ArticleDevelopment (Cambridge, England)2004
The winged helix transcription factor Foxg1 facilitates retinal ganglion cell axon crossing of the ventral midline in the mouse.
Article in Development (Cambridge, England), 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 64 citations in OpenAlex.
- Foxg1 regulates the development of microvillous cells in the olfactory epithelium.Developmental biology · 2026Article
- Article
- Multimodal epigenetic changes and altered NEUROD1 chromatin binding in the mouse hippocampus underlie FOXG1 syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Optic Atrophy 1 Controls Human Neuronal Development by Preventing Aberrant Nuclear DNA Methylation.iScience · 2020Article
- Knockdown of Foxg1 in supporting cells increases the trans-differentiation of supporting cells into hair cells in the neonatal mouse cochlea.Cellular and molecular life sciences : CMLS · 2020Article
- Elucidating the pathogenic and biomarker potentials of FOXG1 in glioblastoma.Oncology reviews · 2020Article
- Hair cell regeneration from inner ear progenitors in the mammalian cochlea.American journal of stem cells · 2020Review
- Review
- A Retino-retinal Projection Guided by Unc5c Emerged in Species with Retinal Waves.Current biology : CB · 2019Article
- Molecular guidance cues in the development of visual pathway.Protein & cell · 2018Review
- The multisystemic functions of FOXD1 in development and disease.Journal of molecular medicine (Berlin, Germany) · 2018Review
- The Transcription Factor Foxg1 Promotes Optic Fissure Closure in the Mouse by Suppressing Wnt8b in the Nasal Optic Stalk.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Transcriptional regulatory dynamics drive coordinated metabolic and neural response to social challenge in mice.Genome research · 2017Article
- The Shark Alar Hypothalamus: Molecular Characterization of Prosomeric Subdivisions and Evolutionary Trends.Frontiers in neuroanatomy · 2016Article
- Foxg1 localizes to mitochondria and coordinates cell differentiation and bioenergetics.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Connecting the retina to the brain.ASN neuro · 2014Review
- Foxg1 is required to limit the formation of ciliary margin tissue and Wnt/β-catenin signalling in the developing nasal retina of the mouse.Developmental biology · 2013Article
- Ebf1 deficiency causes increase of Müller cells in the retina and abnormal topographic projection at the optic chiasm.Biochemical and biophysical research communications · 2011Article
- A role for DNA methylation in regulation of EphA5 receptor expression in the mouse retina.Vision research · 2011Article
- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
During normal development, retinal ganglion cells (RGCs) project axons along the optic nerve to the optic chiasm on the ventral surface of the hypothalamus. In rodents, most RGC growth cones then cross the ventral midline to join the contralateral optic tract; those that do not cross join the ipsilateral optic tract. Contralaterally projecting RGCs are distributed across the retina whereas ipsilaterally projecting RGCs are concentrated in temporal retina. The transcription factor Foxg1 (also known as BF1) is expressed at several key locations along this pathway. Analysis of Foxg1 expression using lacZ reporter transgenes shows that Foxg1 is normally expressed in most, if not all, nasal RGCs but not in most temporal RGCs, neither at the time they project nor earlier in their lineage. Foxg1 is also expressed at the optic chiasm. Mice that lack Foxg1 die at birth and, although the shape of their eyes is abnormal, their retinas still project axons to the brain via the optic chiasm. Using anterograde and retrograde tract tracing, we show that there is an eightfold increase in the ipsilateral projection in Foxg1-/- embryos. The distributions of cells expressing the transcription factors Foxg1 and Nkx2.2, and cell-surface molecules Ephb2, ephrin B2 and SSEA-1 (Fut4) have been correlated to the normally developing retinothalamic projection and we show they are not much altered in the developing Foxg1-/- retina and optic chiasm. As much of the increased ipsilateral projection in Foxg1-/- embryos arises from temporal RGCs that are unlikely to have an autonomous requirement for Foxg1, we propose that the phenotype reflects at least in part a requirement for Foxg1 outwith the RGCs themselves, most likely at the optic chiasm.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.