Feedback control of mitosis in budding yeast

Inducing precocious anaphase in cultured mammalian cells

“…Our studies show that either Mad2⌬C or GST-Mad1F10 can overcome the checkpoint in nocodazole-treated PtK1 cells where kinetochores lack both tension as well as attached microtubules. This result indicates that BubR1 is not able to maintain the spindle checkpoint independently of Mad2 function, a conclusion supported by other studies where Mad2 function was inhibited with antibodies or deleted by genetic manipulations [Canman et al, 2000;Dobles et al, 2000;Gorbsky et al, 1998;Hoyt, 2001;Kitagawa and Rose, 1999;Li and Murray, 1991;Li and Benezra, 1996;Michel et al, 2001;Waters et al, 1998]. How the kinetochore mediates inhibition of APC/C by Cdc20 via Mad2, BubR1, or a direct effect on APC/C remains an important unresolved issue [Gillett and Sorger, 2001;Hoyt, 2001;Sudakin et al, 2001].…”

SAC‐ing mitotic errors: How the spindle assembly checkpoint (SAC) plays defense against chromosome mis‐segregation

“…This can be accomplished by physical manipulation of chromosomes [reviewed in McIntosh et al, 2002; reviewed in Nicklas, 1997], by drug-induced destabilization of spindle microtubules Hoyt et al, 1991;Li and Murray 1991], or by alteration of kinetochore structure Pangilinan and Spencer, 1996].…”

“…Two independent screens in Saccharomyces cerevisiae identified the first SAC genes [mitotic arrest deficient (MAD1-3) and budding uninhibited by benzimidazole (BUB1-3)] based on the sensitivity of strains harboring mutations in these genes to spindle disruption (see Table I for summary of SAC component nomenclature and function) [Hoyt et al, 1991;Li and Murray 1991]. Slowing down or blocking mitosis decreases the sensitivity of these mutants to microtubule-destabilizing drugs, indicating that they mis-segregate chromosomes and lose viability because they fail to arrest the cell cycle long enough to repair spindle damage.…”

Dissection of fission yeast microtubule associating protein p93Dis1: regions implicated in regulated localization and microtubule interaction

“…Kinetochores form on the centromere DNAs of condensed chromosomes, interact with microtubules, and are pulled toward the two ends of the spindle in anaphase (Hyman & Mitchison 1991;Mitchison & Salmon 1992). A mechanism called spindle checkpoint control ensures that sister chromatid separation is prolonged when spindle formation is inhibited (Li & Murray 1991;Hoyt et al 1991). Another mechanism, metaphase checkpoint control, delays anaphase when any one of the chromosomes fails to properly situate in the metaphase spindle (e.g.…”