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

GSE270969 Mus musculus Expression profiling by high throughput sequencing 9 samples Submitted 2024/10/31 Platform GPL24247
Summary
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.
Published in
An essential role for Cmtr2 in mammalian embryonic development
Yermalovich AV, Mohsenin Z, Cowdin M et al. · Developmental biology 2024 · PMID 39094818 · doi:10.1016/j.ydbio.2024.07.019
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Also filed as BioProject PRJNA1129128 and SRA study SRP516629. Searching any of these in the dataset finder brings you back here.

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