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三聚体 PCNA 可提高 Dbh 的活性和保真度,Dbh 是一种易产生单碱基缺失突变的 Y 家族跨损伤 DNA 聚合酶。

Heterotrimeric PCNA increases the activity and fidelity of Dbh, a Y-family translesion DNA polymerase prone to creating single-base deletion mutations.

机构信息

Wadsworth Center, New York State Department of Health, Albany, NY, United States; Department of Biomedical Sciences, University at Albany, Albany, NY, United States.

Wadsworth Center, New York State Department of Health, Albany, NY, United States.

出版信息

DNA Repair (Amst). 2020 Dec;96:102967. doi: 10.1016/j.dnarep.2020.102967. Epub 2020 Sep 6.

Abstract

Dbh is a Y-family translesion DNA polymerase from Sulfolobus acidocaldarius, an archaeal species that grows in harsh environmental conditions. Biochemically, Dbh displays a distinctive mutational profile, creating single-base deletion mutations at extraordinarily high frequencies (up to 50 %) in specific repeat sequences. In cells, however, Dbh does not appear to contribute significantly to spontaneous frameshifts in these same sequence contexts. This suggests that either the error-prone DNA synthesis activity of Dbh is reduced in vivo and/or Dbh is restricted from replicating these sequences. Here, we test the hypothesis that the propensity for Dbh to make single base deletion mutations is reduced through interaction with the S. acidocaldarius heterotrimeric sliding clamp processivity factor, PCNA-123. We first confirm that Dbh physically interacts with PCNA-123, with the interaction requiring both the PCNA-1 subunit and the C-terminal 10 amino acids of Dbh, which contain a predicted PCNA-interaction peptide (PIP) motif. This interaction stimulates the polymerase activity of Dbh, even on short, linear primer-template DNA, by increasing the rate of nucleotide incorporation. This stimulation requires an intact PCNA-123 heterotrimer and a DNA duplex length of at least 18 basepairs, the minimal length predicted from structural data to bind to both the polymerase and the clamp. Finally, we find that PCNA-123 increases the fidelity of Dbh on a single-base deletion hotspot sequence 3-fold by promoting an increase in the rate of correct, but not incorrect, nucleotide addition and propose that PCNA-123 induces Dbh to adopt a more active conformation that is less prone to creating deletions during DNA synthesis.

摘要

Dbh 是一种来自嗜酸热硫化叶菌的 Y 家族跨损伤 DNA 聚合酶,这是一种生长在恶劣环境条件下的古菌物种。从生化角度看,Dbh 表现出独特的突变特征,在特定重复序列中以极高的频率(高达 50%)产生单碱基缺失突变。然而,在细胞中,Dbh 似乎并没有显著导致这些相同序列背景下的自发移框突变。这表明,Dbh 易错 DNA 合成活性在体内降低,或者 Dbh 被限制复制这些序列。在这里,我们通过与嗜酸热硫化叶菌异三聚体滑动夹进程因子 PCNA-123 的相互作用来测试 Dbh 产生单碱基缺失突变倾向降低的假设。我们首先证实 Dbh 与 PCNA-123 发生物理相互作用,这种相互作用需要 PCNA-1 亚基和 Dbh 的 C 末端 10 个氨基酸,其中包含一个预测的 PCNA 相互作用肽(PIP)基序。这种相互作用通过增加核苷酸掺入的速率来刺激 Dbh 的聚合酶活性,即使在短的线性引物 - 模板 DNA 上也是如此。这种刺激需要一个完整的 PCNA-123 异三聚体和至少 18 个碱基对的 DNA 双链长度,这是从结构数据预测的结合聚合酶和夹的最小长度。最后,我们发现 PCNA-123 通过促进正确核苷酸添加速率的增加而将 Dbh 在单碱基缺失热点序列上的保真度提高了 3 倍,而不是错误核苷酸的添加,并且提出 PCNA-123 诱导 Dbh 采用更活跃的构象,从而在 DNA 合成过程中减少缺失的产生。

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