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Aberrant expression of histone homocysteinylation: Implications for neural tube defects

ABSTRACT: Aberrant expression of histone homocysteinylation: Implications for neural tube defects

PROVIDER: PRJNA408231 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6056724.fastq.gz	Fastqsanger.gz
	SRR6056725.fastq.gz	Fastqsanger.gz
	SRR6056726.fastq.gz	Fastqsanger.gz
	SRR6056727.fastq.gz	Fastqsanger.gz
	SRR6056728.fastq.gz	Fastqsanger.gz

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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)

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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)

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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.

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

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

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

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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

CIDR Genome-Wide Association Study of Neural Tube Defects

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CIDR Genome-Wide Association Study of Neural Tube Defects

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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

Abnormal Transcriptome-wide of DNA demethylation in Folate deficiency caused neural tube defects [MeDIP]

Project description:To investigate the associated with abnormal DNA demethylation and neural tube defects (NTDs) with folate deficiency, we etablished mouse embryonic stem cells (mESCs) Sv/129 in folate-deficiency-treated.

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