ArticleNature communications2025
Transcriptomic insights into fate choice of pallial versus subpallial GABAergic neurons.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
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.
Who cites it
4 citing papers in PubMed.
- Disruption of FOXG1 Impairs the Development of Striatal dSPNs, Thereby Contributing to ASD-Like Phenotypes.Neuroscience bulletin · 2026Article
- FOXG1 Transcriptionally Orchestrates ParvalbuminNeuroscience bulletin · 2026Article
- Analysis of 14q12 microdeletions reveals novel regulatory loci for the neurodevelopmental disorder-related gene FOXG1.Nature communications · 2026Article
- Genetic Variants from Large Cohorts and Familial Studies Implicate Common Mechanisms in Schizophrenia.Biology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The activity of the telencephalon is shaped by pallial and subpallial GABAergic neurons, two large populations produced in the embryonic ganglionic eminence. However, knowledge about the fate specification of neuron subtypes is limited, especially whether there is a common mechanism directing the fate choice of pallial versus subpallial populations remains unknown, largely because each population comprises numerous subtypes. Here, using sc-RNA sequencing combined with loss-of-function we profile ganglion eminence lineages and find that Foxg1 deletion causes the pallial population to adopt subpallial fates in mice. We delineate developmental trajectories and reveal FOXG1-driven transcriptional programs that specify neuron subtypes in each GE lineage and transcription factors that direct lineage bifurcation decisions. We uncover a common mechanism that drives pallial fate over subpallial fate across ganglion eminence lineages. Our study illuminates the control of production between pallial and subpallial populations and offers transcriptomic insights into the pathogenesis of GABAergic neuron-related disorders.
Indexed as
Identifiers
What OpenQuestion holds
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.