| First Author | Ragone G | Year | 2009 |
| Journal | Oncogene | Volume | 28 |
| Issue | 10 | Pages | 1329-38 |
| PubMed ID | 19169282 | Mgi Jnum | J:157374 |
| Mgi Id | MGI:4430713 | Doi | 10.1038/onc.2008.489 |
| Citation | Ragone G, et al. (2009) The Tcl1 oncogene defines secondary hair germ cells differentiation at catagen-telogen transition and affects stem-cell marker CD34 expression. Oncogene 28(10):1329-38 |
| abstractText | Overexpression of the TCL1 gene family plays a role in the onset of T-cell leukemias in mice and in humans. The Tcl1 gene is tightly regulated during early embryogenesis in which it participates in embryonic stem (ES)-cells proliferation and during lymphoid differentiation. Here, we provide evidences that Tcl1 is also important in mouse hair follicle (HF) and skin homeostasis. We found that Tcl1(-/-) adult mice exhibit hair loss, leading to alopecia with extensive skin lesions. By analysing Tcl1 expression in the wild-type (wt) skin through different stages of hair differentiation, we observe high levels in the secondary hair germ (HG) cells and hair bulges, during early anagen and catagen-telogen transition phases. The loss of Tcl1 does not result in apparent skin morphological defects during embryonic development and at birth, but its absence causes a reduction of proliferation in anagen HFs. Importantly, we show the that absence of Tcl1 induces a significant loss of the stem-cell marker CD34 (but not alpha6-integrin) expression in the bulge cells, which is necessary to maintain stem-cell characteristics. Therefore, our findings indicate that Tcl1 gene(s) might have important roles in hair formation, by its involvement in cycling and self-renewal of transient amplifying (TA) and stem-cell (SC) populations. |
