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蛋白二硫键异构酶在不使 A1 亚单位展开的情况下将霍乱毒素 A1 亚单位从全毒素中置换出来。

Protein-disulfide isomerase displaces the cholera toxin A1 subunit from the holotoxin without unfolding the A1 subunit.

机构信息

Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, Florida 32826, USA.

出版信息

J Biol Chem. 2011 Jun 24;286(25):22090-100. doi: 10.1074/jbc.M111.237966. Epub 2011 May 4.

Abstract

Protein-disulfide isomerase (PDI) has been proposed to exhibit an "unfoldase" activity against the catalytic A1 subunit of cholera toxin (CT). Unfolding of the CTA1 subunit is thought to displace it from the CT holotoxin and to prepare it for translocation to the cytosol. To date, the unfoldase activity of PDI has not been demonstrated for any substrate other than CTA1. An alternative explanation for the putative unfoldase activity of PDI has been suggested by recent structural studies demonstrating that CTA1 will unfold spontaneously upon its separation from the holotoxin at physiological temperature. Thus, PDI may simply dislodge CTA1 from the CT holotoxin without unfolding the CTA1 subunit. To evaluate the role of PDI in CT disassembly and CTA1 unfolding, we utilized a real-time assay to monitor the PDI-mediated separation of CTA1 from the CT holotoxin and directly examined the impact of PDI binding on CTA1 structure by isotope-edited Fourier transform infrared spectroscopy. Our collective data demonstrate that PDI is required for disassembly of the CT holotoxin but does not unfold the CTA1 subunit, thus uncovering a new mechanism for CTA1 dissociation from its holotoxin.

摘要

蛋白二硫键异构酶(PDI)被认为对霍乱毒素(CT)的催化 A1 亚基具有“展开酶”活性。CTA1 亚基的展开被认为将其从 CT 全毒素中置换出来,并为其易位到细胞质做准备。迄今为止,PDI 的展开酶活性尚未在除 CTA1 以外的任何底物上得到证明。最近的结构研究提出了 PDI 假定的展开酶活性的另一种解释,表明 CTA1 在生理温度下从全毒素中分离出来时会自发展开。因此,PDI 可能只是将 CTA1 从 CT 全毒素中逐出,而不会使 CTA1 亚基展开。为了评估 PDI 在 CT 解体和 CTA1 展开中的作用,我们利用实时测定法监测 PDI 介导的 CTA1 与 CT 全毒素的分离,并通过同位素编辑傅里叶变换红外光谱直接检查 PDI 结合对 CTA1 结构的影响。我们的综合数据表明,PDI 是 CT 全毒素解体所必需的,但不会使 CTA1 亚基展开,从而揭示了 CTA1 与其全毒素解离的新机制。

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