Gene expression in the mTSCs of WT and Pr-set7 KO mTSCs
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA803920 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17901620.fastq.gz | Fastqsanger.gz | |||
| SRR17901621.fastq.gz | Fastqsanger.gz | |||
| SRR17901622.fastq.gz | Fastqsanger.gz | |||
| SRR17901623.fastq.gz | Fastqsanger.gz | |||
| SRR17901624.fastq.gz | Fastqsanger.gz |
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Project description:To detect the gene profiles in WT and Pr-set7 KO mTSCs, mTSCs are collected and subjected to RNA-Seq. After aligned to mouse mm10 by HISAT2, RPKM value was calculated by Edger. Our results show that Pr-set7 as the key regulator for mTSCs. There are also some genes differentially expressed after Pr-set7 KO, some of the DEGs were further confirmed by qPCR, the DEGs were associated with viral mimic inflammatory activities, antiviral innate immune response, genomic instability, and programmed cell death, indicating the essential role of Pr-set7. This RNA-Seq data provides fundamental information for our further physiological study of Pr-set7.
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Project description:To detect the gene profiles in si-NC and si-PR-SET7 KD hTSCs, hTSCs are collected and subjected to RNA-Seq. After aligned to mouse hg38 by HISAT2, RPKM value was calculated by Edger. Our results show that PR-SET7 as the key regulator for hTSCs. There are also some genes differentially expressed after PR-SET7 KD, some of the DEGs were further confirmed by qPCR, the DEGs were associated with viral mimic inflammatory activities, antiviral innate immune response, genomic instability, and programmed cell death, indicating the essential role of PR-SET7. This RNA-Seq data provides fundamental information for our further physiological study of PR-SET7.
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Project description:The ability of neural stem cells (NSCs) to switch between quiescence and proliferation is crucial for brain development and homeostasis. Increasing evidence suggest that variants of histone lysine methyltransferases including KMT5A are associated with neurodevelopmental disorders. However, the function of KMT5A/Pr-set7/SETD8 in the central nervous system is not well established. Here, we show that Drosophila Pr-Set7 is a novel regulator of NSC reactivation. Loss-of-function of pr-set7 causes a delay in NSC reactivation and loss of H4K20 monomethylation in the brain. Through NSC-specific in vivo profiling, we demonstrate that Pr-set7 binds to the promoter region of cyclin dependent kinase 1 (cdk1) and Wnt pathway transcriptional co-activator earthbound1/jerky (ebd1). Further validation indicates that Pr-set7 is required for the expression of cdk1 and ebd1 in the brain. Similar to Pr-set7, Cdk1 and Ebd1 promote NSC reactivation. Moreover, Cdk1 upregulates the Ebd1 levels in NSCs, while Ebd1 appears to downregulate Cdk1 expression, suggesting a negative feedback regulation. Finally, overexpression of Cdk1 and Ebd1 significantly suppressed NSC reactivation defects observed in pr-set7-depleted brains. Therefore, Pr-set7, the sole H4K20 methyltransferase, promotes NSC reactivation through regulating Wnt signaling and cell-cycle progression. Given the conservation of Pr-set7, our findings may contribute to the understanding of mammalian KMT5A/PR-SET7/SETD8 in NSC proliferation and associated neurodevelopmental disorders.
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Project description:PR-SET7-mediated histone-4 lysine-20 methylation has been implicated in mitotic condensation, DNA damage response and replication licencing. Here we show that PR-SET7 function in the liver is pivotal for maintaining genome integrity. Hepatocyte-specific deletion of PR-SET7 in mouse embryos resulted in G2 arrest followed by massive cell death and defect in liver organogenesis. Inactivation at postnatal stages caused cell duplication-dependent hepatocyte necrosis with unusual features of autophagy, termed "endonucleosis". Necrotic death was accompanied by inflammation, fibrosis and compensatory growth induction of neighboring hepatocytes and resident ductal progenitor cells. Prolonged necrotic-regenerative cycles coupled with oncogenic STAT3 activation replaced pre-existing hepatocytes with hepatocellular carcinoma derived entirely from ductal progenitor cells. Hepatocellular carcinoma in these mice displays a cancer stem cell gene signature specified by the co-expression of ductal progenitor markers and oncofetal genes. Mice carrying hepatocyte specific inactivation of PR-SET7 were generated in order to investigate the function of PR-SET7 histone methyl transferase in liver organogenesis, hepatocyte proliferation and liver regeneration. P15 WT mice were injected intra-peritoneally (ip) with 25ml per kg DEN (diethyl nitrosamine). Mice were examined for RNA expression at 8 months old.
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Project description:To detect genes whose expression is signigicantly altered upon depletion of pr-SET7
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