| First Author | Ikeda Y | Year | 1997 |
| Journal | Dev Dyn | Volume | 210 |
| Issue | 2 | Pages | 157-72 |
| PubMed ID | 9337136 | Mgi Jnum | J:43264 |
| Mgi Id | MGI:1097444 | Doi | 10.1002/(SICI)1097-0177(199710)210:2<157::AID-AJA8>3.0.CO;2-F |
| Citation | Ikeda Y, et al. (1997) Expression of reelin, the gene responsible for the reeler mutation, in embryonic development and adulthood in the mouse. Dev Dyn 210(2):157-72 |
| abstractText | reelin has recently been isolated as a candidate gene, the mutation of which gives rise to the reeler phenotype in mice. In this study, we analyzed the expression of reelin during embryonic development in the mouse and in adult mouse tissues, by in situ hybridization. reelin transcripts were present on embryonic day (E) 8.5 in the somite, foregut, yolk sac, and unclosed neural plate. reelin was expressed in the brain, spinal cord, liver, and kidney throughout embryonic development, and transiently in many developing organs such as the optic cup, blood vessels, precartilage, stomach, pituitary, vibrissae, tooth germ, and in cells along growing nerve fibers. These observations indicate a role for reelin in development of organs in addition to that in neuronal migration. Furthermore, we demonstrated the existence of reelin mRNA and its cellular distribution in the adult brain, spinal cord, liver, kidney, testis, and ovary, suggesting additional roles for reelin in stabilizing the cyto-architecture and in remolding in adult organs. However, we detected no obvious phenotype of the reelin-expressing organs except for the brain in the reeler mouse, indicating the functional redundancy of this gene during the development of these organs. |
