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The epithalamus, which is dorsal to the thalamus, consists of the habenula, pineal gland and third ventricle choroid plexus and plays important roles in the stress response and sleep–wake cycle in vertebrates. During development, the epithalamus arises from the most dorsal part of prosomere 2. However, the mechanism underlying epithalamic development remains largely unknown.  Foxg1  is critical for the development of the telencephalon, but its role in diencephalic development has been under-investigated. Patients suffering from FOXG1-related disorders exhibit severe anxiety, sleep disturbance and choroid plexus cysts, indicating that  Foxg1  likely plays a role in epithalamic development. In this study, we identified the specific expression of  Foxg1  in the developing epithalamus. Using a “self-deletion” approach, we found that the habenula significantly expanded and included an increased number of habenular subtype neurons. The innervations, particularly the habenular commissure, were severely impaired. Meanwhile, the  Foxg1  mutants exhibited a reduced pineal gland and more branched choroid plexus. After ablation of  Foxg1  no obvious changes in Shh and Fgf signalling were observed, suggesting that  Foxg1  regulates the development of the epithalamus without the involvement of Shh and Fgfs. Our findings provide new insights into the regulation of the development of the epithalamus.

Foxg1 deletion impairs the development of the epithalamus