| First Author | Inamata Y | Year | 2014 |
| Journal | Development | Volume | 141 |
| Issue | 6 | Pages | 1260-71 |
| PubMed ID | 24553291 | Mgi Jnum | J:208415 |
| Mgi Id | MGI:5563276 | Doi | 10.1242/dev.102327 |
| Citation | Inamata Y, et al. (2014) Dbx1 triggers crucial molecular programs required for midline crossing by midbrain commissural axons. Development 141(6):1260-71 |
| abstractText | Axon guidance by commissural neurons has been well documented, providing us with a molecular logic of how midline crossing is achieved during development. Despite these advances, knowledge of the intrinsic genetic programs is still limited and it remains obscure whether the expression of a single transcription factor is sufficient to activate transcriptional programs that ultimately enable midline crossing. Here, we show in the mouse that the homeodomain transcription factor Dbx1 is expressed by a subset of progenitor cells that give rise to commissural neurons in the dorsal midbrain. Gain- and loss-of-function analyses indicate that the expression of Dbx1 alone is sufficient and necessary to trigger midline crossing in vivo. We also show that Robo3 controls midline crossing as a crucial downstream effector of the Dbx1-activated molecular programs. Furthermore, Dbx1 suppresses the expression of the transcriptional program for ipsilateral neuron differentiation in parallel. These results suggest that a single transcription factor, Dbx1, has an essential function in assigning midline-crossing identity, thereby contributing crucially to the establishment of the wiring laterality in the developing nervous system. |
