Spindle Assembly Checkpoint: Kinetochore Tension & Anaphase Timing

Metaphase Setup

Chromosomes 5

Initial misattachment rate 40%

Aurora B correction rate 1.0x

Checkpoint Status

Spindle assembly checkpoint: WAIT

Mad2 "wait-anaphase" signal inhibits APC/C-Cdc20.

Bi-oriented (tension)

0 / 10

SAC signal strength

100%

Time in metaphase

0.0 s

Segregation result

—

How it works

Each chromosome carries two sister kinetochores that must each capture microtubules from opposite spindle poles (amphitelic attachment). Only that geometry stretches the centromere and generates inter-kinetochore tension. Wrong attachments — both sisters to the same pole (syntelic) or one kinetochore to both poles (merotelic) — produce little or no tension.

Tension-sensing (Aurora B, spatial-separation model):
  low tension  → Aurora B phosphorylates Ndc80/KMN → MT release → retry
  high tension → kinetochore pulled away from Aurora B → attachment stabilized

SAC signal:
  S = (untensioned kinetochore pairs) / (total kinetochore pairs)
  APC/C-Cdc20 blocked while S > 0   (Mad1/Mad2 template → Mitotic Checkpoint Complex)
  anaphase onset triggered only when S = 0

Chromosomes — how many pairs of sister chromatids sit on the metaphase plate.
Initial misattachment rate — the fraction that start out syntelic (both kinetochores to one pole) instead of correctly bi-oriented.
Aurora B correction rate — how fast tension-less attachments are released and re-tried by the spindle.
Force Anaphase — degrades securin/cyclin B immediately, bypassing the checkpoint. Any chromosome still syntelic sends both chromatids to one pole — real-world nondisjunction, the mechanism behind aneuploidies like trisomy 21.

Real cells hold anaphase for minutes to hours until every kinetochore satisfies the checkpoint; overriding it experimentally (or through checkpoint mutations) is a direct source of chromosome mis-segregation in cancer cells.

Bi-oriented (tension) Syntelic error Astral microtubules

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