SUMMARY The past 17 years have been marked by a revolution in our understanding of cellular multisubunit DNA-dependent RNA polymerases (MSDDRPs) at the structural level. A parallel development over the past 15 years has been the emerging story of the giant viruses, which encode MSDDRPs. Here we link the two in an attempt to understand the specialization of multisubunit RNA polymerases in the domain of life encompassing the large nucleocytoplasmic DNA viruses (NCLDV), a superclade that includes the giant viruses and the biochemically well-characterized poxvirus vaccinia virus. The first half of this review surveys the recently determined structural biology of cellular RNA polymerases for a microbiology readership. The second half discusses a reannotation of MSDDRP subunits from NCLDV families and the apparent specialization of these enzymes by virus family and by subunit with regard to subunit or domain loss, subunit dissociability, endogenous control of polymerase arrest, and the elimination/customization of regulatory interactions that would confer higher-order cellular control. Some themes are apparent in linking subunit function to structure in the viral world: as with cellular RNA polymerases I and III and unlike cellular RNA polymerase II, the viral enzymes seem to opt for speed and processivity and seem to have eliminated domains associated with higher-order regulation. The adoption/loss of viral RNA polymerase proofreading functions may have played a part in matching intrinsic mutability to genome size.

概括在过去的17年中，我们在结构水平上对细胞多亚基DNA依赖性RNA聚合酶（MSDDRP）的理解有了革命性的变化。在过去15年中，并行发展是编码MSDDRP的巨型病毒的新兴故事。在这里，我们将两者联系在一起，以试图理解生活中域中多亚基RNA聚合酶的专业化，包括大型核质DNA病毒（NCLDV），这是一个包括巨人病毒和生化特性良好的痘病毒痘苗病毒的超级物种。这篇综述的上半部分为微生物学读者调查了最近确定的细胞RNA聚合酶的结构生物学。下半部分讨论了来自NCLDV家族的MSDDRP亚基的重新注释以及这些酶在病毒亚家族或亚基丢失，亚基可解离性，聚合酶阻滞的内源控制以及调控相互作用的消除/定制方面的明显专一性这将赋予更高级别的细胞控制。在将亚基功能与病毒世界的结构联系起来时，一些主题很明显：与细胞RNA聚合酶I和III一样，与细胞RNA聚合酶II不同，病毒酶似乎选择了速度和合成能力，并且似乎消除了与更高一级蛋白相关的结构域订单规定。病毒RNA聚合酶校对功能的采用/缺失可能在使内在变异性与基因组大小相匹配方面发挥了作用。在将亚基功能与病毒世界的结构联系起来时，一些主题很明显：与细胞RNA聚合酶I和III一样，与细胞RNA聚合酶II不同，病毒酶似乎选择了速度和合成能力，并且似乎消除了与更高一级蛋白相关的结构域订单规定。病毒RNA聚合酶校对功能的采用/缺失可能在使内在变异性与基因组大小相匹配方面发挥了作用。在将亚基功能与病毒世界的结构联系起来时，一些主题很明显：与细胞RNA聚合酶I和III一样，与细胞RNA聚合酶II不同，病毒酶似乎选择了速度和合成能力，并且似乎消除了与更高一级蛋白相关的结构域订单规定。病毒RNA聚合酶校对功能的采用/缺失可能在使内在变异性与基因组大小相匹配方面发挥了作用。