Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of Human Specific Expressed Genes in the Fetal Brain

ABSTRACT: The expansion of human neocortex is the cornerstone of highly developed cognitive abilities which distinguishes human from primates, but the molecular basis underlying it remains elusive. Here, we comprehensively compared the transcriptomes of neural precursor cells-enriched germinal zone (GZ) and neurons-enriched cortical plate (CP) of neocortex among human, macaque and mouse to identify human specific expressed genes (HSEGs) for each layer. The data identified that the HSEGs have evolved to transfer between the layers and also annotated the primate originated HSEGs. Further, we assessed the contributions of regulatory factors to the evolution of HSEGs. Finally, we analyzed such a new identified HSEG named CCNB1IP1 and discovered that the evolution of cis regulatory elements caused the gene to develop human specific pattern. Subsequent functional results showed that CCNB1IP1 could repress the expression of cell cycle related genes by interacting with E2F1, thereby shortening the length of the G1 phase. Thus, our study is firstly to identify HSEGs in the fetal cortex and reveals how CCNB1IP1 regulated cell cycle progress which contributed to the expansion of human cortex potentially.

ORGANISM(S): Homo sapiens

PROVIDER: GSE203351 | GEO | 2026/07/29

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Novel primate miRNAs co-evolved with ancient target genes in germinal zone specific expression patterns [RISC trap immunoprecipitation]

Project description:Major non primate-primate differences in corticogenesis include the dimensions, precursor lineages and developmental timing of the germinal zones (GZ). microRNAs (miRNAs) of laser dissected GZ compartments and cortical plate (CP) from embryonic E80 macaque visual cortex were deep sequenced. The CP and the GZ including Ventricular Zone (VZ), outer and inner subcompartments of the Outer SubVentricular Zone (OSVZ) in area 17 displayed unique miRNA profiles. miRNAs present in primate, but absent in rodent, contributed disproportionately to the differential expression between GZ sub-regions. Prominent among the validated targets of these miRNAs were cell-cycle and neurogenesis regulators. Co-evolution between the emergent miRNAs and their targets suggested that novel miRNAs became integrated into ancient gene circuitry to exert additional control over proliferation. We conclude that multiple cell-cycle regulatory events contribute to the emergence of primate-specific cortical features, including the OSVZ, generated enlarged supragranular layers, largely responsible for the increased primate cortex computational abilities. target mRNAs for selected miRNAs were detected with RISC trap immunoprecipitation

2014-02-27 | E-GEOD-52607 | biostudies-arrayexpress

Evolution of CCNB1IP1 regulating emergence and increase of cortical folding in primates

Project description:Cortical expansion and folding have gradually increased during primate evolution, reaching the highest in the human brain. Indeed, cortical folding has a concerted relationship with neocortex expansion, underlying evolution of human cognitive functions. However, molecular mechanisms underlying concerted evolution remain largely unknown. Here, using Chinese tree shrew as an outgroup of primate, we identify the Cyclin B1 Interacting Protein 1 gene CCNB1IP1 (also named HEI10) as a key regulator of cortically concerted evolution. CCNB1IP1 has acquired brain expression in primates, and is highly expressed in human neuronal progenitor cells. The expression of CCNB1IP1 has gradually increased along primate brain evolution, coinciding with the increase of cortical size and folding. Mechanistically, we elucidated that overexpression of CCNB1IP1, leading to a decrease of G1 duration, and subsequently causes an increase in basal progenitors and neurons. Furthermore, we generated a novel CCNB1IP1 knock-in mouse model and provide confirmation that CCNB1IP1 can induce cortical folding in otherwise smooth mouse brain. Moreover, the CCNB1IP1 knock-in mouse model exhibited traits associated with enhanced learning and memory abilities. Together, our study reveals how the changes in CCNB1IP1 expression may have contributed to the increase of cortical size and folding during human brain evolution.

2026-07-29 | GSE247966 | GEO

Novel primate miRNAs co-evolved with ancient target genes in germinal zone specific expression patterns [RISC trap immunoprecipitation]

2014-02-27 | GSE52607 | GEO

Novel primate miRNAs co-evolved with ancient target genes in germinal zone specific expression patterns [miRNA-Seq]

2014-02-27 | GSE52606 | GEO

Novel primate miRNAs co-evolved with ancient target genes in germinal zone specific expression patterns [miRNA-Seq]

Project description:Major non primate-primate differences in corticogenesis include the dimensions, precursor lineages and developmental timing of the germinal zones (GZ). microRNAs (miRNAs) of laser dissected GZ compartments and cortical plate (CP) from embryonic E80 macaque visual cortex were deep sequenced. The CP and the GZ including Ventricular Zone (VZ), outer and inner subcompartments of the Outer SubVentricular Zone (OSVZ) in area 17 displayed unique miRNA profiles. miRNAs present in primate, but absent in rodent, contributed disproportionately to the differential expression between GZ sub-regions. Prominent among the validated targets of these miRNAs were cell-cycle and neurogenesis regulators. Co-evolution between the emergent miRNAs and their targets suggested that novel miRNAs became integrated into ancient gene circuitry to exert additional control over proliferation. We conclude that multiple cell-cycle regulatory events contribute to the emergence of primate-specific cortical features, including the OSVZ, generated enlarged supragranular layers, largely responsible for the increased primate cortex computational abilities. Seven brain regions (VZ17, OSVZ17int, OSVZ17ext, CP17, VZ18, OSVZ18, CP18). OSVZ17int corresponds to the inner (apical) third of OSVZ 17 and OSVZ17ext to the most outer (basal) third of OSVZ 17, located immediately below the Outer Fiber Layer (Smart et al., 2002; Betizeau et al., 2013)

2014-02-27 | E-GEOD-52606 | biostudies-arrayexpress

Transcriptomes of germinal zones of human and mouse fetal neocortex suggest a role of extracellular matrix in progenitor self-renewal.

