Department of Microbiology and Molecular Medicine, University Medical Centre, Geneva, Switzerland.
Gilead Sciences, Foster City, CA, USA.
Nat Struct Mol Biol. 2022 Sep;29(9):922-931. doi: 10.1038/s41594-022-00829-0. Epub 2022 Sep 12.
In addition to its role in chromosome maintenance, the six-membered Smc5/6 complex functions as a restriction factor that binds to and transcriptionally silences viral and other episomal DNA. However, the underlying mechanism is unknown. Here, we show that transcriptional silencing by the human Smc5/6 complex is a three-step process. The first step is entrapment of the episomal DNA by a mechanism dependent on Smc5/6 ATPase activity and a function of its Nse4a subunit for which the Nse4b paralog cannot substitute. The second step results in Smc5/6 recruitment to promyelocytic leukemia nuclear bodies by SLF2 (the human ortholog of Nse6). The third step promotes silencing through a mechanism requiring Nse2 but not its SUMO ligase activity. By contrast, the related cohesin and condensin complexes fail to bind to or silence episomal DNA, indicating a property unique to Smc5/6.
除了在染色体维持中的作用外,六聚体 Smc5/6 复合物还作为一种限制因子发挥作用,与病毒和其他附加体 DNA 结合并使其转录沉默。然而,其潜在的机制尚不清楚。在这里,我们表明,人 Smc5/6 复合物的转录沉默是一个三步过程。第一步是通过依赖于 Smc5/6 ATP 酶活性的机制和其 Nse4a 亚基的功能来捕获附加体 DNA,其 Nse4b 同源物不能替代该功能。第二步导致 Smc5/6 通过 SLF2(Nse6 的人同源物)募集到早幼粒细胞白血病核体。第三步通过需要 Nse2 但不需要其 SUMO 连接酶活性的机制促进沉默。相比之下,相关的黏合蛋白和凝缩蛋白复合物不能结合或沉默附加体 DNA,这表明 Smc5/6 具有独特的性质。