| First Author | Krawetz R | Year | 2006 |
| Journal | Exp Cell Res | Volume | 312 |
| Issue | 17 | Pages | 3224-40 |
| PubMed ID | 16860319 | Mgi Jnum | J:114373 |
| Mgi Id | MGI:3688930 | Doi | 10.1016/j.yexcr.2006.06.016 |
| Citation | Krawetz R, et al. (2006) Galpha13 activation rescues moesin-depletion induced apoptosis in F9 teratocarcinoma cells. Exp Cell Res 312(17):3224-40 |
| abstractText | Mouse F9 cells differentiate into primitive endoderm when treated with retinoic acid (RA) and into parietal endoderm in response to RA and dibutyryl (db-) cAMP. G protein signaling either blocks or mimics RA-induced differentiation, the latter signaling through the Wnt-beta-catenin pathway. In our study, we found that a constitutively active Galpha13 mutant induces F9 cells to differentiate into parietal endoderm in the absence of exogenous agents. Galpha13 expression and subsequent differentiation are accompanied by beta-catenin translocation to the nucleus. Differentiation and changes in cell morphology are supported by rearrangements to the F-actin cytoskeleton. ERM (ezrin-radixin-moesin) proteins, known to link F-actin to transmembrane receptors, are also redistributed during differentiation. Furthermore, morpholino antisense and shRNA approaches show that moesin expression is essential since its knockdown leads to altered F-actin distribution and subsequent apoptosis. Moesin-depleted cells, however, remain attached to the substrate when Galpha13 is constitutively expressed, but they do not differentiate into extraembryonic endoderm. Our study demonstrates a link between Galpha13 signaling that regulates differentiation of F9 cells through primitive to parietal endoderm and a moesin requirement for cell survival. |
