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Foxn4 specifies subtype identity of spinal sensory neurons. Neuronal subtype diversification is essential for the establishment of functional neural circuits and yet the molecular events underlying neuronal diversity remain largely to be defined. During spinal neurogenesis, the p2 progenitor domain, unlike others in the ventral spinal cord, gives rise to two intermingled but molecularly distinct subtypes of interneurons, termed V2a and V2b. We show that the Foxn4 winged helix/forkhead transcription factor is co-expressed with the bHLH factor Mash1 in a subset of p2 progenitors. Loss of Foxn4 function eliminates Mash1 expression and V2b neurons and causes a fate-switch to V2a neurons while the absence of Mash1 displays a similar but less severe phenotype. Overexpression of Foxn4 alone in spinal neural progenitors promotes the V2a fate at the expense of the V2b fate, whereas, Mash1 suppresses both the V2a and V2b fates. However, co-expression of both Foxn4 and Mash1 promotes the V2b fate while inhibiting the V2a fate, indicating that Foxn4 cooperates with Mash1 to specify the identity of V2b neurons from bi-potential p2 progenitors.

Loss of Foxn4 function causes a V2b-to-V2a fate switch in the spinal cord. PNAS 102:10688-10693 (2005)

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