| First Author | Kang T | Year | 2019 |
| Journal | Mol Cells | Volume | 42 |
| Issue | 8 | Pages | 589-596 |
| PubMed ID | 31402636 | Mgi Jnum | J:284300 |
| Mgi Id | MGI:6391297 | Doi | 10.14348/molcells.2019.0140 |
| Citation | Kang T, et al. (2019) Loss of Pix Causes Defects in Early Embryonic Development, and Cell Spreading and PlateletDerived Growth Factor-Induced Chemotaxis in Mouse Embryonic Fibroblasts. Mol Cells 42(8):589-596 |
| abstractText | betaPix is a guanine nucleotide exchange factor for the Rho family small GTPases, Rac1 and Cdc42. It is known to regulate focal adhesion dynamics and cell migration. However, the in vivo role of betaPix is currently not well understood. Here, we report the production and characterization of betaPix-KO mice. Loss of betaPix results in embryonic lethality accompanied by abnormal developmental features, such as incomplete neural tube closure, impaired axial rotation, and failure of allantoischorion fusion. We also generated betaPix-KO mouse embryonic fibroblasts (MEFs) to examine betaPix function in mouse fibroblasts. betaPix-KO MEFs exhibit decreased Rac1 activity, and defects in cell spreading and platelet-derived growth factor (PDGF)-induced ruffle formation and chemotaxis. The average size of focal adhesions is increased in betaPix-KO MEFs. Interestingly, betaPix-KO MEFs showed increased motility in random migration and rapid wound healing with elevated levels of MLC2 phosphorylation. Taken together, our data demonstrate that betaPix plays essential roles in early embryonic development, cell spreading, and cell migration in fibroblasts. |
