In Archaea repair of uracil and hypoxanthine, which arise by deamination of cytosine and adenine, respectively, is initiated by three enzymes: Uracil-DNA-glycosylase (UDG, which recognises uracil); Endonuclease V (EndoV, which recognises hypoxanthine); and Endonuclease Q (EndoQ), (which recognises both uracil and hypoxanthine). Two archaeal DNA polymerases, Pol-B and Pol-D, are inhibited by deaminated bases in template strands, a feature unique to this domain. Thus the three repair enzymes and the two polymerases show overlapping specificity for uracil and hypoxanthine. Here it is demonstrated that binding of Pol-D to primer-templates containing deaminated bases inhibits the activity of UDG, EndoV, and EndoQ. Similarly Pol-B almost completely turns off EndoQ, extending earlier work that demonstrated that Pol-B reduces catalysis by UDG and EndoV. Pol-B was observed to be a more potent inhibitor of the enzymes compared to Pol-D. Although Pol-D is directly inhibited by template strand uracil, the presence of Pol-B further suppresses any residual activity of Pol-D, to near-zero levels. The results are compatible with Pol-D acting as the replicative polymerase and Pol-B functioning primarily as a guardian preventing deaminated base-induced DNA mutations.

中文翻译：

---

古细菌DNA聚合酶-B作为DNA模板的守护者：在处理脱尿碱基尿嘧啶和次黄嘌呤时，聚合酶与碱基/替代切除修复酶之间的联系。

在古细菌中，尿嘧啶和次黄嘌呤的修复分别通过胞嘧啶和腺嘌呤的脱氨基而产生，它是由三种酶启动的：尿嘧啶-DNA-糖基化酶（UDG，可识别尿嘧啶）；核酸内切酶V（EndoV，识别次黄嘌呤）；和核酸内切酶Q（EndoQ）（可识别尿嘧啶和次黄嘌呤）。两种古细菌DNA聚合酶Pol-B和Pol-D被模板链中的脱氨基碱基所抑制，这是该域特有的功能。因此，三种修复酶和两种聚合酶对尿嘧啶和次黄嘌呤显示出重叠的特异性。在此证明，Pol-D与含有脱氨基碱基的引物模板的结合会抑制UDG，EndoV和EndoQ的活性。同样，Pol-B几乎完全关闭了EndoQ，扩展了先前的工作，证明了Pol-B减少了UDG和EndoV的催化作用。与Pol-D相比，Pol-B被认为是一种更有效的酶抑制剂。尽管Pol-D被模板链尿嘧啶直接抑制，但是Pol-B的存在进一步将Pol-D的任何残留活性抑制到接近零的水平。结果与充当复制性聚合酶的Pol-D和主要充当防止脱氨基碱基诱导的DNA突变的监护人的Pol-B相容。