoint proteins

Section 7 of 9More from the specification

1
Chromatid
  • One of the two identical copies of a replicated chromosome.
2
Daughter cell
  • Cell produced by cell division.
3
Genetically identical
  • Having the same alleles
4
Spindle fibres
  • Protein microtubules that move chromosomes in mitosis.
5
Sister chromatids
  • The two identical DNA copies of a replicated chromosome joined at the centromere.
6
Interphase
  • The stage when the cell grows and DNA is replicated.
7
Organelle
  • A small structure within a cell with a specific function.
8
Cytokinesis
  • Division of the cytoplasm.
9
Fibre
  • Plant material that adds bulk and aids movement of food through the gut.

Section 8 of 9Key terms

TermMeaning
Checkpointcontrol point that can halt the cycle
Cyclinprotein whose level rises and falls through the cycle
CDKcyclin-dependent kinase, active only with cyclin
Tumour suppressorgene that restrains division, e.g. p53
Oncogenemutated proto-oncogene that promotes division
MPFmitosis-promoting factor, a cyclin–CDK complex

Section 9 of 9Exam technique

1
Saying CDKs change concentration — cyclin levels change; CDKs are constant but need cyclin.
2
Thinking oncogenes are suppressors — oncogenes promote division; tumour suppressors inhibit it.
3
Seeing apoptosis only as a fault — it is a controlled process needed in development.
4
Confusing apoptosis with necrosis — apoptosis is tidy and programmed; necrosis causes inflammation.

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