TY - JOUR
T1 - Foxg1 confines Cajal-Retzius neuronogenesis and hippocampal morphogenesis to the dorsomedial pallium
AU - Muzio, Luca
AU - Mallamaci, Antonello
PY - 2005/4/27
Y1 - 2005/4/27
N2 - It has been suggested that cerebral cortex arealization relies on positional values imparted to early cortical neuroblasts by transcription factor genes expressed within the palliai field in graded ways. Foxg1, encoding for one of these factors, previously was reported to be necessary for basal ganglia morphogenesis, proper tuning of cortical neuronal differentiation rates, and the switching of cortical neuroblasts from early generation of primordial plexiform layer to late production of cortical plate. Being expressed along a rostral/lateralhigh-to-caudal/mediallow gradient, Foxg1, moreover, could contribute to shaping the cortical areal profile as a repressor of caudomedial fates. We tested this prediction by a variety of approaches and found that it was correct. We found that overproduction of Cajal-Retzius neurons characterizing Foxg1-/- mutants does not arise specifically from blockage of laminar histogenetic progression of neocortical neuroblasts, as reported previously, but rather reflects lateral-to-medial repatterning of their cortical primordium. Even if lacking a neocortical plate, Foxg1-/- embryos give rise to structures, which, for molecular properties and birthdating profile, are highly reminiscent of hippocampal plate and dentate blade. Remarkably, in the absence of Foxg1, additional inactivation of the medial fates promoter Emx2, although not suppressing cortical specification, conversely rescues overproduction of Reelinon neurons.
AB - It has been suggested that cerebral cortex arealization relies on positional values imparted to early cortical neuroblasts by transcription factor genes expressed within the palliai field in graded ways. Foxg1, encoding for one of these factors, previously was reported to be necessary for basal ganglia morphogenesis, proper tuning of cortical neuronal differentiation rates, and the switching of cortical neuroblasts from early generation of primordial plexiform layer to late production of cortical plate. Being expressed along a rostral/lateralhigh-to-caudal/mediallow gradient, Foxg1, moreover, could contribute to shaping the cortical areal profile as a repressor of caudomedial fates. We tested this prediction by a variety of approaches and found that it was correct. We found that overproduction of Cajal-Retzius neurons characterizing Foxg1-/- mutants does not arise specifically from blockage of laminar histogenetic progression of neocortical neuroblasts, as reported previously, but rather reflects lateral-to-medial repatterning of their cortical primordium. Even if lacking a neocortical plate, Foxg1-/- embryos give rise to structures, which, for molecular properties and birthdating profile, are highly reminiscent of hippocampal plate and dentate blade. Remarkably, in the absence of Foxg1, additional inactivation of the medial fates promoter Emx2, although not suppressing cortical specification, conversely rescues overproduction of Reelinon neurons.
KW - Cajal-Retzius cells
KW - Emx2
KW - Foxg1
KW - Hippocampus
KW - Neocortex
KW - Wnt types
UR - http://www.scopus.com/inward/record.url?scp=18244401109&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=18244401109&partnerID=8YFLogxK
U2 - 10.1523/JNEUROSCI.4804-04.2005
DO - 10.1523/JNEUROSCI.4804-04.2005
M3 - Article
C2 - 15858069
AN - SCOPUS:18244401109
VL - 25
SP - 4435
EP - 4441
JO - Journal of Neuroscience
JF - Journal of Neuroscience
SN - 0270-6474
IS - 17
ER -