Wood T G, McGeady M L, Baroudy B M, Blair D G, Vande Woude G F
Proc Natl Acad Sci U S A. 1984 Dec;81(24):7817-21. doi: 10.1073/pnas.81.24.7817.
Although the molecularly cloned mouse c-mos oncogene locus can be efficiently activated by insertion of a retroviral long terminal repeat (LTR) 5' to its coding region, only low-frequency transformation occurs with the LTR element inserted 3' to this region. Analysis of several of the latter transformed cell lines suggested that loss of 2 kilobases (kb) of normal mouse DNA sequences preceding c-mos was required for oncogene activation. The determination of the transforming potential of deletion mutants containing only portions of this region followed by analysis of their nucleotide sequences identified a region termed upstream mouse sequence (UMS) as a cis-acting locus that prevents c-mos activation by a 3' LTR. The UMS region is approximately 1 kb in length and is located 0.8-1.8 kb upstream from the first ATG in the open reading frame of c-mos. Insertion of UMS 5' to the v-mos coding region also prevents 3' LTR enhancement of its transforming activity, but this inhibition is position dependent and functions only when inserted between v-mos and its putative promoter. The results presented here suggest that UMS may function to regulate c-mos proto-oncogene expression and may explain the lack of detectable c-mos transcripts in normal mouse cells.
尽管分子克隆的小鼠c-mos癌基因位点可通过在其编码区5'端插入逆转录病毒长末端重复序列（LTR）而被有效激活，但当LTR元件插入该区域3'端时，仅发生低频转化。对几种后一种转化细胞系的分析表明，c-mos之前正常小鼠DNA序列缺失2千碱基（kb）是癌基因激活所必需的。对仅包含该区域部分的缺失突变体的转化潜能进行测定，随后分析其核苷酸序列，确定了一个称为上游小鼠序列（UMS）的区域，它是一个顺式作用位点，可阻止3' LTR激活c-mos。UMS区域长度约为1 kb，位于c-mos开放阅读框中第一个ATG上游0.8 - 1.8 kb处。将UMS插入v-mos编码区5'端也可阻止3' LTR增强其转化活性，但这种抑制作用依赖于位置，且仅当插入v-mos与其假定启动子之间时才起作用。本文给出的结果表明，UMS可能起到调节c-mos原癌基因表达的作用，并且可能解释正常小鼠细胞中检测不到c-mos转录本的原因。
