Richt Jürgen A, Kasinathan Poothappillai, Hamir Amir N, Castilla Joaquin, Sathiyaseelan Thillai, Vargas Francisco, Sathiyaseelan Janaki, Wu Hua, Matsushita Hiroaki, Koster Julie, Kato Shinichiro, Ishida Isao, Soto Claudio, Robl James M, Kuroiwa Yoshimi
National Animal Disease Center, Agriculture Research Services, United States Department of Agriculture, 2300 Dayton Avenue, Ames, Iowa 50010, USA.
Nat Biotechnol. 2007 Jan;25(1):132-8. doi: 10.1038/nbt1271. Epub 2006 Dec 31.
Prion diseases are caused by propagation of misfolded forms of the normal cellular prion protein PrP(C), such as PrP(BSE) in bovine spongiform encephalopathy (BSE) in cattle and PrP(CJD) in Creutzfeldt-Jakob disease (CJD) in humans. Disruption of PrP(C) expression in mice, a species that does not naturally contract prion diseases, results in no apparent developmental abnormalities. However, the impact of ablating PrP(C) function in natural host species of prion diseases is unknown. Here we report the generation and characterization of PrP(C)-deficient cattle produced by a sequential gene-targeting system. At over 20 months of age, the cattle are clinically, physiologically, histopathologically, immunologically and reproductively normal. Brain tissue homogenates are resistant to prion propagation in vitro as assessed by protein misfolding cyclic amplification. PrP(C)-deficient cattle may be a useful model for prion research and could provide industrial bovine products free of prion proteins.
朊病毒疾病是由正常细胞朊病毒蛋白PrP(C)的错误折叠形式的传播引起的,例如牛海绵状脑病(BSE)中的PrP(BSE)和人类克雅氏病(CJD)中的PrP(CJD)。在小鼠(一种不会自然感染朊病毒疾病的物种)中破坏PrP(C)的表达,不会导致明显的发育异常。然而,在朊病毒疾病的天然宿主物种中消除PrP(C)功能的影响尚不清楚。在此,我们报告了通过连续基因靶向系统产生的PrP(C)缺陷牛及其特征。在超过20个月大时,这些牛在临床、生理、组织病理学、免疫和生殖方面均正常。通过蛋白质错误折叠循环扩增评估,脑组织匀浆在体外对朊病毒传播具有抗性。PrP(C)缺陷牛可能是朊病毒研究的有用模型,并可提供不含朊病毒蛋白的工业牛产品。