Time-resolved backbone desolvation and mutational hot spots in folding proteins

被引:14
作者
Fernández, A
机构
[1] Max Planck Inst Biochem, D-8000 Munich, Germany
[2] Univ Nacl Sur CONICET, Inst Matemat, Bahia Blanca, Argentina
来源
PROTEINS-STRUCTURE FUNCTION AND GENETICS | 2002年 / 47卷 / 04期
关键词
ab initio simulations; chymotrypsin inhibitor 2; mammalian ubiquitin;
D O I
10.1002/prot.10109
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
A method is presented to identify hot mutational spots and predict the extent of surface burial at the transition state relative to the native fold in two-state folding proteins. The method is based on ab initio simulations of folding histories in which transitions between coarsely defined conformations and pairwise interactions are dependent on the solvent environments created by the chain. The highly conserved mammalian ubiquitin is adopted as a study case to make predictions. The evolution in time of the chain topology suggests a nucleation process with a critical point signaled by a sudden quenching of structural fluctuations. The occurrence of this nucleus is shown to be concurrent with a sudden escalation in the number of three-body correlations whereby hydrophobic units approach residue pairs engaged in amide-carbonyl hydrogen bonding. These correlations determine a pattern designed to structure the surrounding solvent, protecting intramolecular hydrogen bonds from water attack. Such correlations are shown to be required to stabilize the nucleus, with kinetic consequences for the folding process. Those nuclear residues that adopt the dual role of protecting and being protected while engaged in hydrogen bonds are predicted to be the hottest mutational spots. Some such residues are shown not to retain the same protecting role in the native fold. This kinetic treatment of folding nucleation is independently validated vis-a-vis a Phi-value analysis on chymotrypsin inhibitor 2, a protein for which extensive mutational data exists.
引用
收藏
页码:447 / 457
页数:11
相关论文
共 27 条
[21]  
MATTHEWS CR, 1987, METHOD ENZYMOL, V154, P498
[22]   A simple model for calculating the kinetics of protein folding from three-dimensional structures [J].
Muñoz, V ;
Eaton, WA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (20) :11311-11316
[23]  
Park K, 2000, PROTEINS, V40, P237, DOI 10.1002/(SICI)1097-0134(20000801)40:2<237::AID-PROT60>3.0.CO
[24]  
2-P
[25]   Effect of preformed correct tertiary interactions on rapid two-state tendamistat folding: Evidence for hairpins as initiation sites for beta-sheet formation [J].
Schonbrunner, N ;
Pappenberger, G ;
Scharf, M ;
Engels, J ;
Kiefhaber, T .
BIOCHEMISTRY, 1997, 36 (29) :9057-9065
[26]   THE BARRIERS IN PROTEIN-FOLDING [J].
SOSNICK, TR ;
MAYNE, L ;
HILLER, R ;
ENGLANDER, SW .
NATURE STRUCTURAL BIOLOGY, 1994, 1 (03) :149-156
[27]   Folding dynamics with nonadditive forces: A simulation study of a designed helical protein and a random heteropolymer [J].
Takada, S ;
Luthey-Schulten, Z ;
Wolynes, PG .
JOURNAL OF CHEMICAL PHYSICS, 1999, 110 (23) :11616-11629