| First Author | Pohlers M | Year | 2005 |
| Journal | Curr Biol | Volume | 15 |
| Issue | 11 | Pages | 1051-7 |
| PubMed ID | 15936277 | Mgi Jnum | J:99185 |
| Mgi Id | MGI:3581455 | Doi | 10.1016/j.cub.2005.04.060 |
| Citation | Pohlers M, et al. (2005) A role for E2F6 in the restriction of male-germ-cell-specific gene expression. Curr Biol 15(11):1051-7 |
| abstractText | E2F transcription factors play a pivotal role in the regulation of cellular proliferation and can be subdivided into activating and repressing family members [1]. Like other E2Fs, E2F6 binds to E2F consensus sites, but in contrast to E2F1-5, it lacks an Rb binding domain and functions as an Rb-independent transcriptional repressor [2, 3, 4 and 5]. Instead, E2F6 has been shown to complex with Polycomb (PcG) group proteins [6 and 7], which have a well-established role in gene silencing. Here, we show that E2F6 plays an unexpected and essential role in the tissue specificity of gene expression. E2F6-deficient mice ubiquitously express the alpha-tubulin 3 and 7 genes, which are expressed strictly testis-specifically in control mice. Like an additional E2F6 target gene, Tex12, that we identified, tubulin 3 and 7 are normally expressed in male germ cells only. The promoters of the alpha-tubulin and Tex12 genes share a perfectly conserved E2F site, which E2F6 binds to. Mechanistically, E2F6-mediated repression involves CpG hypermethylation locking target promoters in an inactive state. Thus, E2F6 is essential for the long-term somatic silencing of certain male-germ-cell-specific genes, but it is dispensable for cell-cycle regulation. |
