D'Urzo Annalisa, Santambrogio Carlo, Grandori Rita, Ciurli Stefano, Zambelli Barbara
Department of Biotechnology and Biosciences, University of Milano-Bicocca, Milan, Italy.
J Biol Inorg Chem. 2014 Dec;19(8):1341-54. doi: 10.1007/s00775-014-1191-9. Epub 2014 Sep 9.
Urease is an essential Ni(II) enzyme involved in the nitrogen metabolism of bacteria, plants and fungi. Ni(II) delivery into the enzyme active site requires the presence of four accessory proteins, named UreD, UreF, UreG and UreE, acting through a complex protein network regulated by metal binding and GTP hydrolysis. The GTPase activity is catalyzed by UreG, which couples this function to a non-enzymatic role as a molecular chaperone. This moonlighting activity is reflected in a flexible fold that makes UreG the first discovered intrinsically disordered enzyme. UreG binds Ni(II) and Zn(II),which in turn modulate the interactions with other urease chaperones. The aim of this study is to understand the structural implications of metal binding to Sporosarcina pasteurii UreG (SpUreG). A combination of light scattering, calorimetry, mass spectrometry, and NMR spectroscopy revealed that SpUreG exists in monomer-dimer equilibrium (K(d)= 45 µM), sampling three distinct folding populations with different degrees of compactness. Binding of Zn(II) ions, occurring in two distinct sites (K(d1) = 3 nM, K(d2) = 0.53 µM), shifts the protein conformational landscape toward the more compact population, while maintaining the overall protein structural plasticity. Differently, binding of Ni(II) ions occurs in three binding sites (K(d1(= 14 µM; K(d2) = 270 µM; K(d3)= 160 µM), with much weaker influence on the protein conformational equilibrium. These distinct conformational responses of SpUreG to Ni(II) and Zn(II) binding suggest that selective metal binding modulates protein plasticity, possibly having an impact on the protein-protein interactions and the enzymatic activity of UreG.
脲酶是一种参与细菌、植物和真菌氮代谢的必需镍(II)酶。镍(II)传递到酶活性位点需要四种辅助蛋白,即脲酶D(UreD)、脲酶F(UreF)、脲酶G(UreG)和脲酶E(UreE)的存在,它们通过由金属结合和GTP水解调节的复杂蛋白质网络发挥作用。GTPase活性由UreG催化,UreG将此功能与作为分子伴侣的非酶作用联系起来。这种兼职活性体现在一种灵活的折叠中,这使得UreG成为首个被发现的内在无序酶。UreG结合镍(II)和锌(II),进而调节与其他脲酶伴侣的相互作用。本研究的目的是了解金属结合到巴氏芽孢杆菌脲酶G(SpUreG)的结构影响。光散射、量热法、质谱和核磁共振光谱的结合表明,SpUreG以单体-二聚体平衡状态存在(解离常数K(d)= 45 µM),呈现出三种具有不同紧密程度的不同折叠群体。锌(II)离子在两个不同位点结合(K(d1) = 3 nM,K(d2) = 0.53 µM),使蛋白质构象格局向更紧密的群体转变,同时保持蛋白质整体结构可塑性。不同的是,镍(II)离子在三个结合位点结合(K(d1)= 14 µM;K(d2) = 270 µM;K(d3)= 160 µM),对蛋白质构象平衡的影响要弱得多。SpUreG对镍(II)和锌(II)结合的这些不同构象反应表明,选择性金属结合调节蛋白质可塑性,可能对蛋白质-蛋白质相互作用和UreG的酶活性产生影响。