Villafane R, King J
Department of Biology, Massachusetts Institute of Technology, Cambridge 02139.
J Mol Biol. 1988 Dec 5;204(3):607-19. doi: 10.1016/0022-2836(88)90359-2.
Temperature-sensitive folding (tsf) mutations in gene 9 of bacteriophage P22 interfere with the folding and association of the tailspike polypeptide chain at restrictive temperature. We report here the location and amino acid substitutions for 24 independent tsf mutants. The distribution of these and previously identified mutations is distinctly non-random; all of the 32 unambiguous sites of tsf mutations are located in the central 350 residues of the 666 residue tailspike polypeptide chain. No ts mutation has been found among the N-terminal 140 amino acids, and none among the C-terminal 170 amino acids. Since the physiological defect in these mutants is the destabilization of an early intermediate in the folding pathway, the localization of the mutants suggests that the central region of the chain is critical for formation or stabilization of this early intermediate. The majority of amino acids that served as sites for the tsf mutations were hydrophilic residues. Sixty percent of the replacements of these residues represented charge changes. This probably reflects the selection for mutant sites at the mature protein surface where the substitutions can be best tolerated without interfering with function. None of the sites of tsf mutations were at aromatic residues, and only one proline site was found. Substitutions at these residues may cause lethal folding defects which are not recovered as tsf mutants. The local sequences at tsf sites resemble those reported for turns. Structural studies identify beta-sheet as the dominant secondary structure. These mutations may disrupt the formation of conformational features of beta-sheets which are repeated, such as turns, associations between pairs of strands, or sheet/sheet packing interactions. Such a model accounts for the occurrence of tsf mutations with similar defective phenotypes at multiple positions along the chain.
噬菌体P22基因9中的温度敏感折叠(tsf)突变在限制温度下会干扰尾刺多肽链的折叠和缔合。我们在此报告24个独立tsf突变体的位置和氨基酸替换情况。这些突变以及先前鉴定出的突变的分布明显是非随机的;tsf突变的所有32个明确位点都位于666个氨基酸的尾刺多肽链的中央350个残基中。在N端的140个氨基酸中未发现ts突变,在C端的170个氨基酸中也未发现。由于这些突变体的生理缺陷是折叠途径中早期中间体的不稳定,突变体的定位表明链的中央区域对于该早期中间体的形成或稳定至关重要。作为tsf突变位点的大多数氨基酸是亲水性残基。这些残基替换中有60%代表电荷变化。这可能反映了在成熟蛋白质表面选择突变位点,在那里替换能够在不干扰功能的情况下得到最佳耐受。tsf突变位点均不在芳香族残基处,仅发现一个脯氨酸位点。这些残基的替换可能会导致致命的折叠缺陷,而无法作为tsf突变体恢复。tsf位点的局部序列类似于已报道的转角序列。结构研究确定β-折叠是主要的二级结构。这些突变可能会破坏β-折叠的构象特征的形成,这些特征是重复的,如转角、链对之间的缔合或片层/片层堆积相互作用。这样的模型解释了沿着链的多个位置出现具有相似缺陷表型的tsf突变的现象。