Publication Date:
1997-02-28
Description:
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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Juang, Y L -- Huang, J -- Peters, J M -- McLaughlin, M E -- Tai, C Y -- Pellman, D -- New York, N.Y. -- Science. 1997 Feb 28;275(5304):1311-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatric Oncology, The Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9036857" target="_blank"〉PubMed〈/a〉
Keywords:
*Anaphase
;
Base Sequence
;
Cell Cycle Proteins/*metabolism
;
G1 Phase
;
Microtubule-Associated Proteins/*metabolism
;
Mitosis
;
Molecular Sequence Data
;
Morphogenesis
;
Mutagenesis, Site-Directed
;
Saccharomyces cerevisiae/*cytology/metabolism
;
Spindle Apparatus/*metabolism/ultrastructure
;
Telophase
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
