Little is known about molecular recognition of acetylated N termini, despite prevalence of this modification among eukaryotic cytosolic proteins. We report that the family of human DCN-like (DCNL) co-E3s, which promote ligation of the ubiquitin-like protein NEDD8 to cullin targets, recognizes acetylated N termini of the E2 enzymes UBC12 and UBE2F. Systematic biochemical and biophysical analyses reveal 40- and 10-fold variations in affinities among different DCNL-cullin and DCNL-E2 complexes, contributing to varying efficiencies of different NEDD8 ligation cascades. Structures of DCNL2 and DCNL3 complexes with N-terminally acetylated peptides from UBC12 and UBE2F illuminate a common mechanism by which DCNL proteins recognize N-terminally acetylated E2s and how selectivity for interactions dependent on N-acetyl-methionine are established through side chains recognizing distal residues. Distinct preferences of UBC12 and UBE2F peptides for inhibiting different DCNLs, including the oncogenic DCNL1 protein, suggest it may be possible to develop small molecules blocking specific N-acetyl-methionine-dependent protein interactions.

译文

尽管这种修饰在真核胞质蛋白中普遍存在,但对乙酰化N末端的分子识别知之甚少。我们报告说,促进泛素样蛋白NEDD8与cullin靶标连接的人DCN样 (DCNL) co-E3s家族识别E2酶UBC12和UBE2F的乙酰化N末端。系统的生化和生物物理分析显示,不同的DCNL-cullin和DCNL-E2复合物之间的亲和力变化为40倍和10倍,从而导致不同NEDD8连接级联的效率变化。DCNL2和DCNL3复合物与来自UBC12和UBE2F的N末端乙酰化肽的结构阐明了DCNL蛋白识别N末端乙酰化E2s的共同机制,以及如何通过识别远端残基的侧链建立依赖于N-乙酰基-甲硫氨酸的相互作用的选择性。UBC12和UBE2F肽对抑制不同dcnl (包括致癌DCNL1蛋白) 的独特偏好表明,可能有可能开发阻断特定的N-乙酰基-甲硫氨酸依赖性蛋白相互作用的小分子。

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