期刊
VIROLOGY
卷 428, 期 1, 页码 58-63出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2012.03.004
关键词
Forward genetics; AAV5; Furin; Toxin; CHO cells; Anthrax
类别
资金
- National Institute of Health, National Institute of Dental and Craniofacial Research
- Molecular Physiology and Therapeutics Branch, National Institute of Dental and Craniofacial Research
- National Institute of Allergy and Infectious Diseases
Due to its non-pathogenic lifecycle, little is known about the cellular determinants of infection by adeno-associated virus (AAV). To identify these critical cellular factors, we took advantage of the gene transfer abilities of AAV in combination with a forward genetic selection to identify proteins critical for transduction by this virus. AAV serotype 5 (AAV5) vectors encoding the furin gene were used to transduce furin-deficient cells followed by selection with furin-dependent toxins. A population of cells specifically resistant to AAV5 transduction was identified and sequence analysis suggested all had a single amino acid mutation in the leader sequence of the platelet-derived growth factor receptor alpha (PDGFR alpha) gene. Characterization of this mutation suggested it inhibited PDGFR alpha trafficking resulting in limited expression on the plasma membrane. Mutagenesis and transfection experiments confirmed the effect of this mutation on PDGFR alpha trafficking, and the AAV5 resistant phenotype could be rescued by transfection with wild type PDGFR alpha. Published by Elsevier Inc.
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