Kim Kyoung Hoon, An Doo Ri, Yoon Hye Jin, Yang Jin Kuk, Suh Se Won
Department of Chemistry, College of Natural Sciences, Seoul National University, Seoul 151-742, Republic of Korea.
Department of Chemistry, College of Natural Sciences, Soongsil University, Seoul 156-743, Republic of Korea.
Acta Crystallogr F Struct Biol Commun. 2014 Sep;70(Pt 9):1173-9. doi: 10.1107/S2053230X14017385. Epub 2014 Aug 29.
The Rv2416c gene of Mycobacterium tuberculosis (Mtb) encodes the enhanced intracellular survival (Eis) protein that enhances intracellular survival of the pathogen in host macrophages during infection. The Mtb Eis protein is released into the cytoplasm of the phagocyte during intracellular infection and modulates the host immune response. It also contributes to drug resistance by acetylating multiple amine groups of aminoglycosides. Interestingly, the nonpathogenic M. smegmatis (Msm) contains a homologous eis gene (MSMEG_3513). The overall structures of Mtb Eis and Msm Eis are highly similar to each other, reflecting the high level (58%) of amino-acid sequence identity between them. Both Mtb Eis and Msm Eis are active as aminoglycoside acetyltransferases, while only Mtb Eis functions as an N(ℇ)-acetyltransferase to acetylate Lys55 of dual-specificity protein phosphatase 16 (DUSP16)/mitogen-activated protein kinase phosphatase 7 (MKP-7), leading to the suppression of host immune responses. Here, the crystal structure of Msm Eis in the paromomycin-bound form is reported, revealing detailed interactions between an aminoglycoside antibiotic and Msm Eis. The crystal structure of Msm Eis in the paromomycin-bound form has been determined at 3.3 Å resolution. This work provides potentially useful information for structure-guided discovery of Eis inhibitors as a novel antituberculosis drug against drug-resistant Mtb.
结核分枝杆菌(Mtb)的Rv2416c基因编码增强型细胞内存活(Eis)蛋白,该蛋白在感染期间可增强病原体在宿主巨噬细胞中的细胞内存活能力。Mtb Eis蛋白在细胞内感染期间释放到吞噬细胞的细胞质中,并调节宿主免疫反应。它还通过乙酰化氨基糖苷类的多个胺基来促进耐药性。有趣的是,非致病性耻垢分枝杆菌(Msm)含有一个同源的eis基因(MSMEG_3513)。Mtb Eis和Msm Eis的整体结构彼此高度相似,这反映了它们之间58%的高氨基酸序列同一性。Mtb Eis和Msm Eis均作为氨基糖苷类乙酰转移酶具有活性,而只有Mtb Eis作为N(ε)-乙酰转移酶,使双特异性蛋白磷酸酶16(DUSP16)/丝裂原活化蛋白激酶磷酸酶7(MKP-7)的Lys55乙酰化,从而导致宿主免疫反应受到抑制。在此,报道了与巴龙霉素结合形式的Msm Eis的晶体结构,揭示了氨基糖苷类抗生素与Msm Eis之间的详细相互作用。已确定与巴龙霉素结合形式的Msm Eis的晶体结构,分辨率为3.3 Å。这项工作为以结构为导向发现Eis抑制剂作为一种针对耐药Mtb的新型抗结核药物提供了潜在有用的信息。