| First Author | Liu Z | Year | 2019 |
| Journal | Cereb Cortex | Volume | 29 |
| Issue | 6 | Pages | 2653-2667 |
| PubMed ID | 29878134 | Mgi Jnum | J:293452 |
| Mgi Id | MGI:6437426 | Doi | 10.1093/cercor/bhy133 |
| Citation | Liu Z, et al. (2019) Sp9 Regulates Medial Ganglionic Eminence-Derived Cortical Interneuron Development. Cereb Cortex 29(6):2653-2667 |
| abstractText | Immature neurons generated by the subpallial MGE tangentially migrate to the cortex where they become parvalbumin-expressing (PV+) and somatostatin (SST+) interneurons. Here, we show that the Sp9 transcription factor controls the development of MGE-derived cortical interneurons. SP9 is expressed in the MGE subventricular zone and in MGE-derived migrating interneurons. Sp9 null and conditional mutant mice have approximately 50% reduction of MGE-derived cortical interneurons, an ectopic aggregation of MGE-derived neurons in the embryonic ventral telencephalon, and an increased ratio of SST+/PV+ cortical interneurons. RNA-Seq and SP9 ChIP-Seq reveal that SP9 regulates MGE-derived cortical interneuron development through controlling the expression of key transcription factors Arx, Lhx6, Lhx8, Nkx2-1, and Zeb2 involved in interneuron development, as well as genes implicated in regulating interneuron migration Ackr3, Epha3, and St18. Thus, Sp9 has a central transcriptional role in MGE-derived cortical interneuron development. |
