High impact information on Foxn4

• These results indicate that Foxn4 is both necessary and sufficient for commitment to the amacrine cell fate and is nonredundantly required for the genesis of horizontal cells [1].
• Two reports in this issue of Neuron reveal two transcription factors (Foxn4 and Bhlhb4) that contribute to the development of this remarkable cellular diversity [2].
• Loss of Foxn4 function eliminates Mash1 expression and V2b neurons and causes a fate-switch to V2a neurons, whereas the absence of Mash1 displays a similar but less severe phenotype [3].
• Foxn4 acts synergistically with Mash1 to specify subtype identity of V2 interneurons in the spinal cord [3].
• These data, together with the previous findings on Foxn4, provide a model in which the Foxn4-Ptf1a pathway plays a central role in directing the differentiation of retinal progenitors towards horizontal and amacrine cell fates [4].

Anatomical context of Foxn4

• Retinal Foxn4 expression is associated with the zone of proliferating progenitor cells [5].

Regulatory relationships of Foxn4

• We show here that the Foxn4 winged helix/forkhead transcription factor is coexpressed with the bHLH factor Mash1 in a subset of p2 progenitors [3].
• We show here in experiments conducted using mouse and chick that Foxn4 induces expression of delta-like 4 (Dll4) and Mash1 (Ascl1) [6].

Other interactions of Foxn4

• A previously described Whn-like gene from zebrafish, now designated as whna, is shown to be the orthologue of the mouse Foxn4 gene [7].

References