Islam T A, Miller-Martini D M, Horowitz P M
Department of Biochemistry, University of Texas Health Science Center at San Antonio 78284-7760.
J Biol Chem. 1994 Mar 18;269(11):7903-13.
Mutants of rhodanese (EC 2.8.1.1) that substitute Ser for Cys-254 and/or Cys-263, i.e. C254S, C263S, and the double mutant C254/263S, were compared with the wild-type enzyme to test the hypothesis that the persulfide formation to give sulfur-substituted rhodanese (ES) during catalysis can exert a stabilizing influence on the global structure of the protein. All the ES forms were quite refractory toward limited tryptic digestion. Extensive digestion was observed only in the persulfide-free forms (E) of mutants having substitutions of Ser for Cys-254 (C254/263S and C254S). Limited proteolysis of C254/263S produced a species on SDS gels at approximately 21 kDa that was proteolyzed further to give a slightly smaller product. Amino acid sequencing, together with mass spectrometry, indicated that these two components had the same N-terminal sequence as wild-type rhodanese and that they resulted from cleavage in the C-terminal domain, first at residues Arg-186 or Arg-182 and subsequently at Arg-175 or Lys-174. In addition to increased proteolytic susceptibility, the conversion from ES to E of C254/263S was accompanied by increased hydrophobic exposure and increased quenching of the intrinsic protein fluorescence by acrylamide. The substitution of Ser for Cys-254, within the helix suggested to be involved in stabilizing the persulfide bond in ES, seems to promote the formation of flexible conformations of sulfur-free rhodanese. In keeping with this model, C254/263S shows a marked increase in the hysteresis that is observed in rhodanese catalysis at pH 7 and high ionic strength. These results can be understood in terms of a model, suggesting that there is mutual stabilization of the protein structure and the persulfide bond in the ES form of rhodanese.
将半胱氨酸-254和/或半胱氨酸-263替换为丝氨酸的硫氰酸酶(EC 2.8.1.1)突变体,即C254S、C263S和双突变体C254/263S,与野生型酶进行了比较,以检验以下假设:催化过程中形成过硫化物从而产生硫取代硫氰酸酶(ES),这可能会对蛋白质的整体结构产生稳定作用。所有的ES形式对胰蛋白酶的有限消化都相当耐受。只有在半胱氨酸-254被丝氨酸取代的突变体(C254/263S和C254S)的无过硫化物形式(E)中观察到广泛消化。C254/263S的有限蛋白酶解在SDS凝胶上产生了一个约21 kDa的条带,该条带进一步被蛋白酶解,产生了一个稍小的产物。氨基酸测序以及质谱分析表明,这两个组分与野生型硫氰酸酶具有相同的N端序列,并且它们是由C端结构域中的切割产生的,首先是在精氨酸-186或精氨酸-182处,随后是在精氨酸-175或赖氨酸-174处。除了蛋白水解敏感性增加外,C254/263S从ES向E的转变还伴随着疏水性暴露增加以及丙烯酰胺对蛋白质固有荧光的猝灭增加。在被认为参与稳定ES中过硫键的螺旋内,将半胱氨酸-254替换为丝氨酸似乎促进了无硫硫氰酸酶柔性构象的形成。与该模型一致,C254/263S在pH 7和高离子强度下硫氰酸酶催化中观察到的滞后现象显著增加。这些结果可以用一个模型来解释,该模型表明在硫氰酸酶的ES形式中,蛋白质结构和过硫键之间存在相互稳定作用。