Rosson D, Dugan D, Reddy E P
Proc Natl Acad Sci U S A. 1987 May;84(10):3171-5. doi: 10.1073/pnas.84.10.3171.
Activation of the mouse c-myb oncogene in Abelson virus-induced plasmacytoid lymphosarcomas was studied using cDNA cloning and nucleotide sequence analysis. The results presented here show that viral integration in the myb locus generates splicing errors at the 5' and 3' regions. Viral integration results in transcriptional initiation within the viral long terminal repeat and generation of a chimeric mRNA that lacks the first three coding exons. The alterations at the 3' end are caused by an aberrant splicing event in which additional splice-donor and -acceptor sequences within intronic sequences are used to splice an additional 363 nucleotides into the myb transcripts. The resulting insertion of 121 amino acids is in a region of the protein where other activated forms of the myb gene product have deletions. These results suggest that alterations in the 3' end of the myb gene play a crucial role in the activation of this gene.
利用cDNA克隆和核苷酸序列分析技术，研究了阿贝尔森病毒诱导的浆细胞样淋巴瘤中小鼠c-myb癌基因的激活情况。本文给出的结果表明，病毒整合到myb基因座会在5'和3'区域产生剪接错误。病毒整合导致在病毒长末端重复序列内起始转录，并产生一种缺少前三个编码外显子的嵌合mRNA。3'端的改变是由异常剪接事件引起的，在该事件中，内含子序列中的额外剪接供体和受体序列被用于将另外363个核苷酸剪接到myb转录本中。由此产生的121个氨基酸的插入位于蛋白质的一个区域，在该区域myb基因产物的其他激活形式存在缺失。这些结果表明，myb基因3'端的改变在该基因的激活中起关键作用。
