Huang S G, Klingenberg M
Institute of Physical Biochemistry, University of Munich, Germany.
Biochemistry. 1996 Dec 24;35(51):16806-14. doi: 10.1021/bi960989v.
The uncoupling protein (UCP) from brown adipose tissue mitochondria possesses H+ and Cl- transport activities [reviewed in Klingenberg, M. (1990) Trends Biochem. Sci. 15, 108-112]. Being a member of a mitochondrial carrier family, the transport of H+ and Cl- is carrier-like, i.e., much slower as compared to channels. Here we report that UCP reconstituted into giant liposomes displays stable chloride channel properties under patch-clamp conditions. The transport inhibitors (GTP, GDP, ATP, and ADP) also inhibit this channel in a reversible way, showing that the channel activity is associated with UCP. The slightly inward-rectifying chloride channel has a unit conductance of approximately 75 pS in symmetrical 100 mM KCl and closes at high positive potentials on the matrix side of UCP. Channel gatings switch from slow open-closure transitions to fast flickerings as the holding potential increases over +60 mV. Substitution experiments reveal a strong discrimination against cations [P(Cl-)/P(K+) approximately 17] and a permeability ratio order of Cl- > Br- > F- > SCN- > I- > NO3- > SO4(2-) > HPO4(2-) > gluconate. Nucleotide inhibition studies indicate that 70% UCP molecules had its matrix side oriented outside in the giant liposomes. Fatty acids, pH, divalent cations (Ca2+ and Mg2+), and mersalyl do not influence these Cl- currents. The Cl- channel can be blocked by 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS) from the matrix side of UCP. The data are consistent with a dimer consisting of two monomeric 75-pS Cl- channels or with a monomeric 150-pS channel having a 50% subconductance state. The channel current increases with Cl- concentration showing a typical saturation curve with Km approximately 63 mM and gmax approximately 120 pS (100 mM KCl in the pipet). The Cl- conductance measured under these conditions is 6 orders of magnitude higher than the Cl- transport activity reported earlier, suggesting that the UCP has the potential of behaving as an anion channel.
棕色脂肪组织线粒体的解偶联蛋白(UCP)具有H⁺和Cl⁻转运活性[见Klingenberg, M. (1990) Trends Biochem. Sci. 15, 108 - 112中的综述]。作为线粒体载体家族的一员,H⁺和Cl⁻的转运类似载体,即与通道相比要慢得多。在此我们报告,重构到巨型脂质体中的UCP在膜片钳条件下表现出稳定的氯离子通道特性。转运抑制剂(GTP、GDP、ATP和ADP)也以可逆方式抑制该通道,表明通道活性与UCP相关。这种轻微内向整流的氯离子通道在对称的100 mM KCl中单位电导约为75 pS,并且在UCP基质侧的高正电位时关闭。随着保持电位超过 +60 mV,通道门控从缓慢的开闭转换变为快速闪烁。替代实验揭示了对阳离子的强烈歧视[P(Cl⁻)/P(K⁺)约为17]以及渗透率比顺序为Cl⁻ > Br⁻ > F⁻ > SCN⁻ > I⁻ > NO₃⁻ > SO₄²⁻ > HPO₄²⁻ > 葡萄糖酸盐。核苷酸抑制研究表明,70%的UCP分子在巨型脂质体中其基质侧朝外。脂肪酸、pH、二价阳离子(Ca²⁺和Mg²⁺)以及汞撒利不影响这些Cl⁻电流。Cl⁻通道可从UCP的基质侧被4,4'-二异硫氰酸根合芪-2,2'-二磺酸(DIDS)阻断。数据与由两个单体75-pS Cl⁻通道组成的二聚体或具有50%亚电导状态的单体150-pS通道一致。通道电流随Cl⁻浓度增加,呈现典型的饱和曲线,Km约为63 mM,gmax约为120 pS(移液管中为100 mM KCl)。在这些条件下测得的Cl⁻电导比先前报道的Cl⁻转运活性高6个数量级,表明UCP有作为阴离子通道的潜力。