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M6A mRNA modification is a rheostat to maintain colonic epithelial cell homeostasis [scRNA-seq]

ABSTRACT: The function of m6A modification in colonic epithelial cells has been validated in our study that depletion of METTL14 in colonic epithelial cells triggers cell death. To further explore the biological effects of m6A deficiency in colonic epithelial cell heterogeneity, we performed single cell RNA-seq of colonic epithelial cells form 2-week-old Mettl14-KO and WT control mice

ORGANISM(S): Mus musculus

PROVIDER: GSE171422 | GEO | 2022/04/19

REPOSITORIES: GEO

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m6A mRNA modification is a rheostat to maintain colonic epithelial cell homeostasis [bulkRNA-seq]

Project description:The function of m6A modification in colonic epithelial cells has been validated in our study that depletion of METTL14 in colonic epithelial cells triggers cell death. To further explore the biological effects of m6A deficiency in colonic epithelial cells, we performed RNA sequencing analysis of colonic epithelial cells form 2-week-old Mettl14-KO and WT control mice.The bioinformatic analysis revealed that METTL14 depletion increased the mRNA expression of NF-kB inhibitor Nfkbia, which favored TNF-induced cell death.

2022-04-19 | GSE171421 | GEO

m6A modification maps of mRNA in colonic epithelial cells from mouse

Project description:We report the application of sequencing technology for high-throughput profiling of mRNA m6A methylation in mice colonic epithelial cells with or without mettl14 deletion. By obtaining over thirty billion bases of sequence from m6A antibody immunoprecipitated mRNA, we generated m6A methylation maps of mouse colonic epithelial cells with or with mettl14 deletion. We find that GsdmC2, GsdmC3, GadmC3 mRNA methylation is robustly decreased in colonic epithelial cells upon mettl14 deletion, leading to the decrease of Gsdmc expression.

2022-06-22 | GSE181863 | GEO

m6A mRNA modification is a rheostat to maintain colonic epithelial cell homeostasis

Project description:m6A mRNA modification is a rheostat to maintain colonic epithelial cell homeostasis

| PRJNA719489 | ENA

m6A mRNA modification is a rheostat to maintain colonic epithelial cell homeostasis [bulkRNA-seq]

Project description:m6A mRNA modification is a rheostat to maintain colonic epithelial cell homeostasis [bulkRNA-seq]

| PRJNA719512 | ENA

m6A mRNA modification is a rheostat to maintain colonic epithelial cell homeostasis [scRNA-seq]

Project description:m6A mRNA modification is a rheostat to maintain colonic epithelial cell homeostasis [scRNA-seq]

| PRJNA719513 | ENA

METTL14 regulates neuroblastoma through the m6A modification

Project description:RNA methylation is involved in the regulation of cell response and cell fate, and is closely related to the development of tumors. METTL14 is considered to be a m6A methyltransferase. Studies have found that METTL14 is associated with the occurrence and development of a variety of tumors, but the mechanism in neuroblastoma is not clear. The expression of METTL14 in high risk patients was significantly higher than that in low risk patients. Interference with METTL14 expression in SK-N-BE(2) cells significantly interfered with cell cycle and inhibited cell proliferation, migration and invasion. In neuroblastoma, METTL14 activates the PI3K/AKT signaling pathway by targeting YWHAH by upregulating m6A levels in mRNA transcripts. In all findings, it was suggested that METTL14 has a cancer-promoting function in neuroblastoma.

2024-05-10 | GSE244350 | GEO

RNA methylation destabilizes developmental regulators in murine embryonic stem cells (m6A)

Project description:m6A-seq of mouse embryonic stem cell wildtype or mutant depleted of Mettl3 or Mettl14 m6A-mRNA library for mouse embryonic stem cell each having one biological replicate were generated using HiSeq2000 v3 flowcell (Illumina) and sequenced for 100 bases with separate 7 base indexing read in a single lane.

2014-01-06 | E-GEOD-46878 | biostudies-arrayexpress

m6A mRNA modification is a rheostat to maintain colonic epithelial cell homeostasis

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

2022-04-19 | GSE171423 | GEO

m6A modification maps of mRNA in colonic epithelial cells from mouse

Project description:m6A modification maps of mRNA in colonic epithelial cells from mouse

| PRJNA753769 | ENA

Mettl14-dependent m6A modification controls iNKT cells development and function by regulating p53-dependent apoptosis pathway and TCR signaling

Project description:N6-methyladenosine (m6A) is the most common modification to mRNA in mammalian cells linked to development and disease. m6A controls CD4+ T cell homeostasis by targeting the IL-7/STAT5/SOCS family pathway and sustains Treg suppressive function. However, the role of m6A modification in non-conventional T cell development and function remains unknown. Here we showed that m6A modification was indispensable for NKT cell homeostasis using mice with T cell-specific deletion of RNA methylation writer METTL14 (T-Mettl14-/-). Loss of METTL14-dependent m6A modification led to the upregulation of p53-mediated apoptosis in double-positive (DP) thymocytes. The decreased lifespan of DP thymocytes reduced the efficiency of distal Va-Ja rearrangement, including the invariant Va14-Ja18 TCR, and therefore led to a profound decrease in the iNKT cell population. The residual iNKT cells in T-Mettl14-/- mice exhibited increased apoptosis and impaired maturation. In addition, loss of METTL14 upregulated Cish expression, which contributed to decreased proliferative response to IL-2 and IL-15 and impaired cytokine production upon TCR stimulation in METTL14-deficient iNKT cells. Furthermore, knocking down METTL14 in mature iNKT cells diminished their cytokine production, correlated with increased Cish expression and decreased TCR signaling. Collectively, our data reveals a critical role for METTL14- dependent-m6A modification in iNKT cell development and function, highlighting the need to take this effect into consideration for targeting m6A pathway in therapeutic settings.

2022-03-01 | GSE189339 | GEO

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