Allosteric rescue of catalytically impaired ATP phosphoribosyltransferase variants links protein dynamics to active-site electrostatic preorganisation

变构拯救催化功能受损的ATP磷酸核糖转移酶变体将蛋白质动力学与活性位点静电预组织联系起来

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Abstract

ATP phosphoribosyltransferase catalyses the first step of histidine biosynthesis and is controlled via a complex allosteric mechanism where the regulatory protein HisZ enhances catalysis by the catalytic protein HisG(S) while mediating allosteric inhibition by histidine. Activation by HisZ was proposed to position HisG(S) Arg56 to stabilise departure of the pyrophosphate leaving group. Here we report active-site mutants of HisG(S) with impaired reaction chemistry which can be allosterically restored by HisZ despite the HisZ:HisG(S) interface lying ~20 Å away from the active site. MD simulations indicate HisZ binding constrains the dynamics of HisG(S) to favour a preorganised active site where both Arg56 and Arg32 are poised to stabilise leaving-group departure in WT-HisG(S). In the Arg56Ala-HisG(S) mutant, HisZ modulates Arg32 dynamics so that it can partially compensate for the absence of Arg56. These results illustrate how remote protein-protein interactions translate into catalytic resilience by restoring damaged electrostatic preorganisation at the active site.

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