| First Author | Liu J | Year | 2011 |
| Journal | Proc Natl Acad Sci U S A | Volume | 108 |
| Issue | 35 | Pages | 14560-5 |
| PubMed ID | 21841138 | Mgi Jnum | J:175236 |
| Mgi Id | MGI:5285016 | Doi | 10.1073/pnas.1111056108 |
| Citation | Liu J, et al. (2011) Regenerative phenotype in mice with a point mutation in transforming growth factor {beta} type I receptor (TGFBR1). Proc Natl Acad Sci U S A 108(35):14560-5 |
| abstractText | Regeneration of peripheral differentiated tissue in mammals is rare, and regulators of this process are largely unknown. We carried out a forward genetic screen in mice using N-ethyl-N-nitrosourea mutagenesis to identify genetic mutations that affect regenerative healing in vivo. More than 400 pedigrees were screened for closure of a through-and-through punch wound in the mouse ear. This led to the identification of a single pedigree with a heritable, fast, and regenerative wound-healing phenotype. Within 5 wk after ear-punch, a threefold decrease in the diameter of the wound was observed in the mutant mice compared with the wild-type mice. At 22 wk, new cartilage, hair follicles, and sebaceous glands were observed in the newly generated tissue. This trait was mapped to a point mutation in a receptor for TGF-beta, TGFBR1. Mouse embryonic fibroblasts from the affected mice had increased expression of a subset of TGF-beta target genes, suggesting that the mutation caused partial activation of the receptor. Further, bone marrow stromal cells from the mutant mice more readily differentiated to chondrogenic precursors, providing a plausible explanation for the enhanced development of cartilage islands in the regenerated ears. This mutant mouse strain provides a unique model to further explore regeneration in mammals and, in particular, the role of TGFBR1 in chondrogenesis and regenerative wound healing. |
