| First Author | Li Z | Year | 2022 |
| Journal | Cell Death Discov | Volume | 8 |
| Issue | 1 | Pages | 301 |
| PubMed ID | 35773249 | Mgi Jnum | J:361228 |
| Mgi Id | MGI:7856854 | Doi | 10.1038/s41420-022-01088-0 |
| Citation | Li Z, et al. (2022) Transcription factor Sp9 is a negative regulator of D1-type MSN development. Cell Death Discov 8(1):301 |
| abstractText | The striatum is the main input structure of the basal ganglia, receiving information from the cortex and the thalamus and consisting of D1- and D2- medium spiny neurons (MSNs). D1-MSNs and D2-MSNs are essential for motor control and cognitive behaviors and have implications in Parkinson's Disease. In the present study, we demonstrated that Sp9-positive progenitors produced both D1-MSNs and D2-MSNs and that Sp9 expression was rapidly downregulated in postmitotic D1-MSNs. Furthermore, we found that sustained Sp9 expression in lateral ganglionic eminence (LGE) progenitor cells and their descendants led to promoting D2-MSN identity and repressing D1-MSN identity during striatal development. As a result, sustained Sp9 expression resulted in an imbalance between D1-MSNs and D2-MSNs in the mouse striatum. In addition, the fate-changed D2-like MSNs survived normally in adulthood. Taken together, our findings supported that Sp9 was sufficient to promote D2-MSN identity and repress D1-MSN identity, and Sp9 was a negative regulator of D1-MSN fate. |
