| First Author | Tran CM | Year | 1998 |
| Journal | Development | Volume | 125 |
| Issue | 10 | Pages | 1951-6 |
| PubMed ID | 9550727 | Mgi Jnum | J:48373 |
| Mgi Id | MGI:1267266 | Doi | 10.1242/dev.125.10.1951 |
| Citation | Tran CM, et al. (1998) The RXRalpha gene functions in a non-cell-autonomous manner during mouse cardiac morphogenesis. Development 125(10):1951-6 |
| abstractText | Germline mutation in mice of the retinoic acid receptor gene RXR alpha results in a proliferative failure of cardiomyocytes, which leads to an underdeveloped ventricular chamber and midgestation lethality. Mutation of the cell cycle regulator N-myc gene also leads to an apparently identical phenotype, In this study, we demonstrate by chimera analysis that the cardiomyocyte phenotype in RXR alpha(+) embryos is a non-cell-autonomous phenotype, In chimeric embryos made with embryonic stem cells lacking RXR alpha, cardiomyocytes deficient in RXR alpha develop normally and contribute to the ventricular chamber wall in a normal manner, Because the ventricular hypoplastic phenotype reemerges in highly chimeric embryos, we conclude that RXR alpha functions in a non- myocyte lineage of the heart to induce cardiomyocyte proliferation and accumulation, in a manner that is quantitatively sensitive. We further show that RXR alpha is not epistatic to N-myc, and that RXR alpha and N-myc regulate convergent obligate pathways of cardiomyocyte maturation. |
