Stutchfield J, Cockcroft S
Department of Physiology, University College London, England.
Eur J Biochem. 1991 Apr 10;197(1):119-25. doi: 10.1111/j.1432-1033.1991.tb15889.x.
Phospholipase C (specific for inositol lipids) is known to be present both in membranes and cytosol. Receptor-mediated activation of this enzyme occurs via a guanine nucleotide regulatory protein (G-protein), designated Gp. We have compared the stimulation of this enzyme by fMet-Leu-Phe via the G-protein in HL60 membranes and in permeabilised cells. fMet-Leu-Phe stimulated phospholipase C in membranes at 2 min and the response was dependent on exogenously added GTP. GTP alone also stimulated phospholipase C activity such that at 10 min the response to fMet-Leu-Phe was minimal. In comparison, the response to fMet-Leu-Phe in permeabilised cells was greater in extent but did not require added GTP. However, it was antagonized by GDP analogues (GDP[beta S] greater than GDP greater than dGDP) and by pertussis toxin pretreatment, indicating that fMet-Leu-Phe-stimulated phospholipase C activity was also mediated via Gp. GTP and its analogue GTP[gamma S] also stimulated phospholipase C and their effects were strictly additive to the stimulation obtained with fMet-Leu-Phe. Such additivity was also observed when two receptor-directed agonists, fMet-Leu-Phe and ATP, were used to stimulate intact cells. It is concluded that (a) the size of the response with fMet-Leu-Phe in membranes is limited by the loss of a component, possibly phospholipase C, and (b) stoichiometry and physical organisation of multiple species of G-proteins and/or phospholipases C may explain the independent nature of phospholipase C activation by fMet-Leu-Phe, ATP and guanine nucleotides.
磷脂酶C(对肌醇脂质具有特异性)已知存在于细胞膜和细胞质溶胶中。该酶的受体介导激活通过一种鸟嘌呤核苷酸调节蛋白(G蛋白)发生,称为Gp。我们比较了在HL60细胞膜和通透细胞中,甲酰甲硫氨酸 - 亮氨酸 - 苯丙氨酸(fMet-Leu-Phe)通过G蛋白对该酶的刺激作用。fMet-Leu-Phe在2分钟时刺激细胞膜中的磷脂酶C,且该反应依赖于外源添加的GTP。单独的GTP也刺激磷脂酶C活性,使得在10分钟时对fMet-Leu-Phe的反应最小。相比之下,通透细胞中对fMet-Leu-Phe的反应程度更大,但不需要添加GTP。然而,它受到GDP类似物(GDP-β-S大于GDP大于dGDP)和百日咳毒素预处理的拮抗,表明fMet-Leu-Phe刺激的磷脂酶C活性也通过Gp介导。GTP及其类似物GTP-γ-S也刺激磷脂酶C,并且它们的作用与fMet-Leu-Phe获得的刺激严格相加。当使用两种受体导向的激动剂fMet-Leu-Phe和ATP刺激完整细胞时,也观察到这种相加性。得出的结论是:(a)细胞膜中fMet-Leu-Phe的反应大小受到一种成分(可能是磷脂酶C)损失的限制;(b)多种G蛋白和/或磷脂酶C的化学计量和物理组织可能解释了fMet-Leu-Phe、ATP和鸟嘌呤核苷酸对磷脂酶C激活的独立性。