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Mettl3-mediated m6A Methylation Determines the Size of Endocrine Progenitor Pool and Postnatal Islet Mass [scRNA-seq]

ABSTRACT: To investigate the role of RNA methyltransferase-like 3 (Mettl3)-mediated m6A modification in pancreatic endocrine differentiation in early embryonic period. We then performed single cell RNA-seq at E15.5 Mettl3pKO pancreas group and E15.5 WT pancreas group

ORGANISM(S): Mus musculus

PROVIDER: GSE234256 | GEO | 2024/03/18

REPOSITORIES: GEO

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Mettl3-mediated m6A Methylation Determines the Size of Endocrine Progenitor Pool and Postnatal Islet Mass

Project description:To investigate the role of RNA methyltransferase-like 3 (Mettl3)-mediated m6A modification in pancreatic endocrine differentiation in early embryonic period. We then performed m6A MeRIP-seq (GenSeq®️ m6A MeRIP Kit) at E15.5 Mettl3pKO pancreas group and E15.5 WT pancreas group

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Mettl3-mediated m6A Methylation Determines the Size of Endocrine Progenitor Pool and Postnatal Islet Mass

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Mettl3-mediated m6A Methylation Determines the Size of Endocrine Progenitor Pool and Postnatal Islet Mass [scRNA-seq]

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Pdx1-Oc1 cooperatively drive the induction of the endocrine pancreatic program

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The Bruchpilot cytomatrix determines the size of the readily releasable pool of synaptic vesicles.

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Project description:To find the genes with H3K36me3 modificaiton at different stages of pancreas development, we isolated the pancreatic epithelial cells from E11.5, E13.5 and E15.5 fetal pancreas. Considering the low expression of H3K36me3 at E11.5, E11.5 samples worked as a "negantive" control. By compared with the peaks of E11.5, we was able to find genes under direct regulation of H3K36me3 at E13.5 and E15.5.

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Project description:Retinoic acid (RA) signaling is essential for multiple developmental processes, including appropriate pancreas formation from the foregut endoderm. RA is also required to generate pancreatic progenitors from human pluripotent stem cells. However, the role of RA during the later stages of pancreas development is not well understood. In this study, we generated an inducible system to block RA signaling and demonstrate that disruption of the RA pathway within the Neurog3-expressing endocrine progenitor population is required for appropriate mouse b cell differentiation and repression of critical d cell genes, including Somatostatin. In addition, inhibition of the RA pathway in hESC-derived pancreatic progenitors downstream of NEUROG3 induction impairs INSULIN expression. We further determined that RA-regulation of endocrine cell differentiation is mediated through Wnt pathway components. Together, these data demonstrate the importance of RA signaling in endocrine specification and identify conserved mechanisms by which RA signaling directs endocrine cell fate.

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