TY - JOUR
T1 - Nuclear Factor I gene expression in the developing forebrain
AU - Plachez, Céline
AU - Lindwall, Charlotta
AU - Sunn, Nana
AU - Piper, Michael
AU - Moldrich, Randal X.
AU - Campbell, Christine E.
AU - Osinski, Jason M.
AU - Gronostajski, Richard M.
AU - Richards, Linda J.
PY - 2008/5/20
Y1 - 2008/5/20
N2 - Three members of the Nuclear Factor I (Nfi) gene family of transcription factors; Nfia, Nfib, and Nfix are highly expressed in the developing mouse brain. Nfia and Nfib knockout mice display profound defects in the development of midline glial populations and the development of forebrain commissures (das Neves et al. [1999] Proc Natl Acad Sci U S A 96:11946-11951; Shu et al. [2003] J Neurosci 23:203-212; Steele-Perkins et al. [2005] Mol Cell Biol 25:685-698). These findings suggest that Nfi genes may regulate the substrate over which the commissural axons grow to reach targets in the contralateral hemisphere. However, these genes are also expressed in the cerebral cortex and, thus, it is important to assess whether this expression correlates with a cell-autonomous role in cortical development. Here we detail the protein expression of NFIA and NFIB during embryonic and postnatal mouse forebrain development. We find that both NFIA and NFIB are expressed in the deep cortical layers and subplate prenatally and display dynamic expression patterns postnatally. Both genes are also highly expressed in the developing hippocampus and in the diencephalon. We also find that principally neither NFIA nor NFIB are expressed in callosally projecting neurons postnatally, emphasizing the role for midline glial cell populations in commissure formation. However, a large proportion of laterally projecting neurons express both NFIA and NFIB, indicating a possible cell-autonomous role for these transcription factors in corticospinal neuron development. Collectively, these data suggest that, in addition to regulating the formation of axon guidance substrates, these genes also have cell-autonomous roles in cortical development.
AB - Three members of the Nuclear Factor I (Nfi) gene family of transcription factors; Nfia, Nfib, and Nfix are highly expressed in the developing mouse brain. Nfia and Nfib knockout mice display profound defects in the development of midline glial populations and the development of forebrain commissures (das Neves et al. [1999] Proc Natl Acad Sci U S A 96:11946-11951; Shu et al. [2003] J Neurosci 23:203-212; Steele-Perkins et al. [2005] Mol Cell Biol 25:685-698). These findings suggest that Nfi genes may regulate the substrate over which the commissural axons grow to reach targets in the contralateral hemisphere. However, these genes are also expressed in the cerebral cortex and, thus, it is important to assess whether this expression correlates with a cell-autonomous role in cortical development. Here we detail the protein expression of NFIA and NFIB during embryonic and postnatal mouse forebrain development. We find that both NFIA and NFIB are expressed in the deep cortical layers and subplate prenatally and display dynamic expression patterns postnatally. Both genes are also highly expressed in the developing hippocampus and in the diencephalon. We also find that principally neither NFIA nor NFIB are expressed in callosally projecting neurons postnatally, emphasizing the role for midline glial cell populations in commissure formation. However, a large proportion of laterally projecting neurons express both NFIA and NFIB, indicating a possible cell-autonomous role for these transcription factors in corticospinal neuron development. Collectively, these data suggest that, in addition to regulating the formation of axon guidance substrates, these genes also have cell-autonomous roles in cortical development.
KW - Cortical development
KW - Cortical layers
KW - Hippocampus
KW - Midline glia
KW - NFI
KW - Telencephalon
KW - Transcription factor
UR - http://www.scopus.com/inward/record.url?scp=42449114786&partnerID=8YFLogxK
U2 - 10.1002/cne.21645
DO - 10.1002/cne.21645
M3 - Article
C2 - 18335562
AN - SCOPUS:42449114786
SN - 0021-9967
VL - 508
SP - 385
EP - 401
JO - Journal of Comparative Neurology
JF - Journal of Comparative Neurology
IS - 3
ER -