| Autor: |
Harrison JC; Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA., Bardes ES, Ohya Y, Lew DJ |
| Jazyk: |
angličtina |
| Zdroj: |
Nature cell biology [Nat Cell Biol] 2001 Apr; Vol. 3 (4), pp. 417-20. |
| DOI: |
10.1038/35070104 |
| Abstrakt: |
In many cells the timing of entry into mitosis is controlled by the balance between the activity of inhibitory Wee1-related kinases (Swe1p in budding yeast) and the opposing effect of Cdc25-related phosphatases (Mih1p in budding yeast) that act on the cyclin-dependent kinase Cdc2 (Cdc28p in budding yeast). Wee1 and Cdc25 are key elements in the G2 arrest mediated by diverse checkpoint controls. In budding yeast, a 'morphogenesis checkpoint' that involves Swe1p and Mih1p delays mitotic activation of Cdc28p. Many environmental stresses (such as shifts in temperature or osmolarity) provoke transient depolarization of the actin cytoskeleton, during which bud construction is delayed while cells adapt to environmental conditions. During this delay, the morphogenesis checkpoint halts the cell cycle in G2 phase until actin can repolarize and complete bud construction, thus preventing the generation of binucleate cells. A similar G2 delay can be triggered by mutations or drugs that specifically impair actin organization, indicating that it is probably actin disorganization itself, rather than specific environmental stresses, that triggers the delay. The G2 delay involves stabilization of Swe1p in response to various actin perturbations, although this alone is insufficient to produce a long G2 delay. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
|
