Juang Y L, Huang J, Peters J M, McLaughlin M E, Tai C Y, Pellman D
Department of Pediatric Oncology, The Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.
Science. 1997 Feb 28;275(5304):1311-4. doi: 10.1126/science.275.5304.1311.
The molecular mechanisms that link cell-cycle controls to the mitotic apparatus are poorly understood. A component of the Saccharomyces cerevisiae spindle, Ase1, was observed to undergo cell cycle-specific degradation mediated by the cyclosome, or anaphase promoting complex (APC). Ase1 was degraded when cells exited from mitosis and entered G1. Inappropriate expression of stable Ase1 during G1 produced a spindle defect that is sensed by the spindle assembly checkpoint. In addition, loss of ASE1 function destabilized telophase spindles, and expression of a nondegradable Ase1 mutant delayed spindle disassembly. APC-mediated proteolysis therefore appears to regulate both spindle assembly and disassembly.
将细胞周期调控与有丝分裂装置联系起来的分子机制目前还知之甚少。酿酒酵母纺锤体的一个组成部分Ase1,被观察到会经历由细胞周期体或后期促进复合物(APC)介导的细胞周期特异性降解。当细胞从有丝分裂退出并进入G1期时,Ase1会被降解。在G1期稳定的Ase1的不适当表达会产生一种纺锤体缺陷,该缺陷会被纺锤体组装检查点检测到。此外,ASE1功能的丧失会使末期纺锤体不稳定,而不可降解的Ase1突变体的表达会延迟纺锤体的解体。因此,APC介导的蛋白水解似乎同时调节纺锤体的组装和解体。