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| Item Type: | Article |
|---|---|
| Title: | Novel mechanism of C/EBPbeta (NF-M) transcriptional control: activation through derepression |
| Creators Name: | Kowenz-Leutz, E. and Twamley, G. and Ansieau, S. and Leutz, A. |
| Abstract: | Phosphorylation of transcription factors is regarded as a major mechanism to control their activity in regulation of gene expression. C/EBP beta is a transcription factor that becomes activated after phosphorylation to induce genes involved in inflammation, acute-phase response, cytokine expression, cell growth, and differentiation. The chicken homolog NF-M collaborates with Myb and various kinase oncogenes in normal myeloid differentiation as well as in the leukemic transformation of myelomonocytic cells. Here, we examined the structure of NF-M and its mechanism of activation. We show that NF-M is a repressed transcription factor with concealed activation potential. Derepressed NF-M exhibits enhanced transcriptional efficacy in reporter assays. More importantly, NF-M activates resident chromatin-embedded, myelomonocyte-specific target genes, even in heterologous cell types such as fibroblasts or erythroblasts. We identified two regions within NF-M that act to repress trans-activation. Repression is abolished by deletion of these regions, activation of signal transduction kinases including v-erbB, polyoma middle T, ras and mil/raf, or point mutation of a critical phosphorylation site for MAP kinases. We provide evidence that phosphorylation plays a unique role to derepress rather than to enhance the trans-activation domain as a novel mechanism to regulate gene expression by NF-M/C/EBP beta. |
| Keywords: | C/EBPbeta, Oncogenes, Transcription, Phosphorylation, Gene Activation, Animals, Chickens |
| Source: | Genes & Development |
| ISSN: | 0890-9369 |
| Publisher: | Cold Spring Harbor Laboratory Press |
| Volume: | 8 |
| Number: | 22 |
| Page Range: | 2781-2791 |
| Date: | 15 November 1994 |
| Official Publication: | https://doi.org/10.1101/gad.8.22.2781 |
| PubMed: | View item in PubMed |
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