O'Rourke John P, Ness Scott A
Department of Molecular Genetics & Microbiology, MSC08 4660, 1 University of New Mexico, Albuquerque, NM 87131-0001, USA.
Mol Cell Biol. 2008 Mar;28(6):2091-101. doi: 10.1128/MCB.01870-07. Epub 2008 Jan 14.
The c-Myb transcription factor regulates the proliferation and differentiation of hematopoietic cells, and activated alleles of c-myb induce leukemias and lymphomas in animals. Relatively minor changes in the structure of c-Myb protein change the genes that it regulates and can unleash its latent transforming activities. Here, quantitative assays were used to analyze the alternative splicing of human c-myb transcripts. We identified an array of variant transcripts, expressed in highly regulated, lineage-specific patterns, that were formed through the use of alternate exons 8A, 9A, 9B, 10A, 13A, and 14A. Expression levels of the different splice variant transcripts were regulated independently of one another during human hematopoietic cell differentiation, and the alternative splicing of c-myb mRNAs was increased in primary leukemia samples. The alternatively spliced c-myb transcripts were associated with polysomes and encoded a series of c-Myb proteins with identical DNA binding domains but unique C-terminal domains. In several types of assays, the variant c-Myb proteins exhibited quantitative and qualitative differences in transcriptional activities and specificities. The results suggest that the human c-myb gene encodes a family of related proteins with different transcriptional activities. Enhanced alternative splicing may be a mechanism for unmasking the transforming activity of c-myb in human leukemias.
c-Myb转录因子调节造血细胞的增殖和分化,c-myb的激活等位基因可在动物体内诱发白血病和淋巴瘤。c-Myb蛋白结构中相对较小的变化会改变其调控的基因,并可能释放其潜在的转化活性。在此,我们使用定量分析方法来分析人类c-myb转录本的可变剪接。我们鉴定出一系列以高度调控的、谱系特异性模式表达的可变转录本,它们是通过使用外显子8A、9A、9B、10A、13A和14A形成的。在人类造血细胞分化过程中,不同剪接变体转录本的表达水平相互独立调控,并且在原发性白血病样本中c-myb mRNA的可变剪接增加。可变剪接的c-myb转录本与多核糖体相关,并编码一系列具有相同DNA结合结构域但独特C末端结构域的c-Myb蛋白。在几种类型的分析中,变体c-Myb蛋白在转录活性和特异性方面表现出数量和质量上的差异。结果表明,人类c-myb基因编码一个具有不同转录活性的相关蛋白家族。增强的可变剪接可能是在人类白血病中揭示c-myb转化活性的一种机制。