Evidence map›Paper›PMID 22378868›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012

Foxg1 has an essential role in postnatal development of the dentate gyrus.

Chuanxi Tian, Yifan Gong, Ying Yang, Wei Shen, Kun Wang, Junhua Liu, Bokai Xu, Jing Zhao, Chunjie Zhao

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
3.7field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

60 citing papers in PubMed, 90 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Capicua Refines Mossy Fiber-CA3 Axon Targeting in the Late Postnatal Hippocampus.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. PLP1-Targeting Antisense Oligonucleotides Improve FOXG1 Syndrome Mice.International journal of molecular sciences · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Conditional Deletion ofInternational journal of molecular sciences · 2023
    Article
  15. 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 · 2023
    Article
  16. Review
  17. FOXG1 Contributes Adult Hippocampal Neurogenesis in Mice.International journal of molecular sciences · 2022
    Article
  18. Article
  19. Article
  20. Identification of aFrontiers in molecular neuroscience · 2022
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Chuanxi TianKey Laboratory of Developmental Genes and Human Diseases, Ministry of Education, Institute of Life Science, Southeast University, Nanjing 210009, China.
Yifan Gong
Ying Yang
Wei Shen
Kun Wang
Junhua Liu
Bokai Xu
Jing Zhao
Chunjie Zhao
Southeast University · CNNanjing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Foxg1, formerly BF-1, is expressed continuously in the postnatal and adult hippocampal dentate gyrus (DG). This transcription factor (TF) is thought to be involved in Rett syndrome, which is characterized by reduced hippocampus size, indicating its important role in hippocampal development. Due to the perinatal death of Foxg1(-/-) mice, the function of Foxg1 in postnatal DG neurogenesis remains to be explored. Here, we describe the generation of a Foxg1(fl/fl) mouse line. Foxg1 was conditionally ablated from the DG during prenatal and postnatal development by crossing this line with a Frizzled9-CreER(TM) line and inducing recombination with tamoxifen. In this study, we first show that disruption of Foxg1 results in the loss of the subgranular zone and a severely disrupted secondary radial glial scaffold, leading to the impaired migration of granule cells. Moreover, detailed analysis reveals that Foxg1 may be necessary for the maintenance of the DG progenitor pool and that the lack of Foxg1 promotes both gliogenesis and neurogenesis. We additionally show that Foxg1 may be required for the survival and maturation of postmitotic neurons and that Foxg1 may be involved in Reelin signaling in regulating postnatal DG development. Last, prenatal deletion of Foxg1 suggests that it is rarely involved in the migration of primordial granule cells. In summary, we report that Foxg1 is critical for DG formation, especially during early postnatal stage.

Indexed as

AnimalsAnimals, NewbornDentate GyrusFemaleForkhead Transcription FactorsMaleMiceMice, KnockoutMice, TransgenicNerve Tissue ProteinsNeurogenesisReelin ProteinForkhead Transcription FactorsFoxg1 protein, mouseNerve Tissue ProteinsReelin ProteinRELN protein, humanReln protein, mouse

Identifiers

PMID22378868
PMCPMC6622020
OpenAlexW2028101236

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.