Suzuki T, Kajino K, Masui N, Saito I, Miyamura T
Department of Enteroviruses, National Institute of Health, Tokyo, Japan.
Virology. 1990 Dec;179(2):881-5. doi: 10.1016/0042-6822(90)90160-s.
We identified a novel spliced RNA of 2.6 kb from a human hepatoma cell line HepG2 transfected with the hepatitis B virus (HBV) genome. The splicing acceptor site of the novel 2.6-kb RNA (position 489) was shown to be common to that of the previously described 2.1-kb spliced RNA which codes for an altered core antigen lacking the carboxy-terminal amino acid, cysteine. However, the donor site of the 2.6-kb RNA is different from any of the spliced RNA reported and located at 538 nucleotides (nt) downstream of the donor site of the 2.1-kb RNA. Introduction of single-base change mutations in the consensus sequence of the donor site of the 2.1-kb RNA maintained the splicing by using the cryptic donor site. The amount of the 2.6-kb spliced RNA was unchanged by these mutations. These results suggest independent regulations for the synthesis of the 2.1- and 2.6-kb spliced RNAs.
我们从转染了乙型肝炎病毒(HBV)基因组的人肝癌细胞系HepG2中鉴定出一种2.6 kb的新型剪接RNA。新型2.6 kb RNA的剪接受体位点(第489位)与先前描述的2.1 kb剪接RNA的剪接受体位点相同,后者编码一种缺失羧基末端氨基酸半胱氨酸的变异核心抗原。然而,2.6 kb RNA的供体位点与已报道的任何剪接RNA的供体位点都不同,位于2.1 kb RNA供体位点下游538个核苷酸(nt)处。在2.1 kb RNA供体位点的共有序列中引入单碱基变化突变,通过使用隐蔽供体位点维持了剪接。这些突变并未改变2.6 kb剪接RNA的量。这些结果表明2.1 kb和2.6 kb剪接RNA的合成存在独立调控。