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YTHDC1 is essential for cardiac development [RNA-seq]

ABSTRACT: The goal of this study is to investigate how YTHDC1 regulate cardiac development.

ORGANISM(S): Mus musculus

PROVIDER: GSE241271 | GEO | 2024/05/05

REPOSITORIES: GEO

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Project description:The goal of this study is to investigate how YTHDC1 regulates islet β-cell function. Our study represents the first detailed analysis of islet transcriptomes from Ythdc1flox/flox and Ythdc1-βKO mice, generated by RNA-seq technology. The RNA-seq analysis showed that 2869 genes were downregulated and 2825 genes were upregulated in the pancreatic islets of Ythdc1-βKO mice.

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YTHDC1 is essential for cardiac development

Project description:This SuperSeries is composed of the SubSeries listed below.

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Project description:we investigate the role of YTHDC1 in normal hematopoiesis and adult hematopoietic stem/progenitor cell (HSPC) maintenance in vivo. Utilizing conditional Ythdc1 knockout mice ,we show that YTHDC1 is required for hematopoietic stem cell (HSC) maintenance as well as self-renewal of HSC. Transcriptome analysis identified many differentially expressed genes (DEGs) between WT and YTHDC1-KO LT-HSCs.

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Project description:N6-methyladenosine (m6A) is the most common internal modification in eukaryotic messenger RNAs (mRNAs) and plays essential roles in mammals. The function of this chemical modification is deciphered by m6A-specific binding proteins of the YTH family. Recent studies indicated that m6A methyltransferase METTL3 ('writer') and demethylase FTO ('eraser') play critical roles in cardiovascular diseases. However, function of m6A 'reader' proteins in the heart is still largely unknown. Here, we report that cardiac-speciﬁc ablation of Ythdc1 in postnatal heart exhibits progressive dilated cardiomyopathy, heart failure and dramatically increases the incidence of postnatal lethality. Mechanically, the transcript of Titin-the major DCM and heart failure related gene-is decorated by m6A modification and directly recognized by YTHDC1, deficiency of Ythdc1 in heart results in abnormal splicing of TTN and disarray of sarcomeric structures in the cardiomyocytes subsequently. Collectively, we demonstrated that YTHDC1-dependent TTN splicing is crucial for the postnatal heart development and cardiac function, which probably provides a potential target for treating DCM through tuning m6A modification of TTN mRNA.

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