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Characterization of hGFAP-DsRed Transgenic Guangxi Bama Mini-Pigs and Their Offspring

Characterization of hGFAP-DsRed Transgenic Guangxi Bama Mini-Pigs and Their Offspring

Xiangxing Zhu1, Junyu Nie1, Shouneng Quan1,2, Huiyan Xu1, Xiaogan Yang1, Yangqing Lu1, Kehuan Lu1 and Shengsheng Lu1*

1State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources, Guangxi High Education Key Laboratory for Animal Reproduction and Biotechnology, and College of Animal Science and Technology, Guangxi University, Nanning 530004, China
2Reproductive Medicine Center of Guigang City People’s Hospital, Guigang 537100, China

* Corresponding author: shengshenglu@sina.com

 

 

ABSTRACT

Astrocytes, the most abundant cell type in the mammalian central nervous system (CNS), perform many important neurobiological functions. Although a large number of transgenic mouse models carrying astrocyte-specific transgene expression of transgene have made significant contributions to understanding astrocytic structure and function in vitro and in vivo, evidence suggests that mouse models are limited and sometimes do not fully replicate the complete spectrum of neurological phenotypes seen in human diseases. On the contrary, pigs, especially mini-pigs, show exciting potential for modeling human CNS diseases due to similarities in body size, anatomy, life span, CNS structure and neurobiology. Previously, via the somatic cell nuclear transfer technique, we successfully generated transgenic Guangxi Bama mini-pigs carrying a fluorescent protein (DsRed) reporter gene regulated by the 2.2-kb human glial fibrillary acidic protein promoter (hGFAP-DsRed). This study characterized transgene expression in such transgenic Guangxi Bama mini-pigs and their offspring. Our findings indicate that the hGFAP promoter contains matching regulatory elements for directing specific expression in porcine astrocytes. However, the practical application of hGFAP-DsRed transgenic Guangxi Bama mini-pigs in neuroscience research requires solving the germline transmission problem of the phenotype.

 

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