Chao Michael J, Gillis Tammy, Atwal Ranjit S, Mysore Jayalakshmi Srinidhi, Arjomand Jamshid, Harold Denise, Holmans Peter, Jones Lesley, Orth Michael, Myers Richard H, Kwak Seung, Wheeler Vanessa C, MacDonald Marcy E, Gusella James F, Lee Jong-Min
Molecular Neurogenetics Unit, Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA, USA.
Department of Neurology, Harvard Medical School, Boston, MA, USA.
Eur J Hum Genet. 2017 Nov;25(11):1202-1209. doi: 10.1038/ejhg.2017.125. Epub 2017 Aug 23.
Huntington's disease (HD) is an autosomal dominant neurodegenerative disease caused by expansion of a CAG trinucleotide repeat in HTT, resulting in an extended polyglutamine tract in huntingtin. We and others have previously determined that the HD-causing expansion occurs on multiple different haplotype backbones, reflecting more than one ancestral origin of the same type of mutation. In view of the therapeutic potential of mutant allele-specific gene silencing, we have compared and integrated two major systems of HTT haplotype definition, combining data from 74 sequence variants to identify the most frequent disease-associated and control chromosome backbones and revealing that there is potential for additional resolution of HD haplotypes. We have used the large collection of 4078 heterozygous HD subjects analyzed in our recent genome-wide association study of HD age at onset to estimate the frequency of these haplotypes in European subjects, finding that common genetic variation at HTT can distinguish the normal and CAG-expanded chromosomes for more than 95% of European HD individuals. As a resource for the HD research community, we have also determined the haplotypes present in a series of publicly available HD subject-derived fibroblasts, induced pluripotent cells, and embryonic stem cells in order to facilitate efforts to develop inclusive methods of allele-specific HTT silencing applicable to most HD patients. Our data providing genetic guidance for therapeutic gene-based targeting will significantly contribute to the developments of rational treatments and implementation of precision medicine in HD.
亨廷顿舞蹈症(HD)是一种常染色体显性神经退行性疾病,由HTT基因中CAG三核苷酸重复序列的扩增引起,导致亨廷顿蛋白中多聚谷氨酰胺序列延长。我们和其他人之前已经确定,导致HD的扩增发生在多个不同的单倍型骨架上,这反映了同一类型突变的多个祖先起源。鉴于突变等位基因特异性基因沉默的治疗潜力,我们比较并整合了HTT单倍型定义的两个主要系统,结合74个序列变体的数据,以识别最常见的与疾病相关的和对照染色体骨架,并揭示HD单倍型有进一步解析的潜力。我们利用在最近一项关于HD发病年龄的全基因组关联研究中分析的4078名杂合HD受试者的大量数据,来估计这些单倍型在欧洲受试者中的频率,发现HTT基因的常见遗传变异能够区分超过95%的欧洲HD个体的正常染色体和CAG扩增染色体。作为HD研究群体的一种资源,我们还确定了一系列公开可用的源自HD受试者的成纤维细胞、诱导多能干细胞和胚胎干细胞中的单倍型,以便于努力开发适用于大多数HD患者的等位基因特异性HTT沉默的包容性方法。我们提供基于治疗性基因靶向的遗传指导的数据,将显著有助于HD合理治疗的发展和精准医学的实施。