| First Author | Pathania M | Year | 2016 |
| Journal | Differentiation | Volume | 92 |
| Issue | 4 | Pages | 133-147 |
| PubMed ID | 27596755 | Mgi Jnum | J:236785 |
| Mgi Id | MGI:5807285 | Doi | 10.1016/j.diff.2016.08.002 |
| Citation | Pathania M, et al. (2016) beta1-integrin controls cell fate specification in early lens development. Differentiation 92(4):133-147 |
| abstractText | Integrins are heterodimeric cell surface molecules that mediate cell-extracellular matrix (ECM) adhesion, ECM assembly, and regulation of both ECM and growth factor induced signaling. However, the developmental context of these diverse functions is not clear. Loss of beta1-integrin from the lens vesicle (mouse E10.5) results in abnormal exit of anterior lens epithelial cells (LECs) from the cell cycle and their aberrant elongation toward the presumptive cornea by E12.5. These cells lose expression of LEC markers and initiate expression of the Maf (also known as c-Maf) and Prox1 transcription factors as well as other lens fiber cell markers. beta1-integrin null LECs also upregulate the ERK, AKT and Smad1/5/8 phosphorylation indicative of BMP and FGF signaling. By E14.5, beta1-integrin null lenses have undergone a complete conversion of all lens epithelial cells into fiber cells. These data suggest that shortly after lens vesicle closure, beta1-integrin blocks inappropriate differentiation of the lens epithelium into fibers, potentially by inhibiting BMP and/or FGF receptor activation. Thus, beta1-integrin has an important role in fine-tuning the response of the early lens to the gradient of growth factors that regulate lens fiber cell differentiation. |
