TY - JOUR
T1 - The transcription factor gene Nfib is essential for both lung maturation and brain development
AU - Steele-Perkins, George
AU - Plachez, Céline
AU - Butz, Kenneth G.
AU - Yang, Guanhu
AU - Bachurski, Cindy J.
AU - Kinsman, Stephen L.
AU - Litwack, E. David
AU - Richards, Linda J.
AU - Gronostajski, Richard M.
PY - 2005/1
Y1 - 2005/1
N2 - The phylogenetically conserved nuclear factor I (NFI) gene family encodes site-specific transcription factors essential for the development of a number of organ systems. We showed previously that Nfia-deficient mice exhibit agenesis of the corpus callosum and other forebrain defects, whereas Nfic-deficient mice have agenesis of molar tooth roots and severe incisor defects. Here we show that Nfib-deficient mice possess unique defects in lung maturation and exhibit callosal agenesis and forebrain defects that are similar to, but more severe than, those seen in Nfia-deficient animals. In addition, loss of Nfib results in defects in basilar pons formation and hippocampus development that are not seen in Nfia-deficient mice. Heterozygous Nfib-deficient animals also exhibit callosal agenesis and delayed lung maturation, indicating haploinsufficiency at the Nfib locus. The similarity in brain defects in Nfia- and Nfib-deficient animals suggests that these two genes may cooperate in late fetal forebrain development, while Nfib is essential for late fetal lung maturation and development of the pons.
AB - The phylogenetically conserved nuclear factor I (NFI) gene family encodes site-specific transcription factors essential for the development of a number of organ systems. We showed previously that Nfia-deficient mice exhibit agenesis of the corpus callosum and other forebrain defects, whereas Nfic-deficient mice have agenesis of molar tooth roots and severe incisor defects. Here we show that Nfib-deficient mice possess unique defects in lung maturation and exhibit callosal agenesis and forebrain defects that are similar to, but more severe than, those seen in Nfia-deficient animals. In addition, loss of Nfib results in defects in basilar pons formation and hippocampus development that are not seen in Nfia-deficient mice. Heterozygous Nfib-deficient animals also exhibit callosal agenesis and delayed lung maturation, indicating haploinsufficiency at the Nfib locus. The similarity in brain defects in Nfia- and Nfib-deficient animals suggests that these two genes may cooperate in late fetal forebrain development, while Nfib is essential for late fetal lung maturation and development of the pons.
UR - http://www.scopus.com/inward/record.url?scp=11844283949&partnerID=8YFLogxK
U2 - 10.1128/MCB.25.2.685-698.2005
DO - 10.1128/MCB.25.2.685-698.2005
M3 - Article
C2 - 15632069
AN - SCOPUS:11844283949
SN - 0270-7306
VL - 25
SP - 685
EP - 698
JO - Molecular and cellular biology
JF - Molecular and cellular biology
IS - 2
ER -