Murofushi H, Ishiguro K, Takahashi D, Ikeda J, Sakai H
Cell Motil Cytoskeleton. 1986;6(2):83-8. doi: 10.1002/cm.970060203.
Flagellar motility of Triton models of sea urchin spermatozoa was reactivated by cyclic AMP-dependent protein kinase and a protein factor, termed motility activator, both of which were prepared from the detergent-extract of sea urchin spermatozoa. It was shown that phosphorylation of the motility activator by the protein kinase is necessary for the reactivation of flagellar motility [Ishiguro et al, J. Cell Biol. 92:777-782, 1982; Murofushi et al, in "Biological Functions of Microtubules and Related Structures," Academic Press, 1982]. Reactivating factor was also detected in a KCl-extract of the axoneme fraction devoid of the detergent-extractable materials. The activity of this factor was also cyclic AMP- and protein kinase-dependent. Furthermore, when freshly prepared Triton models were treated with phosphoprotein phosphatase prepared from bovine cardiac muscle, the flagellar motility was drastically suppressed. This inhibition of the motility was partially recovered by the addition of cyclic AMP and protein kinase to the phosphatase-treated models.
海胆精子的Triton模型的鞭毛运动通过环磷酸腺苷依赖性蛋白激酶和一种称为运动激活剂的蛋白质因子重新激活,这两种物质均从海胆精子的去污剂提取物中制备。结果表明,蛋白激酶对运动激活剂的磷酸化对于鞭毛运动的重新激活是必要的[石黑等人,《细胞生物学杂志》92:777 - 782,1982;室伏等人,载于《微管及相关结构的生物学功能》,学术出版社,1982]。在缺乏去污剂可提取物的轴丝部分的氯化钾提取物中也检测到了重新激活因子。该因子的活性也依赖于环磷酸腺苷和蛋白激酶。此外,当用从牛心肌制备的磷蛋白磷酸酶处理新鲜制备的Triton模型时,鞭毛运动被显著抑制。通过向经磷酸酶处理的模型中添加环磷酸腺苷和蛋白激酶,这种运动抑制得到了部分恢复。