| First Author | Hutchins AS | Year | 2002 |
| Journal | Mol Cell | Volume | 10 |
| Issue | 1 | Pages | 81-91 |
| PubMed ID | 12150909 | Mgi Jnum | J:126178 |
| Mgi Id | MGI:3760681 | Doi | 10.1016/s1097-2765(02)00564-6 |
| Citation | Hutchins AS, et al. (2002) Gene silencing quantitatively controls the function of a developmental trans-activator. Mol Cell 10(1):81-91 |
| abstractText | How a single cell gives rise to progeny with differing fates remains poorly understood. We examined cells lacking methyl CpG binding domain protein-2 (MBD2), a molecule that has been proposed to link DNA methylation to silent chromatin. Helper T cells from Mbd2(-/-) mice exhibit disordered differentiation. IL-4, the signature of a restricted set of progeny, is expressed ectopically in Mbd2(-/-) parent and daughter cells. Loss of MBD2-mediated silencing renders the normally essential activator, Gata-3, dispensable for IL-4 induction. Gata-3 and MBD2 act in competition, wherein each factor independently, and quantitatively, regulates the binary choice of whether heritable IL-4 expression is established. Gata-3 functions, in part, to displace MBD2 from methylated DNA. These results suggest that activating and silencing signals integrate to provide spatially and temporally restricted patterns of gene activity. |
