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Transcriptional activation by the myb proteins requires a specific local promoter structure Ganter B; Chao ST; Lipsick JSFEBS Lett 1999[Nov]; 460 (3): 401-10The biological effects of the cellular c-Myb and the viral v-Myb proteins are strikingly different. While c-Myb is indispensable for normal hematopoiesis, v-Myb induces acute leukemia. The v-Myb DNA-binding domain (DBD) differs from that of c-Myb mainly by deletion of the first of three repeats which correlates with efficient oncogenic transformation and a decrease in DNA-binding activity. To investigate the difference in DNA-binding and transcriptional activation, oligonucleotide selection and electrophoretic mobility shift assays were employed. The v-Myb DBD (R2R3) shows an intrinsic DNA-binding specificity for an AT-rich downstream extension of the Myb recognition element (MRE) PyAAC(T)/(G)G for efficient binding to this site, whereas R1 within the c-Myb DBD allows for more flexibility for this downstream extension. Therefore, due to the presence of repeat R1, c-Myb can bind to a greater number of target sites. The intrinsic DNA-binding specificity of R2R3 is further supported with the results from in vivo transcriptional activation experiments which demonstrated that both the v-Myb and c-Myb DBDs require an extension of the MRE (motif #1) by a downstream T-stretch (motif #2) for full activity. Surprisingly, the T-stretch improves binding when present on either strand, but is required on a specific strand for transcriptional activation.|Animals[MESH]|Binding Sites/genetics[MESH]|Cells, Cultured[MESH]|DNA, Viral/metabolism[MESH]|DNA-Binding Proteins/metabolism[MESH]|Oncogene Proteins v-myb/*physiology[MESH]|Promoter Regions, Genetic/*genetics[MESH]|Protein Binding/genetics[MESH]|Proto-Oncogene Proteins c-myb/*physiology[MESH]|Quail[MESH]|Regulatory Sequences, Nucleic Acid/genetics[MESH]|Transcriptional Activation/*genetics[MESH] |
