Relationships between hormone-induced calcium release and 86rubidium uptake stimulation in starfish oocytes.

Revue canadienne de biologie Pub Date : 1979-09-01
P Guerrier, M Moreau, M Dorée
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Abstract

86Rubidium+ uptake, but not 86Rubidium efflux, is strongly stimulated after addition of the meiosis inducing hormone 1-methyladenine (1-MeAde) to prophase blocked oocytes of the starfish Marthasterias glacialis. This stimulation is a transient process which does not require the continuous presence of 1-MeAde and is elicited within 1 minute of contact. 1-MeAde and its biologically active structural analogs fully stimulate Rb+ uptake at concentrations which are about two orders of magnitude lower than those required to trigger meiosis reinitiation but which already release underthreshold levels of Ca2+ from the inner part of the plasma membrane. External Ca2+ concentrations effective in triggering meiosis reinitiation also stimulate Rb+ influx, while drugs like D600, theophyllin and caffein which suppress the hormone induced Ca2+ release, simultaneously preclude the stimulation of Rb+ uptake. Dithiothreitol (DTT) which mimicks 1-MeAde action in releasing Ca2+ and inducing meiosis acts both on the efflux and on active and passive Rb+ influxes. Ouabain, the classical inhibitor of the Na+, K+ pump does not preclude meiosis reinitiation under the influence of 1-MeAde, its agonists of mimetics. It suppresses the active component of Rb+ uptake both in control or stimulate oocytes. When applied only in preincubation before starting the hormone treatment, it cannot however inhibit the stimulation of Rb+ uptake, while basal pump inhibition is preserved. These results demonstrate that stimulation of the active Rb+ or K+ transport is not indispensable to meiosis reinitiation. They suggest moreover that the hormone induced Ca2+ release from the plasma membrane may be responsible for unmasking new ouabain sensitive transport sites.

海星卵母细胞激素诱导钙释放与铷摄取刺激的关系。
在马沙星(Marthasterias glacialis)卵母细胞中加入减数分裂诱导激素1-甲基腺嘌呤(1-MeAde)后,能强烈刺激86Rubidium+的摄取,而不是86Rubidium的流出。这种刺激是一个短暂的过程,不需要1- meade的持续存在,并在接触后1分钟内触发。1-MeAde及其生物活性结构类似物充分刺激Rb+摄取,其浓度比触发减数分裂重新开始所需的浓度低两个数量级,但已经从质膜内部释放低于阈值水平的Ca2+。有效触发减数分裂再起始的外部Ca2+浓度也刺激Rb+内流,而D600、茶碱和咖啡因等药物抑制激素诱导的Ca2+释放,同时阻止Rb+摄取的刺激。二硫苏糖醇(DTT)模仿1-MeAde释放Ca2+和诱导减数分裂的作用,同时作用于流出和主动和被动Rb+流入。经典的Na+, K+泵抑制剂Ouabain在1-MeAde的影响下不能阻止减数分裂的重新开始,1-MeAde是其模拟物的激动剂。在控制或刺激卵母细胞时,它抑制Rb+摄取的活性成分。然而,当仅在开始激素治疗前的孵育前应用时,它不能抑制Rb+摄取的刺激,而保留了基础泵抑制作用。这些结果表明,刺激活跃的Rb+或K+转运对减数分裂再起始并不是必不可少的。此外,他们认为激素诱导的Ca2+从质膜释放可能是揭示新的瓦巴因敏感转运位点的原因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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