Department of Physiology and Biophysics, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
J Gen Physiol. 2011 Apr;137(4):343-56. doi: 10.1085/jgp.201010578. Epub 2011 Mar 14.
Anthrax toxin consists of three proteins: lethal factor (LF), edema factor (EF), and protective antigen (PA). This last forms a heptameric channel, (PA(63))(7), in the host cell's endosomal membrane, allowing the former two (which are enzymes) to be translocated into the cytosol. (PA(63))(7) incorporated into planar bilayer membranes forms a channel that translocates LF and EF, with the N terminus leading the way. The channel is mushroom-shaped with a cap containing the binding sites for EF and LF, and an ∼100 Å-long, 15 Å-wide stem. For proteins to pass through the stem they clearly must unfold, but is secondary structure preserved? To answer this question, we developed a method of trapping the polypeptide chain of a translocating protein within the channel and determined the minimum number of residues that could traverse it. We attached a biotin to the N terminus of LF(N) (the 263-residue N-terminal portion of LF) and a molecular stopper elsewhere. If the distance from the N terminus to the stopper was long enough to traverse the channel, streptavidin added to the trans side bound the N-terminal biotin, trapping the protein within the channel; if this distance was not long enough, streptavidin did not bind the N-terminal biotin and the protein was not trapped. The trapping rate was dependent on the driving force (voltage), the length of time it was applied, and the number of residues between the N terminus and the stopper. By varying the position of the stopper, we determined the minimum number of residues required to span the channel. We conclude that LF(N) adopts an extended-chain configuration as it translocates; i.e., the channel unfolds the secondary structure of the protein. We also show that the channel not only can translocate LF(N) in the normal direction but also can, at least partially, translocate LF(N) in the opposite direction.
致死因子(LF)、水肿因子(EF)和保护性抗原(PA)。最后一种在宿主细胞的内体膜上形成一个七聚体通道(PA(63))(7),允许前两种(酶)易位到细胞质中。(PA(63))(7)整合到平面双层膜中形成一个通道,可易位 LF 和 EF,其 N 端先进入。通道呈蕈状,帽状结构包含 EF 和 LF 的结合位点,以及一个约 100 Å 长、15 Å 宽的茎。为了使蛋白质穿过茎,它们显然必须展开,但二级结构是否被保留?为了回答这个问题,我们开发了一种方法来捕获易位蛋白的多肽链在通道内,并确定可以穿过它的最小残基数。我们在 LF(N)(LF 的 263 个残基的 N 端部分)的 N 端连接一个生物素,并在其他地方连接一个分子塞。如果从 N 端到塞子的距离足够长以穿过通道,则添加到转位侧的链霉亲和素与 N 端生物素结合,将蛋白捕获在通道内;如果此距离不够长,则链霉亲和素不会与 N 端生物素结合,并且蛋白不会被捕获。捕获率取决于驱动力(电压)、施加时间的长短以及 N 端和塞子之间的残基数。通过改变塞子的位置,我们确定了跨越通道所需的最小残基数。我们得出结论,LF(N) 在易位时采用伸展链构象;即,通道使蛋白的二级结构展开。我们还表明,该通道不仅可以正常方向易位 LF(N),而且至少可以部分地在相反方向易位 LF(N)。