Project description:The expansion of the neocortex during mammalian brain evolution results primarily from an increase in neural progenitor cell divisions in its two principal germinal zones during development, the ventricular zone (VZ) and the subventricular zone (SVZ). Using mRNA sequencing, we analyzed the transcriptomes of fetal human and embryonic mouse VZ, SVZ and cortical plate (CP). We describe sets of genes that are up- or down-regulated in each germinal zone. These data suggest that cell adhesion and cell-extracellular matrix (ECM) interactions promote the proliferation and self-renewal of neural progenitors in the developing human neocortex. Notably, relevant ECM-associated genes include distinct sets of collagens, laminins, proteoglycans and integrins, along with specific sets of growth factors and morphogens. Our data establish a basis for identifying novel cell-type markers and open up avenues to unravel the molecular basis of neocortex expansion during evolution. Total RNA was isolated from the VZ, inner SVZ (ISVZ), outer SVZ (OSVZ) and CP of six 13-16 weeks post-conception (w.p.c.) human fetuses and from the VZ, SVZ and CP of five E14.5 mouse embryos using laser capture microdissection of Nissl-stained cryosections of dorsolateral telencephalon. Poly A+ RNA was used as template for the preparation of cDNA which were then subjected to single-end 76-bp RNA-Seq.

2012-07-02 | E-GEOD-38805 | biostudies-arrayexpress

Chromatin Accessibility in Developing Human Brain

Project description:<p>Non-coding regions comprise most of the human genome and harbor a significant fraction of risk alleles for neuropsychiatric diseases, yet their functions remain poorly defined. We created a high-resolution map of non-coding elements involved in human cortical neurogenesis by contrasting chromatin accessibility and gene expression in the germinal zone and cortical plate of the developing cerebral cortex. To obtain a high resolution depiction of chromatin structure and gene expression in developing human fetal cortex, we dissected the post-conception week (PCW) 15-17 human neocortex into two major anatomical divisions to distinguish between proliferating neural progenitors and post mitotic neurons: (1) GZ: the neural progenitor-enriched region encompassing the ventricular zone (VZ), subventricular zone (SVZ), and intermediate zone (IZ) and (2) CP: the neuron-enriched region containing the subplate (SP), cortical plate (CP), and marginal zone (MZ). Tissues were obtained from three independent donors and three to four technical replicates from each tissue were processed for ATAC-seq to define the landscape of accessible chromatin and RNA-seq for genome-wide gene expression profiling.</p>

| phs001438 | dbGaP

Transcriptomes of germinal zones of human and mouse fetal neocortex suggest a role of extracellular matrix in progenitor self-renewal.

2012-07-03 | GSE38805 | GEO

Extracellular matrix components HAPLN1, lumican and collagen I cause hyaluronic acid-dependent folding of the developing human neocortex

Project description:Neocortical expansion, thought to underlie the cognitive traits unique to humans, is accompanied by cortical folding. This folding starts around gestational week (GW) 20, but what causes it remains largely unknown. Extracellular matrix (ECM) has been previously implicated in neocortical expansion. Here, we investigate the potential role of ECM in the formation of neocortical folds. We focus on three specific ECM components localized in the human fetal cortical plate (CP): hyaluronan and proteoglycan link protein 1, lumican and collagen I (collectively, HLC). Addition of HLC to cultures of human fetal neocortex (11-22 GW) caused local changes in tissue stiffness and induced CP folding. HLC-induced folding increased CP hyaluronic acid (HA), required the HA-receptor CD168 and downstream ERK signaling, and was prevented/reversed by hyaluronidases. HLC did not induce CP folding in cultures of developing mouse and ferret neocortex. Together, our data suggest a human-specific role of ECM in neocortical folding.

2018-06-27 | GSE106640 | GEO

Single-cell genomics of the mouse olfactory cortex reveals contrasts with neocortex and ancestral signatures of cell type evolution

Project description:Understanding the molecular logic of cortical cell-type diversity can illuminate cortical circuit function and evolution. Here, we performed single-nucleus transcriptome and chromatin accessibility analyses to compare neurons across three- to six-layered cortical areas of adult mice and across tetrapod species. We found that, in contrast to the six-layered neocortex, glutamatergic neurons of the three-layered mouse olfactory (piriform) cortex displayed continuous rather than discrete variation in transcriptomic profiles. Subsets of piriform and neocortical glutamatergic cells with conserved transcriptomic profiles were distinguished by distinct, area-specific epigenetic states. Furthermore, we identified a prominent population of immature neurons in piriform cortex and observed that, in contrast to the neocortex, piriform cortex exhibited divergence between glutamatergic cells in lab versus wild-derived mice. Finally, we showed that piriform neurons displayed greater transcriptomic similarity to cortical neurons of turtles, lizards, and salamanders than to those of the neocortex. In summary, despite over 200 million years of co-evolution alongside the neocortex, olfactory cortex neurons retain molecular signatures of ancestral cortical identity.

2025-02-01 | GSE239477 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data