Blanca Giuseppina, Delagoutte Emmanuelle, Tanguy le Gac Nicolas, Johnson Neil P, Baldacci Giuseppe, Villani Giuseppe
Institut de Pharmacologie et Biologie Structurale CNRS-UMR 5089, 205 route de Narbonne, 31077 Toulouse cedex 4, France.
Biochem J. 2007 Mar 1;402(2):321-9. doi: 10.1042/BJ20060898.
Replicative DNA polymerases, such as T4 polymerase, possess both elongation and 3'-5' exonuclease proofreading catalytic activities. They arrest at the base preceding DNA damage on the coding DNA strand and specialized DNA polymerases have evolved to replicate across the lesion by a process known as TLS (translesion DNA synthesis). TLS is considered to take place in two steps that often require different enzymes, insertion of a nucleotide opposite the damaged template base followed by extension from the inserted nucleotide. We and others have observed that inactivation of the 3'-5' exonuclease function of T4 polymerase enables TLS across a single site-specific abasic [AP (apurinic/apyrimidinic)] lesion. In the present study we report a role for auxiliary replicative factors in this reaction. When replication is performed with a large excess of DNA template over DNA polymerase in the absence of auxiliary factors, the exo- polymerase (T4 DNA polymerase deficient in the 3'-5' exonuclease activity) inserts one nucleotide opposite the AP site but does not extend past the lesion. Addition of the clamp processivity factor and the clamp loader complex restores primer extension across an AP lesion on a circular AP-containing DNA substrate by the exo- polymerase, but has no effect on the wild-type enzyme. Hence T4 DNA polymerase exhibits a variety of responses to DNA damage. It can behave as a replicative polymerase or (in the absence of proofreading activity) as a specialized DNA polymerase and carry out TLS. As a specialized polymerase it can function either as an inserter or (with the help of accessory proteins) as an extender. The capacity to separate these distinct functions in a single DNA polymerase provides insight into the biochemical requirements for translesion DNA synthesis.
复制性DNA聚合酶,如T4聚合酶,具有延伸和3'-5'核酸外切酶校对催化活性。它们会在编码DNA链上DNA损伤前的碱基处停滞,而专门的DNA聚合酶已经进化出通过一种称为跨损伤DNA合成(TLS)的过程跨越损伤部位进行复制的能力。TLS被认为分两步进行,这通常需要不同的酶,即在受损模板碱基对面插入一个核苷酸,然后从插入的核苷酸处延伸。我们和其他人已经观察到,T4聚合酶的3'-5'核酸外切酶功能失活能够使TLS跨越单个位点特异性无碱基[AP(脱嘌呤/脱嘧啶)]损伤。在本研究中,我们报道了辅助复制因子在该反应中的作用。当在没有辅助因子的情况下,用大量过量的DNA模板与DNA聚合酶进行复制时,外切酶缺陷型聚合酶(缺乏3'-5'核酸外切酶活性的T4 DNA聚合酶)在AP位点对面插入一个核苷酸,但不会延伸越过损伤部位。添加钳位持续合成因子和钳位装载复合物可恢复外切酶缺陷型聚合酶在含AP的环状DNA底物上跨越AP损伤的引物延伸,但对野生型酶没有影响。因此,T4 DNA聚合酶对DNA损伤表现出多种反应。它可以作为复制性聚合酶发挥作用,或者(在没有校对活性的情况下)作为专门的DNA聚合酶进行TLS。作为专门的聚合酶,它既可以作为插入酶发挥作用,也可以(在辅助蛋白的帮助下)作为延伸酶发挥作用。在单一DNA聚合酶中分离这些不同功能的能力为深入了解跨损伤DNA合成的生化要求提供了线索。