Release of mouse eggs from metaphase arrest by protein synthesis inhibition in the absence of a calcium signal or microtubule assembly.
Mouse egg activation, which includes release from meiotic metaphase II arrest, results from fertilization-induced increase in intracellular calcium concentration ([Ca2+]i). However, during egg activation caused by exposure to the protein synthesis inhibitor, cycloheximide, [Ca2+]i did not change. Although eggs fertilized in the presence of microtubule inhibitors remain arrested at metaphase, eggs treated for 32 hr with cycloheximide and the microtubule inhibitor, colcemid, formed nuclei. In untreated eggs aged in culture for 24 hr, the microtubule spindles became deformed. These eggs formed nuclei after exposure to cycloheximide, but not the calcium ionophore A23187. Our results indicate that eggs in which protein synthesis is inhibited are released from metaphase without an increase in [Ca2+]i, and despite disruption of the spindle.
Moses
R M
RM
Department of Zoology, University of Toronto, Canada.
Kline
D
D
D000818:Animals; D002118:Calcium / Q000502:physiology*; D003513:Cycloheximide / Q000494:pharmacology; D003703:Demecolcine / Q000494:pharmacology; D005314:Embryonic and Fetal Development; D005260:Female; D008677:Metaphase / Q000187:drug effects; D051379:Mice; D008870:Microtubules / Q000187:drug effects / Q000502:physiology*; D010063:Ovum / Q000254:growth & development* / Q000502:physiology; D015398:Signal Transduction
D003513:Cycloheximide; D002118:Calcium; D003703:Demecolcine