ArticleBMC developmental biology2008
The transcription factor Nfix is essential for normal brain development.
Article in BMC developmental biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.
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Who cites it
94 citing papers in PubMed, 183 citations in OpenAlex.
- Dynamic NFIX Promoter Usage Shapes Stem and Committed Myogenic States.International journal of molecular sciences · 2026Article
- Nuclear factor IC promoting porcine reproductive and respiratory syndrome virus (PRRSV) replication and suppressing type I interferon transcription.BMC veterinary research · 2026Article
- Structural basis of Nuclear Factor 1-X DNA recognition provides prototypic insight into the NFI family.Nature communications · 2025Article
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- Transcriptional programs of cell identity and p53-induced stress responses are associated with distinctive features of spatial genome organization.Nucleic acids research · 2025Article
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- Overgrowth-intellectual disability disorders: progress in biology, patient advocacy and innovative therapies.Disease models & mechanisms · 2025Review
- Multiomic single-cell profiling identifies critical regulators of postnatal brain.Nature genetics · 2025Article
- Topological identification and interpretation for single-cell epigenetic regulation elucidation in multi-tasks using scAGDE.Nature communications · 2025Article
- Posttranscriptional Control of Neural Progenitors Temporal Dynamics During Neocortical Development by Syncrip.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Mechanistic insights intoFrontiers in genetics · 2025Article
- Roles of the NFI/CTF gene family in transcription and development: update 2025.Academia biology · 2025Article
- Regulatory Role ofInternational journal of molecular sciences · 2024Article
- A Patient Case of Malan Syndrome Involving 19p13.2 Deletion ofJournal of clinical medicine · 2024Article
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- Evolution of glial cells: a non-bilaterian perspective.Neural development · 2024Review
- MEK-inhibitors decrease Nfix in muscular dystrophy but induce unexpected calcifications, partially rescued with Cyanidin diet.iScience · 2024Article
- Multi-omics data integration for the identification of biomarkers for bull fertility.PloS one · 2024Article
- A high-resolution transcriptomic and spatial atlas of cell types in the whole mouse brain.Nature · 2023Article
- Erythroid lineage chromatin accessibility maps facilitate identification and validation of NFIX as a fetal hemoglobin repressor.Communications biology · 2023Article
34 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundThe Nuclear Factor I (NFI) multi-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; Nfib-deficient mice have defects in lung maturation and show callosal agenesis and forebrain defects resembling those seen in Nfia-deficient animals, while Nfic-deficient mice have defects in tooth root formation. Recently the Nfix gene has been disrupted and these studies indicated that there were largely uncharacterized defects in brain and skeletal development in Nfix-deficient mice.
resultsHere we show that disruption of Nfix by Cre-recombinase mediated excision of the 2nd exon results in defects in brain development that differ from those seen in Nfia and Nfib KO mice. In particular, complete callosal agenesis is not seen in Nfix-/- mice but rather there appears to be an overabundance of aberrant Pax6- and doublecortin-positive cells in the lateral ventricles of Nfix-/- mice, increased brain weight, expansion of the cingulate cortex and entire brain along the dorsal ventral axis, and aberrant formation of the hippocampus. On standard lab chow Nfix-/- animals show a decreased growth rate from ~P8 to P14, lose weight from ~P14 to P22 and die at ~P22. If their food is supplemented with a soft dough chow from P10, Nfix-/- animals show a lag in weight gain from P8 to P20 but then increase their growth rate. A fraction of the animals survive to adulthood and are fertile. The weight loss correlates with delayed eye and ear canal opening and suggests a delay in the development of several epithelial structures in Nfix-/- animals.
conclusionThese data show that Nfix is essential for normal brain development and may be required for neural stem cell homeostasis. The delays seen in eye and ear opening and the brain morphology defects appear independent of the nutritional deprivation, as rescue of perinatal lethality with soft dough does not eliminate these defects.
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