Changes between Version 173 and Version 174 of ChromosomeSegregation

Mar 18, 2015, 9:50:16 AM (6 years ago)



  • ChromosomeSegregation

    v173 v174  
    3535||Pad1/Rpn11 and Mts3/Rpn12 are subunits of the lid subcomplex|| in PMID: 16149916 Mutations in the genes encoding these two subunits were isolated in a screen for mutants that were both esistant to methyl 2-benzimidazolecarbamate, a microtubule in- hibitor, and Ts for cell-cycle progression [19,20]. Ts mutations in both genes cause arrest of the cells in mitosis, probably because of a failure to degrade cyclin B/Cdc13 and securin/Cut2. ||-||
    3636|| mde4 || Previous results showed that in interphase, when Mde4 is dephosphorylated, the Mde4-Pcs1 complex localizes to the nucleolus and to the kinetochores, which cluster at the nuclear periphery next to the spindle pole bodies (SPBs) [6,8]. As cells enter mitosis and Mde4 becomes phosphorylated, Mde4- Pcs1 leave the nucleolus but remain at the kinetochores [6,8]. [6. PubMed: 17627824]  [8. PubMed: 12689592]||
    3837||cdc20|| When Cdc20 is overexpressed, securin can be degraded during interphase, whereas other destruction box proteins will remain stable. In cells lacking Cdc20, securin remains stable, and sister chromatids will not separate (Visintin et al., 1997).||
     38||cut7||In the temperature-sensitive cut7 mutant, spindle formation is blocked shortly after duplication of the SPB. The mitotic spindle radiating from the opposite poles cannot interdigitate and thus remains as a V shape (Hagan and Yanagida, 1992). The cut7- specific defect generates a condition whereby the bipolar attachment of the spindle to kinetochores is not achieved. Previously, we demonstrated that this defect causes an arrest in a mad2+-dependent manner (Kim et al., 1998). At the restrictive temperature the majority of Mad2-GFP was found on condensed chromosomes as one or more speckles (Fig. 4).||