Bohne Jens, Schambach Axel, Zychlinski Daniela
Experimental Hematology, Hannover Medical School, Carl-Neuberg-Strasse 1, OE 6960, D-30625 Hanover, Germany.
J Virol. 2007 Apr;81(7):3652-6. doi: 10.1128/JVI.02105-06. Epub 2007 Jan 17.
Alternative splicing has been recognized as a major mechanism for creating proteomic diversity from a limited number of genes. However, not all determinants regulating this process have been characterized. Using subviral human immunodeficiency virus (HIV) env constructs we observed an enhanced splicing of the RNA when expression was under control of the cytomegalovirus (CMV) promoter instead of the HIV long terminal repeat (LTR). We extended these observations to LTR- or CMV-driven murine leukemia proviruses, suggesting that retroviral LTRs are adapted to inefficient alternative splicing at most sites in order to maintain balanced gene expression.
可变剪接已被公认为是一种从有限数量的基因中产生蛋白质组多样性的主要机制。然而,并非所有调节这一过程的决定因素都已得到表征。利用亚病毒人类免疫缺陷病毒(HIV)env构建体,我们观察到当表达受巨细胞病毒(CMV)启动子而非HIV长末端重复序列(LTR)控制时,RNA的剪接受增强。我们将这些观察结果扩展到LTR驱动或CMV驱动的鼠白血病前病毒,这表明逆转录病毒LTR为了维持基因表达平衡,在大多数位点适应了低效的可变剪接。