Ask about this productRelated genes to: FOXP2 antibody
- Gene:
- FOXP2 NIH gene
- Name:
- forkhead box P2
- Previous symbol:
- TNRC10, SPCH1
- Synonyms:
- CAGH44
- Chromosome:
- 7q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-11-20
- Date modifiied:
- 2016-10-05
Related products to: FOXP2 antibody
Related articles to: FOXP2 antibody
- Vocal communication is fundamental for social interaction across species, yet the neural mechanisms that shape vocal circuit development remain poorly understood despite their relevance to neurodevelopmental disorders. Here, we investigate vocal circuit development in mice using isolation-induced ultrasonic vocalizations (USVs) in neonates. An activity-tagging approach identifies the ventromedial prefrontal cortex (vmPFC) as a cortical region strongly activated during USV emission. We find a predictable temporal correlation between vmPFC activity and USV emission using in vivo fiber photometry. Selective activation and inhibition of vmPFC neurons establishes a causal role of vmPFC in vocalization. Interestingly, chronic activation of vmPFC neurons not only increases Foxp2, a gene implicated in childhood speech apraxia, but also Vglut1-labeled synapses in the striatum, suggesting that activity-dependent increases in Foxp2 may promote corticostriatal synaptogenesis. Consistent with this finding, neonatal vmPFC activation partially rescues USV deficits in Foxp2 heterozygous mutant mice. Collectively, our results identify the vmPFC-striatal circuit as a key regulator of neonatal vocalization and suggest that Foxp2 may mediate activity-dependent development of vocal circuits. - Source: PubMed
Publication date: 2026/05/19
Chen Shih-YunPang Hao-YuFan Pao-WenWu Guan-YingLin Wan-TingLiu Fu-ChinKuo Hsiao-Ying - Humans possess human-specific traits such as spoken language and lineage-specific traits such as ape-specific taillessness . Previous efforts to identify the DNA sequences responsible for such human traits were limited by necessary accommodations for poor genome assembly quality and lack of population genomic sampling . Here, we implement new algorithms that combine the near-complete human reference pangenome alignment with a new near-complete simian cross-species alignment to define human- and lineage-specific DNA sequences fixed across human haplotypes. Previously reported amino acid substitutions linked to human spoken language and transposable element insertion contributing to ape taillessness were unique to their respective clades and fixed in sampled humans. In contrast, widely used sets of candidate human-mutated loci showed limited enrichment for either human specificity or fixation. Integration with candidate -regulatory elements identified putative regulatory sequences specific to humans and linked to human-specific traits like hair reduction and brain transcriptome patterning . Although brain-associated fixed regulatory changes were present in all lineages, enrichment for spoken language was human-specific and enrichment for receptive language was ape-specific. This study provides a new pangenome-aware comparative framework and catalogs of candidate genomic loci to trace the evolutionary origins of common human traits and disease risks. - Source: PubMed
Publication date: 2026/05/04
Goh Chern-SingDavenport Matthew HLee ChulJarvis Erich D - Sulfate is a vital nutrient for healthy brain development. More than 90 sulfate-related genes are highly conserved across mammalian species, with 16 of these genes being clinically reportable for adverse brain conditions. To determine the potential involvement of additional sulfate-related genes in human neuropathology, this study curated the spatial and temporal expression patterns of all known sulfate biology genes in the human fetal brain from 8 to 37 post conception weeks (pcw) using data from the BrainSpan database and performed network analysis to cluster sulfate-related genes with genes involved in neurodevelopmental processes. A total of 64 sulfate-related genes were abundantly or moderately expressed in 11 brain regions throughout gestation. Steady state expression was observed for some of these genes from 8 to 37 pcw, including genes that encode sulfotransferases (, ), sulfatases (, , , ), sulfatase modifying enzyme (), key enzymes in amino acid metabolism (, ), sulfate transporter (), as well as genes involved in neurodevelopmental processes (, , , , , ). Between 21-24 weeks, there were numerous clusters of sulfate biology genes with neurodevelopmental genes involved in neuronal migration ( and synaptogenesis (, , , ). At 8-13 and 17-21 pcw, fifteen sulfate genes (, , , , , , , , , , , , , , ) were expressed in the hippocampus and clustered with genes involved in neurogenesis, differentiation and synaptogenesis (, , ). Overall, this study identified 48 sulfate-related genes with moderate/abundant expression in the fetal brain that are coexpressed with genes for neurodevelopmental processes but are not considered in clinical settings. These findings provide information for future studies into the physiological roles of sulfate-related genes that are expressed in the fetal brain. - Source: PubMed
