Mulberg A E, Tulk B M, Forgac M
Department of Molecular and Cellular Physiology, Tufts University School of Medicine, Boston, Massachusetts.
J Biol Chem. 1991 Nov 5;266(31):20590-3.
We have previously shown that activity of a Cl- channel is required for acidification of clathrin-coated vesicles by the coated vesicle (H+)-ATPase (Arai, H., Pink, S. and Forgac, M. (1989) Biochemistry 28, 3075-3082). We demonstrate that activity of the coated vesicle Cl- channel is modulated by phosphorylation. Cl- conductance was measured in a reconstituted preparation of coated vesicle membrane proteins using the Cl(-)-sensitive fluorescence probe, 6-methoxy-N-(3-sulfopropyl)quinolinium. Treatment of coated vesicle membranes with alkaline phosphatase resulted in a 25 +/- 5% decrease in Cl- channel activity. A parallel decrease in ATP-dependent acidification of coated vesicles was also observed. The decrease in Cl- conductance and ATP-dependent acidification was reversed by treatment with protein kinase A and MgATP; the alkaline phosphatase inhibitor, sodium orthovanadate, blocked the inhibition of acidification. These results indicate that Cl- conductance in coated vesicles is modulated by a protein kinase A-dependent phosphorylation and that this modulation in turn affects ATP-dependent acidification.
我们之前已经表明,网格蛋白包被囊泡(H⁺)-ATP酶使网格蛋白包被囊泡酸化需要Cl⁻通道的活性(荒井,H.,平克,S.和福加克,M.(1989年)《生物化学》28卷,3075 - 3082页)。我们证明了网格蛋白包被囊泡Cl⁻通道的活性受磷酸化调节。使用对Cl⁻敏感的荧光探针6 - 甲氧基 - N -(3 - 磺丙基)喹啉鎓,在网格蛋白包被囊泡膜蛋白的重组制剂中测量Cl⁻电导。用碱性磷酸酶处理网格蛋白包被囊泡膜导致Cl⁻通道活性降低25±5%。同时也观察到网格蛋白包被囊泡的ATP依赖性酸化有平行降低。用蛋白激酶A和MgATP处理可逆转Cl⁻电导和ATP依赖性酸化的降低;碱性磷酸酶抑制剂原钒酸钠可阻断酸化的抑制作用。这些结果表明,网格蛋白包被囊泡中的Cl⁻电导受蛋白激酶A依赖性磷酸化调节,并且这种调节反过来影响ATP依赖性酸化。