Department of Biological Sciences, University of Alberta, Edmonton, Alberta, Canada T6G 2E9.
J Mol Biol. 2010 Jul 16;400(3):295-308. doi: 10.1016/j.jmb.2010.05.030. Epub 2010 May 21.
Structure-based protein sequence alignments of family B DNA polymerases revealed a conserved motif that is formed from interacting residues between loops from the N-terminal and palm domains and between the N-terminal loop and a conserved proline residue. The importance of the motif for function of the bacteriophage T4 DNA polymerase was revealed by suppressor analysis. T4 DNA polymerases that form weak replicating complexes cannot replicate DNA when the dGTP pool is reduced. The conditional lethality provides the means to identify amino acid substitutions that restore replication activity under low-dGTP conditions either by correcting the defect produced by the first amino acid substitution or by generally increasing the stability of polymerase complexes; the second type are global suppressors that can effectively counter the reduced stability caused by a variety of amino acid substitutions. Some amino acid substitutions that increase the stability of polymerase complexes produce a new phenotype-sensitivity to the antiviral drug phosphonoacetic acid. Amino acid substitutions that confer decreased ability to replicate DNA under low-dGTP conditions or drug sensitivity were identified in the new motif, which suggests that the motif functions in regulating the stability of polymerase complexes. Additional suppressor analyses revealed an apparent network of interactions that link the new motif to the fingers domain and to two patches of conserved residues that bind DNA. The collection of mutant T4 DNA polymerases provides a foundation for future biochemical studies to determine how DNA polymerases remain stably associated with DNA while waiting for the next available dNTP, how DNA polymerases translocate, and the biochemical basis for sensitivity to antiviral drugs.
基于结构的 B 族 DNA 聚合酶的蛋白质序列比对揭示了一个保守基序,该基序由 N 端和手掌结构域之间的环以及 N 端环与保守脯氨酸残基之间相互作用的残基形成。噬菌体 T4 DNA 聚合酶中该基序对于功能的重要性通过抑制分析揭示。形成弱复制复合物的 T4 DNA 聚合酶在 dGTP 池减少时不能复制 DNA。条件致死性提供了一种识别氨基酸取代的方法,这些取代可以在低 dGTP 条件下恢复复制活性,要么通过纠正第一个氨基酸取代产生的缺陷,要么通过普遍增加聚合酶复合物的稳定性;第二类是全局抑制剂,可以有效地对抗由各种氨基酸取代引起的稳定性降低。一些增加聚合酶复合物稳定性的氨基酸取代产生了一个新的表型——对抗病毒药物膦甲酸钠的敏感性。在新基序中鉴定出了在低 dGTP 条件下复制 DNA 的能力降低或对药物敏感的氨基酸取代,这表明该基序在调节聚合酶复合物的稳定性方面起作用。额外的抑制分析揭示了一个明显的相互作用网络,将新基序与手指结构域和与 DNA 结合的两个保守残基斑块联系起来。突变 T4 DNA 聚合酶的集合为未来的生化研究提供了基础,以确定 DNA 聚合酶如何在等待下一个可用的 dNTP 时保持与 DNA 的稳定结合、DNA 聚合酶如何易位以及对抗病毒药物敏感的生化基础。