Kattmann Dana, Klempnauer Karl-Heinz
Institut für Biochemie, Westfälische-Wilhelms-Universität Münster, Wilhelm-Klemm-Str. 2, D-48149 Münster, Germany.
Oncogene. 2002 Jul 11;21(30):4663-72. doi: 10.1038/sj.onc.1205579.
Numerous studies have shown that the retroviral oncogene v-myb encodes a transcription factor (v-Myb) which interferes with the differentiation program of myelomonocytic cells. It is generally thought that v-Myb deregulates the expression of specific target genes and thereby causes transformation of these cells. By using an estrogen-inducible version of v-Myb we have previously identified the gene for the chicken A2B adenosine receptor (A2B-AR), a member of the seven-pass transmembrane receptor superfamily, as a bona fide target gene for v-Myb. The chicken A2B-AR gene is expressed in v-myb transformed myeloblasts as well as in c-myb expressing erythroblasts, offering the opportunity to study how Myb transcription factors activate a target gene in two different hematopoietic lineages. Here, we report the characterization of the promoter of the A2B-AR gene. We show that the A2B-AR promoter region contains an exceptionally large number of Myb binding sites, many of which contribute to the Myb-inducibility of the promoter. The same sites were required for promoter activity in myelomonocytic and erythroid cells. In contrast to the promoters of other Myb target genes the A2B-AR promoter was not activated synergistically by Myb and other lineage-specific transcription factors that have been identified as Myb cooperation partners before. Taken together, our data suggest that the activation of the A2B-AR promoter by Myb depends on the simultaneous binding of a large number of Myb molecules.
众多研究表明,逆转录病毒癌基因v-myb编码一种转录因子(v-Myb),该因子会干扰骨髓单核细胞的分化程序。一般认为,v-Myb会使特定靶基因的表达失调,从而导致这些细胞发生转化。通过使用雌激素诱导型v-Myb,我们之前已将鸡A2B腺苷受体(A2B-AR)基因鉴定为v-Myb的一个真正靶基因,A2B-AR是七次跨膜受体超家族的成员。鸡A2B-AR基因在v-myb转化的成髓细胞以及表达c-myb的成红细胞中均有表达,这为研究Myb转录因子如何在两种不同造血谱系中激活靶基因提供了机会。在此,我们报告了A2B-AR基因启动子的特征。我们发现,A2B-AR启动子区域含有异常大量的Myb结合位点,其中许多位点有助于启动子的Myb诱导性。骨髓单核细胞和红细胞中的启动子活性需要相同的位点。与其他Myb靶基因的启动子不同,A2B-AR启动子不会被Myb和其他之前已被鉴定为Myb合作伙伴的谱系特异性转录因子协同激活。综上所述,我们的数据表明,Myb对A2B-AR启动子的激活取决于大量Myb分子的同时结合。