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

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

PROVIDER: PRJNA408236 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6056727.fastq.gz	Fastqsanger.gz
	SRR6056728.fastq.gz	Fastqsanger.gz

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Aberrant expression of histone homocysteinylation: Implications for neural tube defects

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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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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.

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