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Published 24 April 2006. doi:10.1083/jcb.200601172
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 173, Number 2, 153-157
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 Structural activation of Mad2 in the mitotic spindle checkpoint: the two-state Mad2 model versus the Mad2 template model

Hongtao Yu

Department of Pharmacology, University of Texas Southwestern Medical Center, Dallas, TX 75390

Correspondence to Hongtao Yu: hongtao.yu{at}utsouthwestern.edu

The inheritance of a normal assortment of chromosomes during each cell division relies on a cell-cycle surveillance system called the mitotic spindle checkpoint. The existence of sister chromatids that do not achieve proper bipolar attachment to the mitotic spindle in a cell activates this checkpoint, which inhibits the ubiquitin ligase activity of the anaphase-promoting complex or cyclosome (APC/C) and delays the onset of anaphase. The mitotic arrest deficiency 2 (Mad2) spindle checkpoint protein inhibits APC/C through binding to its mitotic-specific activator, Cdc20. Binding of Mad2 to Cdc20 involves a large conformational change of Mad2 and requires the Mad1–Mad2 interaction in vivo. Two related but distinct models of Mad1-assisted activation of Mad2, the "two-state Mad2" and the "Mad2 template" models, have been proposed. I review the recent structural, biochemical, and cell biological data on Mad2, discuss the differences between the two models, and propose experiments that test their key principles.

Abbreviations used in this paper: APC/C, the anaphase-promoting complex or cyclosome; Bub, budding uninhibited by benomyl; Mad, mitotic arrest deficiency; MCC, mitotic checkpoint complex; NMR, nuclear magnetic resonance.


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