Gilski Miroslaw, Kazmierczyk Maciej, Krzywda Szymon, Zábranská Helena, Cooper Seth, Popović Zoran, Khatib Firas, DiMaio Frank, Thompson James, Baker David, Pichová Iva, Jaskolski Mariusz
Department of Crystallography, Faculty of Chemistry, A. Mickiewicz University, 60-780 Poznan, Poland.
Acta Crystallogr D Biol Crystallogr. 2011 Nov;67(Pt 11):907-14. doi: 10.1107/S0907444911035943. Epub 2011 Oct 19.
Mason-Pfizer monkey virus (M-PMV), a D-type retrovirus assembling in the cytoplasm, causes simian acquired immunodeficiency syndrome (SAIDS) in rhesus monkeys. Its pepsin-like aspartic protease (retropepsin) is an integral part of the expressed retroviral polyproteins. As in all retroviral life cycles, release and dimerization of the protease (PR) is strictly required for polyprotein processing and virion maturation. Biophysical and NMR studies have indicated that in the absence of substrates or inhibitors M-PMV PR should fold into a stable monomer, but the crystal structure of this protein could not be solved by molecular replacement despite countless attempts. Ultimately, a solution was obtained in mr-rosetta using a model constructed by players of the online protein-folding game Foldit. The structure indeed shows a monomeric protein, with the N- and C-termini completely disordered. On the other hand, the flap loop, which normally gates access to the active site of homodimeric retropepsins, is clearly traceable in the electron density. The flap has an unusual curled shape and a different orientation from both the open and closed states known from dimeric retropepsins. The overall fold of the protein follows the retropepsin canon, but the C(α) deviations are large and the active-site 'DTG' loop (here NTG) deviates up to 2.7 Å from the standard conformation. This structure of a monomeric retropepsin determined at high resolution (1.6 Å) provides important extra information for the design of dimerization inhibitors that might be developed as drugs for the treatment of retroviral infections, including AIDS.
梅森 - 辉瑞猴病毒(M-PMV)是一种在细胞质中组装的D型逆转录病毒,可导致恒河猴患猿猴获得性免疫缺陷综合征(SAIDS)。其胃蛋白酶样天冬氨酸蛋白酶(逆转胃蛋白酶)是所表达的逆转录病毒多蛋白的一个组成部分。与所有逆转录病毒生命周期一样,蛋白酶(PR)的释放和二聚化对于多蛋白加工和病毒体成熟是严格必需的。生物物理和核磁共振研究表明,在没有底物或抑制剂的情况下,M-PMV PR应折叠成稳定的单体,但尽管进行了无数次尝试,该蛋白的晶体结构仍无法通过分子置换法解析。最终,使用在线蛋白质折叠游戏Foldit的玩家构建的模型,在mr-rosetta中获得了解决方案。该结构确实显示为单体蛋白,其N端和C端完全无序。另一方面,通常控制同二聚体逆转胃蛋白酶活性位点通道的瓣环在电子密度中清晰可辨。该瓣具有不寻常的卷曲形状,且与二聚体逆转胃蛋白酶已知的开放和关闭状态的取向不同。该蛋白的整体折叠遵循逆转胃蛋白酶规则,但C(α)偏差较大,活性位点“DTG”环(此处为NTG)与标准构象的偏差高达2.7 Å。这种高分辨率(1.6 Å)测定的单体逆转胃蛋白酶结构为设计二聚化抑制剂提供了重要的额外信息,这些抑制剂可能被开发为治疗包括艾滋病在内的逆转录病毒感染的药物。