| First Author | Hunt A | Year | 2011 |
| Journal | Mol Cell Biol | Volume | 31 |
| Issue | 13 | Pages | 2544-51 |
| PubMed ID | 21536648 | Mgi Jnum | J:172659 |
| Mgi Id | MGI:5008507 | Doi | 10.1128/MCB.01458-10 |
| Citation | Hunt A, et al. (2011) Mtg16/Eto2 contributes to murine T-cell development. Mol Cell Biol 31(13):2544-51 |
| abstractText | Mtg16/Eto2 is a transcriptional corepressor that is disrupted by t(16;21) in acute myeloid leukemia. Using mice lacking Mtg16, we found that Mtg16 is a critical regulator of T-cell development. Deletion of Mtg16 led to reduced thymocyte development in vivo, and after competitive bone marrow transplantation, there was a nearly complete failure of Mtg16(-/-) cells to contribute to thymocyte development. This defect was recapitulated in vitro as Mtg16(-/-) Lineage(-)/Sca1(+)/c-Kit(+) (LSK) cells of the bone marrow or DN1 cells of the thymus failed to produce CD4(+)/CD8(+) cells in response to a Notch signal. Complementation of these defects by reexpressing Mtg16 showed that 3 highly conserved domains were somewhat dispensable for T-cell development but required the capacity of Mtg16 to suppress E2A-dependent transcriptional activation and to bind to the Notch intracellular domain. Thus, Mtg16 integrates the activities of signaling pathways and nuclear factors in the establishment of T-cell fate specification. |
