Laurberg M, Kristensen O, Martemyanov K, Gudkov A T, Nagaev I, Hughes D, Liljas A
Department of Molecular Biophysics, Centre for Chemistry and Chemical Engineering, Lund University, Lund, SE-221 00, Sweden.
J Mol Biol. 2000 Nov 3;303(4):593-603. doi: 10.1006/jmbi.2000.4168.
The crystal structure of Thermus thermophilus elongation factor G (EF-G) carrying the point mutation His573Ala was determined at a resolution of 2.8 A. The mutant has a more closed structure than that previously reported for wild-type EF-G. This is obtained by a 10 degrees rigid rotation of domains III, IV and V with regard to domains I and II. This rotation results in a displacement of the tip of domain IV by approximately 9 A. The structure of domain III is now fully visible and reveals the double split beta-alpha-beta motif also observed for EF-G domain V and for several ribosomal proteins. A large number of fusidic acid resistant mutations found in domain III have now been possible to locate. Possible locations for the effector loop and a possible binding site for fusidic acid are discussed in relation to some of the fusidic acid resistant mutations.
对携带His573Ala点突变的嗜热栖热菌延伸因子G(EF-G)的晶体结构进行了测定,分辨率为2.8埃。该突变体具有比先前报道的野生型EF-G更封闭的结构。这是通过结构域III、IV和V相对于结构域I和II进行10度的刚性旋转实现的。这种旋转导致结构域IV的尖端位移约9埃。结构域III的结构现在完全可见,揭示了在EF-G结构域V和几种核糖体蛋白中也观察到的双分裂β-α-β基序。现在已经能够定位在结构域III中发现的大量对夫西地酸耐药的突变。结合一些对夫西地酸耐药的突变,讨论了效应环的可能位置和夫西地酸的可能结合位点。