Olfactory information regulates both acquired and innate behaviors in animals, with learning-dependent circuits processed in the ventral zone (V zone) and innate circuits processed in the dorsal zone (D zone) of the olfactory epithelium. These zones are distinguished by their molecular characteristics, including the forkhead transcription factor Foxg1, which is consistently expressed in the V zone from embryonic development through adulthood. However, embryos lacking Foxg1 fail to establish the olfactory epithelium, leaving its role in zone formation and zone-specific function unclear.

This year, we employed a tamoxifen-inducible Cre/Flp recombination system to achieve cell-autonomous Foxg1 deletion in olfactory epithelial stem cells and performed lineage tracing of Foxg1-deficient cells using a lineage-dependent GFP reporter. Our results revealed that in control mice, Foxg1-lineage cells remained confined to the V zone and primarily differentiated into neurons. In contrast, Foxg1-deficient stem cells partially invaded the D zone, and those remaining in the V zone differentiated into sustentacular cells. Postnatal analysis further revealed that conditional Foxg1 removal disrupts the V zone-specific expansion of the olfactory epithelium. Given that the V zone in rodents occupies approximately three times the surface area of the D zone, reflecting their strong reliance on olfactory information, these findings suggest that Foxg1 regulates the selective expansion of the V zone and learning-dependent circuit formation by maintaining zone-specific expression.

These results were presented at the 25^th Biennial Meeting of the International society for Developmental Neuroscience, the 17th Meeting of the International Society of Olfaction and Taste, and at the 18th Annual Meeting of the Neurogenesis Society.