Howard Hughes Medical Institute, California Institute of Technology, Pasadena, CA 91125, USA.
Mol Cell. 2011 Apr 8;42(1):75-83. doi: 10.1016/j.molcel.2011.03.016.
During ubiquitin conjugation, the thioester bond that links "donor" ubiquitin to ubiquitin-conjugating enzyme (E2) undergoes nucleophilic attack by the ɛ-amino group of an acceptor lysine, resulting in formation of an isopeptide bond. Models of ubiquitination have envisioned the donor ubiquitin to be a passive participant in this process. However, we show here that the I44A mutation in ubiquitin profoundly inhibits its ability to serve as a donor for ubiquitin chain initiation or elongation, but can be rescued by computationally predicted compensatory mutations in the E2 Cdc34. The donor defect of ubiquitin-I44A can be partially suppressed either by using a low pKa amine (hydroxylamine) as the acceptor or by performing reactions at higher pH, suggesting that the discharge defect arises in part due to inefficient deprotonation of the acceptor lysine. We propose that interaction between Cdc34 and the donor ubiquitin organizes the active site to promote efficient ubiquitination of substrate.
在泛素缀合过程中,将“供体”泛素连接到泛素缀合酶 (E2) 的硫酯键通过受体赖氨酸的ε-氨基进行亲核攻击,导致形成异肽键。泛素化的模型设想供体泛素是该过程的被动参与者。然而,我们在这里表明,泛素中的 I44A 突变极大地抑制了其作为泛素链起始或延伸的供体的能力,但可以通过计算预测的 E2 Cdc34 中的补偿突变来挽救。泛素-I44A 的供体缺陷可以通过使用低 pKa 胺(羟胺)作为受体或在较高 pH 下进行反应来部分抑制,这表明释放缺陷部分是由于受体赖氨酸的去质子化效率低下引起的。我们提出,Cdc34 与供体泛素之间的相互作用将活性位点组织起来,以促进底物的有效泛素化。