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M6A modification in DP and iNKT cells

ABSTRACT: m6A modification in DP and iNKT cells

PROVIDER: PRJNA865276 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20751003_1.fastq.gz	Fastqsanger.gz
	SRR20751003_2.fastq.gz	Fastqsanger.gz
	SRR20751004_1.fastq.gz	Fastqsanger.gz
	SRR20751004_2.fastq.gz	Fastqsanger.gz
	SRR20751005_1.fastq.gz	Fastqsanger.gz

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m6A modification in DP and iNKT cells

Project description:Invariant natural killer T (iNKT) cells are a specific innate-like counterpart of T lymphocytes, which response to lipid-based antigens and provide a functional bridge between the innate and adaptive immunity. The physiological role of m6A modification involved in NK cells differentiation remains unclear. We found that N6-Methyladenosine (m6A) methyltransferase METTL3 is intrinsically required for iNKT cell development and function in an m6A-dependent manner. To investigate the molecular mechanisms, m6A-LACE-seq was performed using iNKT cells and Merip-seq was performed using DP cells in thymocytes isolated from WT and KO mice to investigate the regulatory network.

2023-12-31 | GSE210325 | GEO

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.

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m6A RNA modification controls cell fate transition in mammalian embryonic stem cells

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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