Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-nuclus sequencing analysis reveals aberrant brain development in fetuses with neural tube defects

ABSTRACT: Single-nuclus sequencing analysis reveals aberrant brain development in fetuses with neural tube defects

PROVIDER: PRJNA1107802 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Aberrant expression of histone homocysteinylation: Implications for neural tube defects

Project description:Aberrant expression of histone homocysteinylation: Implications for neural tube defects

| PRJNA408231 | ENA

Single-nuclus sequencing analysis reveals aberrant brain development in fetuses with neural tube defects

Project description:Background: Neural tube defects (NTDs) are congenital malformations that occur when the neural tube fails to close properly during early embryonic development. However, the identity of affected celltypes and pathogenic mechanisms remain unclear due to the lack of clinical samples. Method: We utilized single-nucleus RNA sequencing to analyze 37,064 neural tube cells from NTDs and normal abortus at 14 and 15 gestational weeks. Multiplexed immunofluorescence staining was performed to further validate some phenotypes. Results: Firstly, we revealed that the most affected celltypes are excitatory neurons, inhibitory neurons, and astrocytes. We further elucidated that the main subtypes mediating abnormal development in NTDs is IGF2high subtypes in inhibitory neurons and MEG3high subtypes in astrocytes. Importantly, our findings highlighted IGF2 as a pivotal gene for abnormal development and abnormal cell-cell communications in NTDs. Conclusions: In summary, this study presents the first single-cell atlas of NTDs and provides new insights for further research into the underlying mechanisms of NTDs.

2024-05-15 | GSE266595 | GEO

Aberrant expression of histone homocysteinylation: Implications for neural tube defects (RNA-seq)

Project description:Aberrant expression of histone homocysteinylation: Implications for neural tube defects (RNA-seq)

| PRJNA408236 | ENA

Aberrant expression of histone homocysteinylation: Implications for neural tube defects (ChIP-seq)

Project description:Aberrant expression of histone homocysteinylation: Implications for neural tube defects (ChIP-seq)

| PRJNA408235 | ENA

Aberrant expression of histone homocysteinylation: Implications for neural tube defects (ChIP-seq)

Project description:Neural tube defects (NTDs) are serious congenital malformations. Excessive maternal homocysteine (Hcy) increases the risk of NTDs, while its mechanism remains elusive. In this study, we evaluated the role of histone homocysteinylation in neural tube closure (NTC). A total of 39 histone homocysteinylation sites were identified in samples from human embryonic brain tissue using mass spectrometry. Elevated levels of histone KHcy and H3K79Hcy were detected at increased cellular Hcy levels in human fetal brains. Using ChIP-seq and RNA-seq assays, we demonstrated that increase in H3K79Hcy level downregulated the expression of selected NTC-related genes including Cecr2, Smarca4, and Dnmt3b. In human NTD brain tissues, decrease in expression of Cecr2, Smarca4, and Dnmt3b was also detected along with high levels of Hcy and H3K79Hcy. Our results suggest that higher levels of Hcy contribute to the onset of NTDs through upregulation of histone H3K79Hcy, leading to abnormal expression of selected NTC-related genes.

2018-06-08 | GSE104093 | GEO

Aberrant expression of histone homocysteinylation: Implications for neural tube defects (RNA-seq)

2018-06-08 | GSE104094 | GEO

CIDR Genome-Wide Association Study of Neural Tube Defects

Project description:CIDR Genome-Wide Association Study of Neural Tube Defects

| PRJNA658175 | ENA

CIDR Genome-Wide Association Study of Neural Tube Defects

Project description:CIDR Genome-Wide Association Study of Neural Tube Defects

| PRJNA658177 | ENA

mRNA expression profiles of Neural Tube Defects (NTDs) in the 2nd trimester of human fetus

Project description:Neural Tube Defects (NTDs) are serious health problems of infants, accounting for large proportion of live birth defects in infants and miscarriage in women worldwide. Although some epidemiologic studies suggest both genetic and environmental factors were involved in the progression of the diseases, the etiologies of NTDs are not well understood at present. The objective of our study was to generate and to compare mRNA profiles of NTDs with those of normal controls in the 2nd trimesters of pregnancy. Illumina microarray chips (beadarrays) were utilized to identify the altered mRNA transcripts in the organ samples recruited from Luliang Prefecture in Shanxi Province, China, which has the highest occurrence of NTDs in world. The beadarrays identified 101 un-regulated and 194 down-regulated mRNA transcripts in the NTDs compared with the controls in the spinal cord. A number of genes in the cholesterol biosynthesis pathway were down-regulated. In particular, SIRT2, a key regulator of cholesterol biosynthesis, was significantly down-regulated in NTD samples. Our findings provide evidences that, the decrease of cholesterol biosynthesis in the spinal cord of NTD may affect the neural tube closure in the affected fetuses.

2019-10-10 | GSE33111 | GEO

Folate deficiency reduced aberrant level of DOT1L-mediated histone H3K79 methylation causes disruptive SHH gene expression involved in neural tube defects

Project description:Neural tube defects (NTDs) are one of the most severe congenital abnormalities. Maternal folate deficiency could impact the occurrence of NTDs. Histone H3 methyltransferase disruptor of telomeric silencing 1-like (DOT1L) expression was significantly downregulated, and low levels of H3K79me2 were found in the corresponding NTDs samples with their maternal serum folate under low levels. Using ChIP-seq assays, we found that a decrease of H3K79me2 downregulates the expression of Shh and Sufu in mouse embryonic stem cells (mESC) under folate deficiency. Our results indicate that abnormal Shh and Sufu genes expression reduced by aberrant Dot1l-mediated H3K79me2 levels could be the cause of NTDs occurrence.

2023-07-25 | GSE238081 | 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