| Literature DB >> 29606351 |
Sen Yan1, Zhuchi Tu1, Zhaoming Liu2, Nana Fan2, Huiming Yang3, Su Yang3, Weili Yang1, Yu Zhao2, Zhen Ouyang2, Chengdan Lai2, Huaqiang Yang2, Li Li2, Qishuai Liu2, Hui Shi2, Guangqing Xu4, Heng Zhao5, Hongjiang Wei5, Zhong Pei4, Shihua Li6, Liangxue Lai7, Xiao-Jiang Li8.
Abstract
Huntington's disease (HD) is characterized by preferential loss of the medium spiny neurons in the striatum. Using CRISPR/Cas9 and somatic nuclear transfer technology, we established a knockin (KI) pig model of HD that endogenously expresses full-length mutant huntingtin (HTT). By breeding this HD pig model, we have successfully obtained F1 and F2 generation KI pigs. Characterization of founder and F1 KI pigs shows consistent movement, behavioral abnormalities, and early death, which are germline transmittable. More importantly, brains of HD KI pig display striking and selective degeneration of striatal medium spiny neurons. Thus, using a large animal model of HD, we demonstrate for the first time that overt and selective neurodegeneration seen in HD patients can be recapitulated by endogenously expressed mutant proteins in large mammals, a finding that also underscores the importance of using large mammals to investigate the pathogenesis of neurodegenerative diseases and their therapeutics.Entities:
Keywords: CRISPR/Cas9; huntingtin; knockin; large animal; neurodegeneration; polyglutamine; striatum
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Year: 2018 PMID: 29606351 PMCID: PMC5935586 DOI: 10.1016/j.cell.2018.03.005
Source DB: PubMed Journal: Cell ISSN: 0092-8674 Impact factor: 41.582