| First Author | Kablar B | Year | 2004 |
| Journal | Int J Dev Neurosci | Volume | 22 |
| Issue | 4 | Pages | 215-24 |
| PubMed ID | 15245757 | Mgi Jnum | J:101960 |
| Mgi Id | MGI:3605964 | Doi | 10.1016/j.ijdevneu.2004.04.001 |
| Citation | Kablar B (2004) MyoD-lacZ transgenes are early markers in the neural retina, but MyoD function appears to be inhibited in the developing retinal cells. Int J Dev Neurosci 22(4):215-24 |
| abstractText | Recent findings suggest that eye and skeletal muscle development in vertebrates share the same regulatory network. In that network, Pax3 gene is apparently activated through Dach/Eya/Six feedback loop to mediate MyoD-driven myogenesis. The purpose of this study was to investigate previously reported MyoD-lacZ expression in the developing mouse neural retina and to gain insight into the potential role of MyoD in the embryonic retinal cells. The analysis of MD6.0-lacZ and 258/-2.5lacZ transgenic embryos revealed that the retinal temporal expression pattern of the two transgenes resembled their expression pattern in the MyoD-dependent precursor muscle cells. However, MyoD transcripts and protein could not be found in the sites of MyoD-lacZ retinal expression. Furthermore, our immunohistochemical analysis suggests the existence of diverse factors (e.g., Pax6 and Chx10) within the retinal cells that differentially and inappropriately activate the two transgenes. Finally, the retinal phenotype observed in Pax7-/- knock-out mice suggests a role for Pax7 in photoreceptor cell differentiation, retinal lamination and in the etiopathology of retinoblastoma. Taken together, our data suggest that the MyoD gene evolved a different mechanism to achieve its down-regulation within the retina than that of the Myf5 gene. |
