3 cytoskeleton

What is the mechanism of microtubule depolymerizing agents?

These drugs grab the free tubulin dimers so microtubules can’t grow.

When tubulin falls off a microtubule, the drug locks it up and keeps it from being reused — so no new polymerization happens.

Examples:

• Colchicine / Colcemid

• Nocodazole

• Podophyllotoxin

• Exisulind

• Vinblastine / Vincristine

• SAMC (S-Allylmercaptocysteine)

What is the overall effect of microtubule depolymerizing agents on the cell?

They block mitosis by preventing spindle formation → arrest in metaphase → apoptosis.

What is the mechanism of microtubule polymerizing agents?

They stabilize microtubules by binding along their length and preventing loss of tubulin subunits, locking MTs in a polymerized state.

Examples:

• Paclitaxel (Taxol)

• Epothilones

• Cryptophsins

What is the overall effect of microtubule polymerizing agents on the cell?

They prevent microtubule depolymerization, freezing the mitotic spindle, leading to mitotic arrest and apoptosis (also metaphase arrest).

Which microtubule drug class includes vinblastine and vincristine, and what do they do?

Microtubule depolymerizing agents (vinca alkaloids).

They bind β-tubulin, prevent polymerization, and collapse the mitotic spindle.

Which microtubule drug stabilizes microtubules and prevents their depolymerization?

Paclitaxel (Taxol) — locks microtubules in polymerized form.

What is a real-world analogy for depolymerizing vs polymerizing microtubule drugs?

Depolymerizing drugs (vincristine, colchicine): “Steal the bricks” → MTs fall apart.

Polymerizing drugs (taxol): “Glue the bricks together” → MTs become rigid and nonfunctional.

Which drugs cause metaphase arrest?

Both classes of MT drugs:

Depolymerizing (vincristine, colchicine)

Polymerizing (taxol)

Both disrupt spindle dynamics → metaphase arrest.