INVOLVEMENT OF CAMP-DEPENDENT PROTEIN-KINASE AND PROTEIN-PHOSPHORYLATION IN REGULATION OF MOUSE OOCYTE MATURATION

INVOLVEMENT OF CAMP-DEPENDENT PROTEIN-KINASE AND PROTEIN-PHOSPHORYLATION IN REGULATION OF MOUSE OOCYTE MATURATION
复制标题

DOI:
10.1016/0012-1606(86)90209-5
复制
发表时间:
1986-04-01
影响因子:
2.7
通讯作者:
SCHULTZ, RM
SCHULTZ, RM
中科院分区:
生物学3区
文献类型:
--
作者:
BORNSLAEGER, EA;MATTEI, P;SCHULTZ, RM

文献摘要

被引文献

相似文献

我们报告的实验结果支持这一假设,在小鼠卵母细胞中,减少卵母细胞内的环磷酸腺苷(cAMP)启动减数分裂成熟;卵母细胞显微注射环核苷酸磷酸二酯酶(PDE)进行了生殖囊泡破裂(GVBD)的存在下,3-异丁基-1-甲基黄嘌呤(IBMX),抑制GVBD在卵母细胞不注射PDE和注射热灭活PDE的卵母细胞。环腺苷酸依赖性蛋白激酶(PK)已被提出介导的维持减数分裂阻滞的cAMP。支持这一假设的是观察到不激活PK的2“-脱氧cAMP不像cAMP那样维持减数分裂停滞;这一结果是通过显微注射这些化合物和在其膜可渗透的N6-单丁酰衍生物存在下孵育卵母细胞获得的。此外,在二丁酰cAMP(dbcAMP)或IBMX的存在下,向卵母细胞中微量注射热稳定的PK抑制剂PKI诱导GVBD。然而,在没有dbcAMP或IBMX的情况下,通过显微注射PK的催化亚基而不是通过与PKI共注射的催化亚基来维持减数分裂阻滞。此外,在dbcAMP的存在下,通过显微注射PKI,诱导减数分裂恢复之前的卵母细胞磷蛋白的特定变化;这些变化也与卵母细胞恢复减数分裂的承诺紧密结合。这些结果进行了讨论,在我们的模型调节减数分裂停滞和成熟。
We report the results of experiments which support the hypothesis that, in mouse oocytes, a decrease in intraoocyte cyclic AMP (cAMP) initiates meiotic maturation; oocytes microinjected with cyclic nucleotide phosphodiesterase (PDE) underwent germinal vesicle breakdown (GVBD) in the presence of 3-isobutyl-1-methylxanthine (IBMX), which inhibited GVBD both in oocytes not injected with PDE and in oocytes injected with heat-inactivated PDE. Cyclic AMP-dependent protein kinase (PK) has been proposed to mediate maintenance of meiotic arrest by cAMP. In support of this hypothesis is the observation that 2''-deoxy cAMP, which does not activate PK, did not maintain meiotic arrest as did cAMP; this result was obtained both by microinjection of these compounds and by incubating oocytes in the presence of their membrane-permeable N6-monobutyryl derivatives. Furthermore, microinjection into oocytes of the heat-stable inhibitor of PK, PKI, induced GVBD in the presence of either dibutyryl cAMP (dbcAMP) or IBMX. Meiotic arrest was maintained in the absence of dbcAMP or IBMX, however, by microinjected catalytic subunit of PK, but not by catalytic subunit co-injected with PKI. In addition, specific changes in oocyte phosphoproteins that preceded resumption of meiosis were induced, in the presence of dbcAMP, by microinjected PKI; these changes were also tightly coupled with commitment of oocytes to resume meiosis. These results are discussed in terms of our model for regulation of meiotic arrest and maturation.