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An essential role for Cmtr2 in mammalian embryonic development [RNA-Seq]

ABSTRACT: An essential role for Cmtr2 in mammalian embryonic development [RNA-Seq]

PROVIDER: PRJNA1130850 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29759223_1.fastq.gz	Fastqsanger.gz
	SRR29759223_2.fastq.gz	Fastqsanger.gz
	SRR29759224_1.fastq.gz	Fastqsanger.gz
	SRR29759224_2.fastq.gz	Fastqsanger.gz
	SRR29759225_1.fastq.gz	Fastqsanger.gz

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An essential role for Cmtr2 in mammalian embryonic development [scRNA-Seq]

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Project description:CMTR2 is an mRNA cap methyltransferase with poorly understood physiological functions. It catalyzes 2'-O-ribose methylation of the second transcribed nucleotide of mRNAs, potentially serving to mark RNAs as “self” to evade the cellular innate immune response. Here we analyze the consequences of Cmtr2 deficiency in mice. We discover that constitutive deletion of Cmtr2 results in mouse embryos that die during mid-gestation, exhibiting defects in embryo size, placental malformation and yolk sac vascularization. Endothelial cell deletion of Cmtr2 in mice results in vascular and hematopoietic defects, and perinatal lethality. Detailed characterization of the constitutive Cmtr2 KO phenotype shows an activation of the p53 pathway and decreased proliferation, but no evidence of interferon pathway activation. In summary, our study reveals the essential roles of Cmtr2 in mammalian cells beyond its immunoregulatory function.

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Project description:Eukaryotic RNA pol II transcripts are capped at the 5′ end by the methylated guanosine (m7G) moiety. In higher eukaryotes, CMTR1 and CMTR2 catalyse cap-proximal ribose methylations on the first (cap1) and second (cap2) nucleotides, respectively. These modifications mark RNAs as ‘self’, blocking the activation of the innate immune response pathway. Here we show that loss of mouse Cmtr1 or Cmtr2 leads to embryonic lethality, with non-overlapping sets of transcripts being regulated, without activation of the interferon pathway. In contrast, Cmtr1 mutant adult mouse livers exhibit a chronic activation of the interferon pathway, with multiple interferon-stimulated genes (ISGs) being expressed. Conditional deletion of Cmtr1 in the male germline leads to infertility, while global translation is unaffected in the Cmtr1 mutant mouse liver and human cells. Thus, mammalian cap1 and cap2 modifications have an essential role in embryonic gene regulation that is independent of their established role in evading the innate immune system.

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