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Cell movement: ameboid crawling, chemotaxis and ciliary beating

  • Mechanism
  • For completeness

White cells crawl by pushing out a front edge and pulling up the back; cilia beat like oars, driven by dynein, to sweep mucus out of the airways.

Updated

Also called: Ameboid locomotion, Chemotaxis, Mucociliary clearance, Dynein

See it in 3D: Trachea

What it is

Cells move in two main ways. Crawling (ameboid) cells such as neutrophils and macrophages extend the front by polymerizing actin, stick to the surface, and pull the rear forward; chemical gradients steer them (chemotaxis). Ciliated cells stay in place and move fluid: dynein motors slide microtubule doublets to produce a fast power stroke and a slow recovery stroke. Both use ATP.

How it works, step by step

  1. A receptor on the cell surface detects a chemoattractant more strongly on one side.
  2. Signalling at that side drives actin polymerization, which pushes the membrane forward as a pseudopod.
  3. Integrins in the pseudopod bind the surface and form new attachment points; old ones at the rear are released.
  4. Myosin II in the rear cortex contracts and pulls the cell body toward the front; membrane is recycled by endocytosis at the rear and added at the front.
  5. In cilia, dynein arms walk along the neighbouring microtubule doublet using ATP; because nexin links tie the doublets, sliding becomes bending.
  6. Bending switches side to side in sequence (power then recovery stroke), and neighbouring cilia beat in waves that move the mucus layer.
  7. Mucus sits on a thin watery periciliary layer; if that layer is too dry (as in cystic fibrosis), cilia cannot beat and clearance fails.

Two ways to move

FeatureAmeboid crawlingCiliary beating
MotorActin polymerization + myosin IIAxonemal dynein on microtubules
What movesThe whole cellFluid over a fixed cell (sperm: the cell itself, flagellum)
ExamplesNeutrophils, monocytes/macrophages, fibroblasts in wound repair, tumour cellsAirway epithelium, uterine tube, ependyma; sperm flagellum
SteeringChemotactic gradientsCoordinated waves; direction is fixed
Typical failureLeukocyte adhesion defects: recurrent infections, no pusPrimary ciliary dyskinesia; dehydrated airway surface

Clinical notes

  • Primary ciliary dyskinesia: stagnant mucus causes recurrent infections and bronchiectasis; immotile sperm cause infertility; random left–right patterning causes situs inversus in about half.
  • Cystic fibrosis: cilia are normal but the airway surface liquid is depleted, so mucus sticks and clearance fails.
  • Smoking slows ciliary beating and damages ciliated cells, part of why smokers cough to clear mucus.
  • Leukocyte adhesion deficiency: neutrophils cannot stick and crawl out of vessels, so the blood count is very high but infected sites lack pus.

Test yourself

Think of the answer, then tap the question to see it.

What drives the leading edge of a crawling neutrophil forward?

Actin polymerization just under the membrane at the front, steered by the chemoattractant gradient; myosin II then pulls the rear along.

Which protein generates ciliary bending, and what does it consume?

Axonemal dynein, an ATPase; it slides adjacent microtubule doublets, and nexin links turn the sliding into bending.

A man has chronic sinusitis, bronchiectasis, infertility and dextrocardia. What is the defect?

Primary ciliary dyskinesia (Kartagener syndrome): defective dynein arms leave cilia and sperm flagella immotile.

In cystic fibrosis cilia are structurally normal. Why does mucociliary clearance fail?

Defective CFTR reduces Cl⁻ and water secretion, the periciliary liquid layer collapses, and cilia are trapped in thick mucus.

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Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: Primary ciliary dyskinesia: MedlinePlus Genetics (MedlinePlus, US National Library of Medicine, 2025); Bronchiectasis (StatPearls (NCBI Bookshelf), 2025); Anatomy, Thorax, Tracheobronchial Tree (StatPearls (NCBI Bookshelf), 2025).

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