Publication date: 2026/05/08
Vijayakumar PrasidheeSummers Kim MDawson Paul A - Huntington's disease (HD) is an autosomal dominant neurodegenerative disease characterised by the loss of GABAergic medium spiny neurons (MSNs). Cellular models of HD are mainly derived from human embryonic stem cells or induced pluripotent stem cells. These models are limited by their DNA embryonic age, low neuronal yields and limited disease pathology. We propose direct reprogramming, which maintains the aging signature of the cells, to human induced lateral ganglionic eminence precursors (hiLGEP) results in the generation of high yields of functionally mature MSNs exhibiting pathological hallmarks of HD. hiLGEPs were derived from normal and HD fibroblasts by direct reprogramming and differentiated to MSNs. hiLGEP and MSN fate acquisition was compared between normal and HD through gene and protein expression. Known pathological hallmarks of HD were investigated within the hiLGEP-derived MSNs. The formation of functional synapses was investigated using live cell calcium imaging. We demonstrate that HD fibroblasts can be reprogrammed to hiLGEPs expressing key linage markers and displaying disease-related changes in expression of FOXP1 and FOXP2. HD hiLGEPs can be differentiated to high yields of MSNs co-expressing DARPP32, GABA, or GAD65/67, and SYN1 and PSD-95. HD MSNs show a reduced expression of BDNF, HAP1, TRKB, Rhes and PGC1α, exhibit MW8+ mHTT aggregates and display smaller cell somas, reduced total neurite length and reduced branched neurites when compared to normal MSNs. An administration of 100 µM dopamine was necessary to generate a calcium response in HD MSNs. This study establishes a directly reprogrammed hiLGEP-derived MSN model of HD which recapitulates pathological signatures. - Source: PubMed
Publication date: 2026/05/06
McCaughey-Chapman AmyConnor Bronwen - Prefrontal neurons exhibit diverse activity during cognitive functions such as working memory, attention, and timing; however, the importance of this heterogeneity is unclear. Our goal was to better understand the diversity of prefrontal activity through anatomical connectivity. We harnessed circuit-specific tools in mice to capture activity within prefrontal projections during interval timing, a highly translational cognitive process that requires working memory for temporal rules and attention to the passage of time to estimate a temporal interval of several seconds. We used neuronal recordings to capture prefrontal activity during interval timing, with major patterns characterized by monotonic time-dependent ramping over a temporal interval. We then leveraged retrograde viruses to interrogate prefrontal cortex (PFC) projections to the mediodorsal thalamus (PFC-MD) and the dorsomedial striatum (PFC-DMS). We report three main findings. First, circuit-specific fiber photometry revealed that PFC-MD and PFC-DMS activity encoded distinct temporal signals, with PFC-MD projections ramping down and PFC-DMS ramping up to interval timing response times. Second, circuit-specific inactivation revealed that suppressing PFC-DMS projections disrupted animals' internal estimates of time. Third, circuit-specific single-nucleus RNA sequencing of projection-defined prefrontal neurons revealed distinct transcriptomic profiles of PFC-MD and PFC-DMS projections, with enrichment of cortical layer-associated genes as well as genes such as and . These data suggest that differences in gene expression and connectivity distinguish prefrontal activity during interval timing. These findings advance our fundamental understanding of prefrontal function and dysfunction in human disease. - Source: PubMed
Publication date: 2026/05/06
Ding XinWeber Matthew AButler Trevor CBova Alexandra SGuerrero Stephanie GHunter Christopher MCole Rachel CStutt Hannah RMcMurrin Madison SSpicer Mackenzie MConlon Mackenzie MHeiney Shane AKim YoungchoResch Jon MNarayanan Nandakumar S