Laboratory of Molecular Biology, NIDDK, National Institutes of Health, Bethesda, MD 20892, USA.
Laboratory of Molecular Biology, NIDDK, National Institutes of Health, Bethesda, MD 20892, USA.
J Mol Biol. 2024 May 15;436(10):168557. doi: 10.1016/j.jmb.2024.168557. Epub 2024 Apr 4.
Retroviral DNA integration is mediated by nucleoprotein complexes (intasomes) in which a pair of viral DNA ends are bridged by a multimer of integrase (IN). Most of the high-resolution structures of HIV-1 intasomes are based on an HIV-1 IN with an Sso7d protein domain fused to the N-terminus. Sso7d-IN aggregates much less than wild-type IN and has been critical for structural studies of HIV-1 intasomes. Unexpectedly, these structures revealed that the common core architecture that mediates catalysis could be assembled in various ways, giving rise to both tetrameric and dodecameric intasomes, together with other less well-characterized species. This differs from related retroviruses that assemble unique multimeric intasomes, although the number of protomers in the intasome varies between viruses. The question of whether the additional Sso7d domain contributes to the heterogeneity of HIV-1 intasomes is therefore raised. We have addressed this by biochemical and structural studies of intasomes assembled with wild-type HIV-1 IN. Negative stain and cryo-EM reveal a similar range of multimeric intasome species as with Sso7d-IN with the same common core architecture. Stacks of intasomes resulting from domain swapping are also seen with both wild-type and Sso7d-IN intasomes. The propensity to assemble multimeric intasome species is, therefore, an intrinsic property of HIV-1 IN and is not conferred by the presence of the Sso7d domain. The recently solved intasome structures of different retroviral species, which have been reported to be tetrameric, octameric, dodecameric, and hexadecameric, highlight how a common intasome core architecture can be assembled in different ways for catalysis.
逆转录病毒 DNA 整合是由核蛋白复合物(intasomes)介导的,其中一对病毒 DNA 末端由整合酶(IN)的多聚体桥接。大多数 HIV-1 intasomes 的高分辨率结构都是基于 HIV-1 IN 与 Sso7d 蛋白结构域融合到 N 端。Sso7d-IN 比野生型 IN 聚集得少得多,并且对 HIV-1 intasomes 的结构研究至关重要。出乎意料的是,这些结构表明,介导催化的常见核心架构可以以各种方式组装,导致形成四聚体和十二聚体 intasomes,以及其他特征不太明确的物种。这与组装独特的多聚体 intasomes的相关逆转录病毒不同,尽管 intasome 中的原体数量在不同病毒之间有所不同。因此,提出了额外的 Sso7d 结构域是否有助于 HIV-1 intasomes 异质性的问题。我们通过对野生型 HIV-1 IN 组装的 intasomes 的生化和结构研究来解决这个问题。负染和 cryo-EM 揭示了与 Sso7d-IN 相似的多聚体 intasome 物种范围,具有相同的常见核心架构。也可以看到来自结构域交换的 intasome 堆栈与野生型和 Sso7d-IN intasomes 都存在。组装多聚体 intasome 物种的倾向是 HIV-1 IN 的固有特性,而不是由 Sso7d 结构域的存在赋予的。最近报道的不同逆转录病毒物种的 intasome 结构,已被报道为四聚体、八聚体、十二聚体和十六聚体,突出了共同的 intasome 核心架构如何以不同的方式组装用于催化。