Journal
MOLECULAR AND CELLULAR BIOLOGY
Volume 25, Issue 2, Pages 685-698Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.25.2.685-698.2005
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Funding
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL060907, R29HL060907] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK058401, R01DK048796] Funding Source: NIH RePORTER
- NHLBI NIH HHS [R01 HL060907, R29 HL060907, HL60907] Funding Source: Medline
- NICHD NIH HHS [HD34901] Funding Source: Medline
- NIDDK NIH HHS [R01 DK058401, R01 DK048796, DK48796, DK58401] Funding Source: Medline
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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 a genesis 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 ports formation aud 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.
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