Siddiqui J F, Van Mater D, Sowden M P, Smith H C
Department of Biochemistry and Biophysics, Health Science, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Rochester, New York 14642, USA.
Exp Cell Res. 1999 Oct 10;252(1):154-64. doi: 10.1006/excr.1999.4598.
Apolipoprotein B (apoB) mRNA editing is a site-specific (nucleotide 6666) cytidine to uridine transition catalyzed by a cytidine deaminase, APOBEC-1, in the context of a multiprotein complex referred to as the C/U editosome. This report quantifies for the first time the effect of altering APOBEC-1 protein abundance on the proportion of edited apoB mRNAs using transfected McArdle rat hepatoma cells which had been sorted by flow cytometry into populations expressing different levels of green fluorescent protein-APOBEC-1 chimera, GFP-APOBEC. A correlation was observed in which increased expression of GFP-APOBEC protein resulted in a higher proportion of edited apoB mRNA. The number of enzyme molecules required to increase the proportion of edited apoB RNAs was disproportionately high relative to that which might have been predicted from a typical catalytic relationship. Moreover, editing of apoB mRNA at inappropriate sites (promiscuous editing) occurred in response to overexpressing GFP-APOBEC. The data suggest that experimental manipulation of APOBEC-1 abundance in the absence of other regulatory considerations will always result in some level of promiscuous editing. Coordinate expression of APOBEC-1 and the auxiliary proteins and/or regulation of their interactions may be required to increase editing activity without losing editing-site fidelity.
载脂蛋白B(apoB)信使核糖核酸(mRNA)编辑是一种位点特异性(核苷酸6666)的胞苷向尿苷的转变,由胞苷脱氨酶APOBEC-1在一种被称为C/U编辑体的多蛋白复合物的背景下催化。本报告首次使用经流式细胞术分选成表达不同水平绿色荧光蛋白-APOBEC-1嵌合体(GFP-APOBEC)的群体的转染麦克阿德尔大鼠肝癌细胞,量化了改变APOBEC-1蛋白丰度对编辑后的apoB mRNA比例的影响。观察到一种相关性,即GFP-APOBEC蛋白表达增加导致编辑后的apoB mRNA比例更高。相对于从典型催化关系中可能预测到的数量,增加编辑后的apoB RNA比例所需的酶分子数量高得不成比例。此外,响应于GFP-APOBEC的过表达,apoB mRNA在不适当的位点发生编辑(乱序编辑)。数据表明,在没有其他调控因素的情况下,对APOBEC-1丰度进行实验操作将总是导致一定程度的乱序编辑。可能需要APOBEC-1与辅助蛋白的协调表达和/或对它们相互作用的调控,以增加编辑活性而不丧失编辑位点的保真度。