Schirm S, Moscovici G, Bishop J M
Department of Microbiology and Immunology, University of California Medical Center, San Francisco 94143.
J Virol. 1990 Feb;64(2):767-73. doi: 10.1128/JVI.64.2.767-773.1990.
The oncogene v-myb of avian myeloblastosis virus is expressed from an mRNA that arises by splicing of the viral genome. In previous work, we described a mutant strain of avian myeloblastosis virus (tsAMV) that elicits temperature-sensitive transformation and suggested that the mutation affects production of the mRNA for v-myb. We now report that the principal determinant of the biochemical phenotype of tsAMV is a point mutation located in a crucial region of the splice acceptor site for v-myb mRNA. The mutation reduces v-myb mRNA production but could account for the conditional phenotype only in combination with an independent effect of temperature on the splicing of both wild-type and mutant viral RNAs, which we also describe here. Our findings dramatize the manner in which retroviruses normally control the splicing of their RNAs and implicate the sequence of the splice acceptor site in the control.
禽成髓细胞瘤病毒的致癌基因v-myb由通过病毒基因组剪接产生的mRNA表达。在先前的工作中,我们描述了一种禽成髓细胞瘤病毒的突变株(tsAMV),它引发温度敏感型转化,并表明该突变影响v-myb mRNA的产生。我们现在报告,tsAMV生化表型的主要决定因素是位于v-myb mRNA剪接受体位点关键区域的一个点突变。该突变减少了v-myb mRNA的产生,但只有与温度对野生型和突变型病毒RNA剪接的独立影响相结合,才能解释这种条件表型,我们在此也描述了这种影响。我们的发现凸显了逆转录病毒通常控制其RNA剪接的方式,并表明剪接受体位点的序列参与了这种控制。