The profiles of m6A modification in villous tissues with embryo damage
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA786693 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17188245_1.fastq.gz | Fastqsanger.gz | |||
| SRR17188245_2.fastq.gz | Fastqsanger.gz | |||
| SRR17188246_1.fastq.gz | Fastqsanger.gz | |||
| SRR17188246_2.fastq.gz | Fastqsanger.gz | |||
| SRR17188247_1.fastq.gz | Fastqsanger.gz |
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Project description:A growing number of studies have demonstrated that N6 methyladenine (m6A) acts as an important role in the pathogenesis of reproductive diseases, which makes it essential to profile the genome-wide m6A modifications in embryo damage. In this study, due to the microscopicity of early villous tissue, we performed high-throughput sequencing for villous tissues from three patients with embryo damage and three patients with painless abortion. Based on meRIP-seq data, we identified 18,568 m6A peaks from these two samples. These m6A peaks were mainly located in the coding region near the stop codon and were mainly characterized by AUGGAC and UGGACG motif. Compared with the normal group, the embryo damage group had 2,159 significantly upregulated m6A peaks and 281 downregulated m6A peaks. Genes with altered m6A peaks were mainly involved in Hippo and Wnt signaling pathways. Based on RNA-seq data, we found that differentially expressed genes were mainly involved in Th17 cell differentiation, TNF signaling pathway, and ECM-receptor interaction. Based on the conjoint analysis of meRIP-seq and RNA-seq data, we identified 36 genes with differentially methylated m6A peaks and synchronously differential expression. These genes were mainly involved in the Wnt signaling pathway, phosphatase activity regulation, protein phosphatase inhibitor activity, and transcription inhibitor activity. In general, our study revealed the transcriptome-wide m6A methylome in early embryonic development, which may provide novel insights into the pathogenesis and treatment of embryo damage.
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Project description:N6-methyl-adenosine (m6A) is the most abundant modification on messenger RNAs and is linked to human diseases, but its functions in mammalian development are poorly understood. Here we reveal the evolutionary conservation and function of m6A by mapping the m6A methylome in mouse and human embryonic stem cells. Thousands of messenger and long noncoding RNAs show conserved m6A modification, including transcripts encoding core pluripotency transcription factors. m6A is enriched over 3M-bM-^@M-^Y untranslated regions at defined sequence motifs, and marks unstable transcripts, including transcripts turned over upon differentiation. Genetic inactivation or depletion of mouse and human Mettl3, one of the m6A methylases, led to m6A erasure on select target genes, prolonged Nanog expression upon differentiation, and impaired ESCM-bM-^@M-^Ys exit from self-renewal towards differentiation into several lineages in vitro and in vivo. Thus, m6A is a mark of transcriptome flexibility required for stem cells to differentiate to specific lineages. Examing m6A modification differences in two different cell types
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Project description:Our study demonstrated that the expression of Igf2bp1 in activated microglia was significantly up-regulated, implying a role of Igf2bp1 in LPS-induced m6A modifications in microglia. To understand the roles of Igf2bp1 on LPS-induced m6A modification in microglia, we performed Igf2bp1 loss-of-function (LOF) approach. Microglia stimulated by LPS were transfected with either scrambled siRNA control or Igf2bp1 siRNA for 48 hours. To m6A modification profiles in control and Igf2bp1 LOF microglia were determined by MeRIP-seq analysis.
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Project description:Here we determine the map of RNA methylation (m6A) in mouse embrionic stem cells, and Mettl3 knock out cells Examination of m6A modification sites on the transcriptome of mouse Embryonic stem cells and Embryonic Mettl3 knock out cells, using a m6A specific antibody.
