Chitrala Kumaraswamy Naidu, Nagarkatti Prakash, Nagarkatti Mitzi
Dept. of Pathology, Microbiology and Immunology, University of South Carolina School of Medicine, Columbia, SC, 29208, USA; Fels Cancer Institute for Personalized Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA.
Dept. of Pathology, Microbiology and Immunology, University of South Carolina School of Medicine, Columbia, SC, 29208, USA.
J Psychiatr Res. 2021 Jun;138:207-218. doi: 10.1016/j.jpsychires.2021.03.048. Epub 2021 Mar 31.
Post-traumatic stress disorder (PTSD) is one of the prevalent neurological disorder which is drawing increased attention over the past few decades. Major risk factors for PTSD can be categorized into environmental and genetic factors. Among the genetic risk factors, polymorphisms in the catechol-O-methyltransferase (COMT) gene is known to be associated with the risk for PTSD. In the present study, we analysed the impact of deleterious single nucleotide polymorphisms (SNPs) in the COMT gene conferring risk to PTSD using computational based approaches followed by molecular dynamic simulations. The data on COMT gene associated with PTSD were collected from several databases including Online Mendelian Inheritance in Man (OMIM) search. Datasets related to SNP were downloaded from the dbSNP database. To study the structural and dynamic effects of COMT wild type and mutant forms, we performed molecular dynamics simulations (MD simulations) at a time scale of 300 ns. Results from screening the SNPs using the computational tools SIFT and Polyphen-2 demonstrated that the SNP rs4680 (V158M) in COMT has a deleterious effect with phenotype in PTSD. Results from the MD simulations showed that there is some major fluctuations in the structural features including root mean square deviation (RMSD), radius of gyration (Rg), root mean square fluctuation (RMSF) and secondary structural elements including α-helices, sheets and turns between wild-type (WT) and mutant forms of COMT protein. In conclusion, our study provides novel insights into the deleterious effects and impact of V158M mutation on COMT protein structure which plays a key role in PTSD.
创伤后应激障碍(PTSD)是一种常见的神经疾病,在过去几十年中受到越来越多的关注。PTSD的主要风险因素可分为环境因素和遗传因素。在遗传风险因素中,儿茶酚-O-甲基转移酶(COMT)基因的多态性与PTSD风险相关。在本研究中,我们使用基于计算的方法,随后进行分子动力学模拟,分析了COMT基因中有害单核苷酸多态性(SNP)对PTSD风险的影响。从包括在线人类孟德尔遗传(OMIM)搜索在内的几个数据库中收集了与PTSD相关的COMT基因数据。与SNP相关的数据集从dbSNP数据库下载。为了研究COMT野生型和突变型的结构和动力学效应,我们在300 ns的时间尺度上进行了分子动力学模拟(MD模拟)。使用计算工具SIFT和Polyphen-2筛选SNP的结果表明,COMT中的SNP rs4680(V158M)对PTSD的表型有有害影响。MD模拟结果表明,野生型(WT)和突变型COMT蛋白之间的结构特征包括均方根偏差(RMSD)、回转半径(Rg)、均方根波动(RMSF)以及包括α螺旋、片层和转角在内的二级结构元素存在一些主要波动。总之,我们的研究为V158M突变对COMT蛋白结构的有害影响和作用提供了新的见解,而COMT蛋白结构在PTSD中起关键作用。