CAJ | 학술논문

哺乳动物卵母细胞在排卵后停滞在第二次减数分裂中期,受精和多种物理或是化学刺激可以克服这一阻滞使卵母细胞活化.蛋白合成抑制剂亚胺环己酮可以诱导小鼠卵母细胞发生孤雌活化,但其机制尚未完全阐明.以前的研究提示亚胺环己酮可能是通过抑制蛋白激酶MOS的合成来发挥孤雌激活的作用的.本实验发现,CHX诱导的卵母细胞孤雌活化是Ca2+依赖性的,其效率可被钙离子载体A23187大大提高.免疫蛋白印迹结果表明,卵母细胞孤雌活化后MAPK发生去磷酸化.蛋白磷酸酶抑制剂冈田酸可以克服CHX+A23187对小鼠卵母细胞活化作用,并且部分阻止MAPK去磷酸化.以上结果表明,抑制MOS的合成并非CHX诱导的孤雌活化过程的惟一原因,并且蛋白磷酸酶抑制剂可以阻断这一激活事件.
포유동물란모세포재배란후정체재제이차감수분렬중기,수정화다충물리혹시화학자격가이극복저일조체사란모세포활화.단백합성억제제아알배기동가이유도소서란모세포발생고자활화,단기궤제상미완전천명.이전적연구제시아알배기동가능시통과억제단백격매MOS적합성래발휘고자격활적작용적.본실험발현,CHX유도적란모세포고자활화시Ca2+의뢰성적,기효솔가피개리자재체A23187대대제고.면역단백인적결과표명,란모세포고자활화후MAPK발생거린산화.단백린산매억제제강전산가이극복CHX+A23187대소서란모세포활화작용,병차부분조지MAPK거린산화.이상결과표명,억제MOS적합성병비CHX유도적고자활화과정적유일원인,병차단백린산매억제제가이조단저일격활사건.
M Ⅱ mouse eggs can be released from M Ⅱ arrest by various physical and chemical stimuli. Cycloheximide(CHX), a protein synthesis inhibitor, can activate mouse eggs but the underlying mechanism is not fully known. Previousstudies suggest that CHX activation occurs through the inhibition of MOS (a Ser/Thr protein kinase) synthesis. In thisexperiment, mouse eggs were cultured in a medium containing various reagents, including cycloheximide, Ca2 + ionophoreA23187 and Ca2+ chelator. The results show that the parthenogenetic activation of mouse eggs by CHX was calcium-de-pendent, and was enhanced by A23187. Egg activation induced by CHX + A23187 was suppressed by okadaic acid, andMAP kinase dephosphorylation was partially reversed as well. Our results suggest that inhibition of MOS synthesis maynot be the only mechansism by which CHX induces egg activation and that such egg activation can be blocked by proteinphosphotase inhibition.