Ybx1 binding sites and Ybx1-binding m5C sites in zebrafish embryo sample.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA493828 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7942635_1.fastq.gz | Fastqsanger.gz | |||
| SRR7942635_2.fastq.gz | Fastqsanger.gz | |||
| SRR7942636_1.fastq.gz | Fastqsanger.gz | |||
| SRR7942636_2.fastq.gz | Fastqsanger.gz | |||
| SRR7942637_1.fastq.gz | Fastqsanger.gz |
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Project description:The maternal-to-zygotic transition (MZT) is a conserved and fundamental process during which the embryo undergoes dramatic reprogramming to convert maternal environment to embryonic-driven programing. However, how the maternally supplied transcripts are dynamically regulated during MZT remains largely unknown. Herein, through genome-wide profiling of RNA 5-methylcytosine (m5C) in zebrafish early embryos, we show that m5C methylated maternal mRNAs display higher stability during MZT. We identify that the Y box-binding protein 1 (Ybx1) prefers to recognizing m5C-modified mRNAs through p-p interaction with a key residue Trp45 in its cold shock domain (CSD), which plays essential roles in maternal mRNA stability and early embryogenesis of zebrafish. Cooperated with an mRNA stabilizer Pabpc1a, Ybx1 promotes the stability of its target mRNAs in an m5C-dependent manner. Our study demonstrates a novel mechanism of RNA m5C methylation-regulated maternal mRNA stability during zebrafish MZT, highlighting the critical role of m5C mRNA methylation in early development.
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Project description:The maternal-to-zygotic transition (MZT) is a conserved and fundamental process during which the embryo undergoes dramatic reprogramming to convert maternal environment to embryonic-driven programing. However, how the maternally supplied transcripts are dynamically regulated during MZT remains largely unknown. Herein, through genome-wide profiling of RNA 5-methylcytosine (m5C) in zebrafish early embryos, we show that m5C methylated maternal mRNAs display higher stability during MZT. We identify that the Y box-binding protein 1 (Ybx1) prefers to recognizing m5C-modified mRNAs through p-p interaction with a key residue Trp45 in its cold shock domain (CSD), which plays essential roles in maternal mRNA stability and early embryogenesis of zebrafish. Cooperated with an mRNA stabilizer Pabpc1a, Ybx1 promotes the stability of its target mRNAs in an m5C-dependent manner. Our study demonstrates a novel mechanism of RNA m5C methylation-regulated maternal mRNA stability during zebrafish MZT, highlighting the critical role of m5C mRNA methylation in early development.
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Project description:The modification and recognition of 5-methylcytosine (m5C) are involved in the initiation and progression of various tumor types. However, the precise role and potential mechanism of Y-box-binding protein 1 (YBX1) in esophageal squamous cell carcinoma (ESCC) remains unclear. Here, we found that YBX1 was frequently upregulated in ESCC compared with matched nontumor tissues. Gain- and loss-of-function assays showed that YBX1 promoted the proliferation and metastasis of ESCC cells both in vitro and in vivo. Functional studies revealed that NOP2/Sun RNA methyltransferase family member 2 (NSUN2) is a critical RNA methyltransferase that facilitates YBX1-mediated ESCC progression. Mechanistically, integrated analysis based on RNA immunoprecipitation sequencing (RIP-seq) and m5C methylated RNA immunoprecipitation and sequencing (MeRIP-seq) assays identified spermine oxidase (SMOX) as a target gene containing an m5C site in its coding sequence (CDS) region, which coincided well with the binding site of YBX1. Overexpression of SMOX-WT but not SMOX-Mut partially restored the proliferation and invasion ability of ESCC cells curbed by YBX1 knockdown. Moreover, YBX1 activated the mTORC1 signaling pathway by stabilizing SMOX mRNA. Our study revealed that YBX1 promotes ESCC development by stabilizing SMOX mRNA in an m5C-dependent manner, thus providing a valuable therapeutic target for ESCC.
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Project description:The reversible epitranscriptomic mark, 5-methylcytosine (m5C) modification, is implicated in numerous cellular processes, but its role in neuronal development remains largely unexplored. In this study, we discovered high expression of the m5C reader Ybx1 in the developing mouse cortex. To elucidate its role in cortical development, Ybx1 was deleted in mouse embryonic cortical neural stem cells (NSCs). Interestingly, the deletion of Ybx1 led to perinatal mortality in mice, along with abnormal cortical development. Cortical progenitor cells lacking Ybx1 exhibited impaired proliferation and differentiation. Multi-omics analysis identified the target mRNAs of Ybx1, which encode the key cell cycle regulatory proteins, such as cyclin D2 (Ccnd2). Ybx1 was found to regulate the stability of its target transcripts. Both knockdown and overexpression of Ybx1 targets via in utero electroporation confirmed that they mediated the Ybx1 regulation of proliferation and differentiation of neural precursor cells. Further mechanistic analysis showed that deletion of Ybx1 resulted in the blocking of G1 to S phase transition in the cortical progenitor cells. This study highlights the crucial function of the m5C reader protein Ybx1 in promoting cell cycle progression of the embryonic cortical progenitors, essential for proper cortical development.
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Project description:The reversible epitranscriptomic mark, 5-methylcytosine (m5C) modification, is implicated in numerous cellular processes, but its role in neuronal development remains largely unexplored. In this study, we discovered high expression of the m5C reader Ybx1 in the developing mouse cortex. To elucidate its role in cortical development, Ybx1 was deleted in mouse embryonic cortical neural stem cells (NSCs). Interestingly, the deletion of Ybx1 led to perinatal mortality in mice, along with abnormal cortical development. Cortical progenitor cells lacking Ybx1 exhibited impaired proliferation and differentiation. Multi-omics analysis identified the target mRNAs of Ybx1, which encode the key cell cycle regulatory proteins, such as cyclin D2 (Ccnd2). Ybx1 was found to regulate the stability of its target transcripts. Both knockdown and overexpression of Ybx1 targets via in utero electroporation confirmed that they mediated the Ybx1 regulation of proliferation and differentiation of neural precursor cells. Further mechanistic analysis showed that deletion of Ybx1 resulted in the blocking of G1 to S phase transition in the cortical progenitor cells. This study highlights the crucial function of the m5C reader protein Ybx1 in promoting cell cycle progression of the embryonic cortical progenitors, essential for proper cortical development.
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