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​Maf  ( c-Maf ) and  Mafb  transcription factors (TFs) have compensatory roles in repressing somatostatin (SST + ) interneuron (IN) production in medial ganglionic eminence (MGE) secondary progenitors in mice.  Maf  and  Mafb  conditional deletion (cDKO) decreases the survival of MGE-derived cortical interneurons (CINs) and changes their physiological properties. Herein, we show that (1)  Mef2c  and  Snap25  are positively regulated by  Maf  and  Mafb  to drive IN morphological maturation; (2)  Maf  and  Mafb  promote  Mef2c  expression which specifies parvalbumin (PV + ) INs; (3)  Elmo1 ,  Igfbp4  and  Mef2c  are candidate markers of immature PV +  hippocampal INs (HIN). Furthermore,  Maf / Mafb  neonatal cDKOs have decreased CINs and increased HINs, that express  Pnoc , an HIN specific marker. Our findings not only elucidate key gene targets of  Maf  and  Mafb  that control IN development, but also identify for the first time TFs that differentially regulate CIN vs. HIN production.

Maf and Mafb control mouse pallial interneuron fate and maturation through neuropsychiatric disease gene regulation