Hazelbaker Dane, Radman-Livaja Marta, Landy Arthur
Department of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, RI 02912, USA.
J Mol Biol. 2005 Sep 2;351(5):948-55. doi: 10.1016/j.jmb.2005.06.077.
Bacteriophage lambda integrase (Int) catalyzes the integration and excision of the phage lambda chromosome into and out of the Esherichia coli host chromosome. The seven carboxy-terminal residues (C-terminal tail) of Int comprise a context-sensitive regulatory element that links catalytic function with protein multimerization and also coordinates Int functions within the multimeric recombinogenic complex. The experiments reported here show that the beta5-strand of Int is not simply a placeholder for the C-terminal tail but rather exerts its own allosteric effects on Int function in response to the incoming tail. Using a mutant integrase in which the C-terminal tail has been deleted (W350ter), we demonstrate that the C-terminal tail is required for efficient and accurate resolution of Holliday junctions by tetrameric Int. Addition of a free heptameric peptide of the same sequence as the C-terminal tail partially reverses the W350ter defects by stimulating Holliday junction resolution. The peptide also stimulates the topoisomerase function of monomeric W350ter. Single residue alterations in the peptide sequence and a mutant of the beta5 strand indicate that the observed stimulation arises from specific contacts with the beta5 strand (residues 239-243). The peptide does not stimulate binding of W350ter to its cognate DNA sites and therefore appears to recapitulate the effects of the normal C-terminal tail intermolecular contacts in wild-type Int. Models for the allosteric stimulation of Int activity by beta5 strand contacts are discussed.
噬菌体λ整合酶(Int)催化噬菌体λ染色体与大肠杆菌宿主染色体之间的整合与切除。Int的七个羧基末端残基(C末端尾巴)构成一个上下文敏感的调控元件,该元件将催化功能与蛋白质多聚化联系起来,并在多聚体重组复合物中协调Int的功能。本文报道的实验表明,Int的β5链并非仅仅是C末端尾巴的占位符,而是会响应进入的尾巴对Int功能发挥自身的变构效应。使用C末端尾巴已被删除的突变整合酶(W350ter),我们证明C末端尾巴对于四聚体Int高效准确地解析Holliday连接体是必需的。添加与C末端尾巴序列相同的游离七聚体肽,通过刺激Holliday连接体的解析,部分逆转了W350ter的缺陷。该肽还刺激单体W350ter的拓扑异构酶功能。肽序列中的单残基改变以及β5链的一个突变体表明,观察到的刺激源于与β5链(残基239 - 243)的特定接触。该肽不刺激W350ter与其同源DNA位点的结合,因此似乎重现了野生型Int中正常C末端尾巴分子间接触的效应。讨论了β5链接触对Int活性变构刺激的模型。