Olivares Eric C, Hollis Roger P, Chalberg Thomas W, Meuse Leonard, Kay Mark A, Calos Michele P
Department of Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA.
Nat Biotechnol. 2002 Nov;20(11):1124-8. doi: 10.1038/nbt753. Epub 2002 Oct 15.
We used the integrase from phage phiC31 to integrate the human Factor IX (hFIX) gene permanently into specific sites in the mouse genome. A plasmid containing attB and an expression cassette for hFIX was delivered to the livers of mice by using high-pressure tail vein injection. When an integrase expression plasmid was co-injected, hFIX serum levels increased more than tenfold to approximately 4 microg/ml, similar to normal FIX levels, and remained stable throughout the more than eight months of the experiment. hFIX levels persisted after partial hepatectomy, suggesting genomic integration of the vector. Site-specific integration was proven by characterizing and quantifying genomic integration in the liver at the DNA level. Integration was documented at two pseudo-attP sites, native sequences with partial identity to attP, with one site highly predominant. This study demonstrates in vivo gene transfer in an animal by site-specific genomic integration.
我们使用噬菌体phiC31的整合酶将人凝血因子IX(hFIX)基因永久性地整合到小鼠基因组的特定位点。通过高压尾静脉注射,将含有attB和hFIX表达盒的质粒导入小鼠肝脏。当共注射整合酶表达质粒时,hFIX血清水平增加了十多倍,达到约4微克/毫升,与正常FIX水平相似,并且在超过八个月的实验过程中保持稳定。部分肝切除术后hFIX水平持续存在,表明载体已整合到基因组中。通过在DNA水平上对肝脏中的基因组整合进行表征和定量,证实了位点特异性整合。在两个假attP位点记录到了整合,这两个位点是与attP具有部分同源性的天然序列,其中一个位点占主导地位。本研究通过位点特异性基因组整合证明了在动物体内进行基因转移。