Eckberg William R, Carroll Alan G
Department of Zoology, Howard University, Washington, DC 20059 USA and The Marine Biological Laboratory, Woods Hole, MA 02543 USA.
Natinal Cancer Institute, National Institutes of Health, Buliding 37, Room 4C24, Bethesda, MD 20892 USA.
Dev Growth Differ. 1987 Oct;29(5):489-496. doi: 10.1111/j.1440-169X.1987.00489.x.
We have examined the possible involvement of protein kinase C (C-kinase) in the initiation of germinal vesicle breakdown (GVBD) in Chaetopterus oocytes. Two tumor-promoting phorbol esters (phorbol-12, 13-dibezoate and 12-0-tetradecanoylphorbol-13-acetate [TPA]) and a permeant diacylglycerol (1-oleoyl-2-acetylglycerol), potent activators of C-Kinase, triggered GVBD. Two other phorbol esters (phorbol-13-monoacetate and 4α-phorbol-12, 13-didecanoate), which do not activate C-kinase, were inactive. Three C-kinase antagonists (W-7, H-7 and retinol) inhibited both naturally-and TPA-induced GVBD, whereas W-5, a much less inhibitory W-7 analog, had no effect on GVBD. Triggering of GVBD by TPA was independent of extracellular Ca . Although naturally-induced GVBD was blocked by micromolar concentrations of the calmodulin antagonist, calmidazolium (R24571), and by millimolar concentrations of the permeant cAMP analog, dibutryryl cAMP, TPA-induced GVBD was not affected by these agents. These results support the hypothesis that both C-kinase and calmodulin are involved in the sequence of events leading to GVBD in this species.
我们研究了蛋白激酶C（C激酶）在毛翼虫卵母细胞生发泡破裂（GVBD）起始过程中可能的作用。两种促肿瘤佛波酯（佛波醇-12,13-二苯甲酸酯和12-O-十四酰佛波醇-13-乙酸酯[TPA]）以及一种可渗透的二酰甘油（1-油酰-2-乙酰甘油），作为C激酶的强效激活剂，可引发GVBD。另外两种不激活C激酶的佛波酯（佛波醇-13-单乙酸酯和4α-佛波醇-12,13-二癸酸酯）则无此作用。三种C激酶拮抗剂（W-7、H-7和视黄醇）可抑制自然诱导和TPA诱导的GVBD，而W-5，一种抑制作用小得多的W-7类似物，对GVBD无影响。TPA引发GVBD与细胞外钙无关。虽然微摩尔浓度的钙调蛋白拮抗剂卡咪唑（R24571）和毫摩尔浓度的可渗透cAMP类似物二丁酰cAMP可阻断自然诱导的GVBD，但TPA诱导的GVBD不受这些试剂影响。这些结果支持了这样一种假说，即C激酶和钙调蛋白都参与了该物种中导致GVBD的一系列事件。
