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. 2011 Jul 15;22(14):2448–2457. doi: 10.1091/mbc.E09-01-0029

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© 2011 Barnhart et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 6: — Two classes of models for the spindle checkpoint defect in MAD2/mad2Δ cells. (A) Class I. Two types of kinetochores can generate a diffusible signal (shown in gray) that can inhibit the APC: kinetochores that are attached to microtubules but are not under tension (relaxed), and kinetochores that are not attached (naked). Both wild-type MAD2/MAD2 and heterozygous MAD2/mad2Δ cells can respond to loss of attachment induced by microtubule depolymerization (top). The relaxed kinetochores can signal in cells that have the normal Mad2:Mad1 ratio but cannot signal in MAD2/mad2Δ heterozygotes, whereas the naked kinetochores signal in either cell type. In addition, even though relaxed kinetochores release microtubules, reattachment is faster than release, so most kinetochores remain attached to microtubules. In this scenario, reducing the tension on all the kinetochores cannot arrest a MAD2/mad2Δ cell (bottom). (B) class II. Only kinetochores that are not attached to microtubules (naked) can generate a signal that inhibits the APC, and this signal is generated more slowly in MAD2/mad2Δ cells. Both wild-type MAD2/MAD2 and heterozygous MAD2/mad2Δ cells can respond to loss of attachment induced by microtubule depolymerization (top). In MAD2/mad2Δ cells, the reduced Mad2:Mad1 ratio increases the lag before naked kinetochores begin to generate a signal that inhibits the APC and arrests the cell cycle. Without microtubules, the kinetochores cannot reattach, and they eventually generate a signal that arrests the cell cycle (top). However, in the absence of tension when relaxed kinetochores detach from microtubules there is a race between generating the signal that inhibits the APC and reattaching to microtubules (bottom). In MAD2/MAD2 cells, we propose that naked kinetochores can generate a signal that can arrest the cell cycle before they reattach to a microtubule, but the naked kinetochores in MAD2/mad2Δ cells reattach to a microtubule before they can generate a signal sufficient to halt the cell cycle (bottom).