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Project description:In this study we performed MeRIP-Seq to study N6-methyl adenosine (m6A) and and N6,2′ -O-dimethyladenosine (m6Am) modification of mRNA. We investigated the effect of the microbiota on the transcriptome and epitranscriptomic modifications in murine liver and cecum. We compared m6A/m modification profiles in cecum of conventionally raised (CONV) and germ-free (GF) mice. We additionally included GF mice colonised with the flora of CONV mice for four weeks (ex-GF), for which show that they exhibit similar patterns of the most abundant genera of gut bacteria as CONV mice. We added mice treated with several antibiotics to deplete the gut flora (abx)and vancomycin treated mice in which the genera Akkermansia, Escherichia/Shigella and Lactobacillus were enriched. Furthermore, we included GF mice colonised with the commensal bacterium Akkermansia muciniphila (Am), Lactobacillus plantarum (Lp) and Escherichia coli Nissle (Ec) and analysed their m6A/m modification profiles. In addition, we analysed changes in m6A/m- modified liver RNA for CONV, GF, and Am, Lp and Ec mice.
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Project description:Posttranscriptional and posttranslational modifications play crucial roles in plant immunity. However, how plant fine-tune these two modifications to activate antiviral immunity remains unknown. Here, we report that the m6A methyltransferase TaHAKAI is utilized by wheat yellow mosaic virus (WYMV) to increase viral genomic m6A modification and promotes viral replication. However, TaHAKAI also functions as an E3 ligase that targets the viral RNA silencing suppressor P2 for degradation and inhibits viral infection. A major allele of TaHAKAI in susceptible cultivar reduced the E3 ligase activity but not m6A methyltransferase activity, promoting viral infection. Interestingly, TaHAKAIR attenuates the mRNA stability of TaWPS1, the negative regulator of spike development, to increase panicle length and spikelet number by modulating its m6A modification. Our study reveals a new mechanisms of balancing disease resistance and yield by fine-tuning m6A modification and ubiquitination.
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Project description:RNA modifications, including m6A, critically modulate protein expression program in a range of cellular processes. Although cellular senescence has been linked to age-related diseases and functional declines, the landscape and impact of m6A modification are poorly understood. Here, we report a robust m6A modification of Patched-Domain Containing Protein 4 (PTCHD4) mRNA at m6A in senescent cells. The METTL3/METTL14 complex was found to mediate the m6A modification of PTCHD4 mRNA, which increased PTCHD4 mRNA stability and PTCHD4 production. MeRIP RT-qPCR and eCLIP analyses were used to map this m6A modification to the last exon of PTCHD4 mRNA. Further investigation identified IGF2BP1, but not other m6A readers, as being responsible for stabilization and increased abundance of PTCHD4 mRNA by m6A modification. Silencing PTCHD4, a transmembrane protein, enhanced growth arrest and DNA damage in pre-senescent cells, and sensitized them to senolytic treatments and apoptosis. Our results support the notion that m6A modifications critically control senescence programs, and that factors such as METTL3/METTL14 and IGF2BP1, implicated in PTCHD4 mRNA m6A metabolism, could be exploited to eliminate senescent cells for therapeutic benefit.
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Project description:RNA modifications, including m6A, critically modulate protein expression program in a range of cellular processes. Although cellular senescence has been linked to age-related diseases and functional declines, the landscape and impact of m6A modification are poorly understood. Here, we report a robust m6A modification of Patched-Domain Containing Protein 4 (PTCHD4) mRNA at m6A in senescent cells. The METTL3/METTL14 complex was found to mediate the m6A modification of PTCHD4 mRNA, which increased PTCHD4 mRNA stability and PTCHD4 production. MeRIP RT-qPCR and eCLIP analyses were used to map this m6A modification to the last exon of PTCHD4 mRNA. Further investigation identified IGF2BP1, but not other m6A readers, as being responsible for stabilization and increased abundance of PTCHD4 mRNA by m6A modification. Silencing PTCHD4, a transmembrane protein, enhanced growth arrest and DNA damage in pre-senescent cells, and sensitized them to senolytic treatments and apoptosis. Our results support the notion that m6A modifications critically control senescence programs, and that factors such as METTL3/METTL14 and IGF2BP1, implicated in PTCHD4 mRNA m6A metabolism, could be exploited to eliminate senescent cells for therapeutic benefit.
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