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秀丽隐杆线虫ZK177.8蛋白的生化功能与结构:艾卡迪-古铁雷斯综合征SAMHD1 dNTP酶直系同源物

Biochemical functions and structure of Caenorhabditis elegans ZK177.8 protein: Aicardi-Goutières syndrome SAMHD1 dNTPase ortholog.

作者信息

Maehigashi Tatsuya, Lim Christopher, Wade Lydia R, Bowen Nicole E, Knecht Kirsten M, Alvarez Natalie N, Kelly William G, Schinazi Raymond F, Kim Dong-Hyun, Xiong Yong, Kim Baek

机构信息

Department of Pediatrics, School of Medicine, Emory University, Atlanta, Georgia, USA.

Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, Connecticut, USA.

出版信息

J Biol Chem. 2023 Sep;299(9):105148. doi: 10.1016/j.jbc.2023.105148. Epub 2023 Aug 9.

Abstract

Mutations in sterile alpha motif domain and histidine-aspartate domain-containing protein 1 (SAMHD1) are found in a neurodevelopmental disorder, Aicardi-Goutières syndrome, and cancers, and SAMHD1, which is a deoxynucleoside triphosphate (dNTP) triphosphorylase, was identified as a myeloid-specific HIV-1 restriction factor. Here, we characterized the enzymology and structure of an SAMHD1 ortholog of Caenorhabditis elegans, ZK177.8, which also reportedly induces developmental defects upon gene knockdown. We found ZK177.8 protein is a dNTPase allosterically regulated by dGTP. The active site of ZK177.8 recognizes both 2' OH and triphosphate moieties of dNTPs but not base moiety. The dGTP activator induces the formation of the enzymatically active ZK177.8 tetramers, and ZK177.8 protein lowers cellular dNTP levels in a human monocytic cell line. Finally, ZK177.8 tetramers display very similar X-ray crystal structure with human and mouse SAMHD1s except that its lack of the canonical sterile alpha motif domain. This striking conservation in structure, function, and allosteric regulatory mechanism for the hydrolysis of the DNA building blocks supports their host developmental roles.

摘要

在一种神经发育障碍——艾卡迪-古铁雷斯综合征以及癌症中发现了含无菌α基序结构域和组氨酸-天冬氨酸结构域蛋白1(SAMHD1)的突变,并且SAMHD1作为一种脱氧核苷三磷酸(dNTP)三磷酸酶,被鉴定为一种髓系特异性HIV-1限制因子。在此,我们对秀丽隐杆线虫的SAMHD1直系同源物ZK177.8的酶学和结构进行了表征,据报道该同源物在基因敲低时也会诱导发育缺陷。我们发现ZK177.8蛋白是一种受dGTP变构调节的dNTP酶。ZK177.8的活性位点识别dNTP的2'-OH和三磷酸基团,但不识别碱基基团。dGTP激活剂诱导形成具有酶活性的ZK177.8四聚体,并且ZK177.8蛋白可降低人单核细胞系中的细胞dNTP水平。最后,ZK177.8四聚体与人和小鼠的SAMHD1显示出非常相似的X射线晶体结构,只是它缺乏典型的无菌α基序结构域。DNA构建模块水解在结构、功能和变构调节机制上的这种显著保守性支持了它们在宿主发育中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b61/10485159/94212c32003e/gr1.jpg

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