Yates Susan P, Merrill Allan R
Department of Chemistry and Biochemistry, Guelph-Waterloo Centre for Graduate Work in Chemistry and Biochemistry, University of Guelph, Guelph, Ontario, Canada N1G 2W1.
Biochem J. 2004 May 1;379(Pt 3):563-72. doi: 10.1042/BJ20031731.
Pseudomonas aeruginosa produces the virulence factor, ETA (exotoxin A), which catalyses an ADP-ribosyltransferase reaction of its target protein, eEF2 (eukaryotic elongation factor-2). Currently, this protein-protein interaction is poorly characterized and this study was aimed at identifying the contact sites between eEF2 and the catalytic domain of ETA (PE24H, an ETA from P. aeruginosa, a 24 kDa C-terminal fragment containing a His6 tag). Single-cysteine residues were introduced into the toxin at 21 defined surface-exposed sites and labelled with the fluorophore, IAEDANS [5-(2-iodoacetylaminoethylamino)-1-napthalenesulphonic acid]. Fluorescence quenching studies using acrylamide, and fluorescence lifetime and wavelength emission maxima analyses were conducted in the presence and absence of eEF2. Large changes in the microenvironment of the AEDANS [5-(2-aminoethylamino)-1-naphthalenesulphonic acid] probe after eEF2 binding were not observed as dictated by both fluorescence lifetime and wavelength emission maxima values. This supported the proposed minimal contact model, which suggests that only small, discrete contacts occur between these proteins. As dictated by the bimolecular quenching constant (k(q)) for acrylamide, binding of eEF2 with toxin caused the greatest change in acrylamide accessibility (>50%) when the fluorescence label was near the active site or was located within a known catalytic loop. All mutant proteins showed a decrease in accessibility to acrylamide once eEF2 bound, although the relative change varied for each labelled protein. From these data, a low-resolution model of the toxin-eEF2 complex was constructed based on the minimal contact model with the intention of enhancing our knowledge on the mode of inactivation of the ribosome translocase by the Pseudomonas toxin.
铜绿假单胞菌产生毒力因子ETA(外毒素A),它催化其靶蛋白eEF2(真核延伸因子-2)的ADP-核糖基转移酶反应。目前,这种蛋白质-蛋白质相互作用的特征尚不明确,本研究旨在确定eEF2与ETA催化结构域(PE24H,一种来自铜绿假单胞菌的ETA,一个含有His6标签的24 kDa C端片段)之间的接触位点。在毒素的21个确定的表面暴露位点引入单半胱氨酸残基,并用荧光团IAEDANS[5-(2-碘乙酰氨基乙基氨基)-1-萘磺酸]进行标记。在有和没有eEF2的情况下,使用丙烯酰胺进行荧光猝灭研究,并进行荧光寿命和波长发射最大值分析。根据荧光寿命和波长发射最大值,未观察到eEF2结合后AEDANS[5-(2-氨基乙基氨基)-1-萘磺酸]探针微环境的大变化。这支持了所提出的最小接触模型,该模型表明这些蛋白质之间仅发生小的、离散的接触。根据丙烯酰胺的双分子猝灭常数(k(q)),当荧光标记靠近活性位点或位于已知的催化环内时,eEF2与毒素的结合导致丙烯酰胺可及性的最大变化(>50%)。一旦eEF2结合,所有突变蛋白的丙烯酰胺可及性均降低,尽管每种标记蛋白的相对变化有所不同。基于这些数据,根据最小接触模型构建了毒素-eEF2复合物的低分辨率模型,旨在增强我们对铜绿假单胞菌毒素使核糖体转位酶失活模式的认识。