Patterning of frontal cortex subdivisions by Fgf17.
The frontal cortex (FC) is the seat of higher cognition. The genetic mechanisms that control formation of the functionally distinct subdivisions of the FC are unknown. Using a set of gene expression markers that distinguish subdivisions of the newborn mouse FC, we show that loss of Fgf17 selectively reduces the size of the dorsal FC whereas ventral/orbital FC appears normal. These changes are complemented by a rostral shift of sensory cortical areas. Thus, Fgf17 functions similar to Fgf8 in patterning the overall neocortical map but has a more selective role in regulating the properties of the dorsal but not ventral FC.
Cholfin
Jeremy A
JA
Medical Scientist Training Program, University of California, San Francisco, CA 94143-2611, USA.
Rubenstein
John L R
JL
D000818:Animals; D015415:Biomarkers; D019521:Body Patterning; D051524:Fibroblast Growth Factor 8 / Q000378:metabolism; D005346:Fibroblast Growth Factors / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D005625:Frontal Lobe / Q000196:embryology* / Q000378:metabolism; D018507:Gene Expression Regulation, Developmental; D051379:Mice; D018345:Mice, Knockout; D009154:Mutation / Q000235:genetics
D015415:Biomarkers; C484726:Fgf17 protein, mouse; C496457:Fgf8 protein, mouse; D051524:Fibroblast Growth Factor 8; D005346:Fibroblast Growth Factors