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

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

PROVIDER: PRJNA1129128 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29632500.fastq.gz	Fastqsanger.gz
	SRR29632501.fastq.gz	Fastqsanger.gz
	SRR29632502.fastq.gz	Fastqsanger.gz
	SRR29632503.fastq.gz	Fastqsanger.gz
	SRR29632504.fastq.gz	Fastqsanger.gz

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

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

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

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.

2024-10-31 | GSE270969 | GEO

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

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Essential roles of RNA cap-proximal ribose methylation in mammalian embryonic development and fertility

Project description:Essential roles of RNA cap-proximal ribose methylation in mammalian embryonic development and fertility

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Essential roles of RNA cap-proximal ribose methylation in mammalian embryonic development and fertility

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.

2023-07-14 | GSE235348 | GEO

Essential requirement of mammalian Pumilio family in embryonic development.

Project description:Mouse PUMILIO1 (PUM1) and PUMILIO2 (PUM2) belong to the PUF (Pumilio/FBF) family, a highly conserved RNA binding protein family whose homologues play critical roles in embryonic development and germ line stem cell maintenance in invertebrates. However, their roles in mammalian embryonic development and stem cell maintenance remained largely uncharacterized. Here we report an essential requirement of the Pum gene family in early embryonic development. A loss of both Pum1 and Pum2 genes led to gastrulation failure, resulting in embryo lethality at E8.5. Pum-deficient blastocysts, however, appeared morphologically normal, from which embryonic stem cells (ESCs) could be established. Both mutant ESCs and embryos exhibited reduced growth and increased expression of endoderm markers Gata6 and Lama1, making defects in growth and differentiation the likely causes of gastrulation failure. Furthermore, ESC Gata6 transcripts could be pulled down via PUM1 immunoprecipitation and mutation of conserved PUM-binding element on 3'UTR (untranslated region) of Gata6 enhanced the expression of luciferase reporter, implicating PUM-mediated posttranscriptional regulation of Gata6 expression in stem cell development and cell lineage determination. Hence, like its invertebrate homologues, mouse PUM proteins are conserved posttranscriptional regulators essential for embryonic and stem cell development.

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Filamin C is Essential for Mammalian Myocardial Integrity

Project description:Filamin C is Essential for Mammalian Myocardial Integrity

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scRNA-seq of embryonic skin development (developmental time series in full-thickness dorsal skin of mouse embryos)

Project description:In this study, we analysed early embryonic skin development (mus musculus; C57BL/6J) at the transcriptional level. Major questions concerned the cell type composition of early embryonic skin, and the emergence of transcriptional heterogeneity among epithelial and stromal precursor cells. Cells were isolated from embryonic dorsal skin and randomly sequenced (scRNA-Seq using 10X Genomics v2) without any cell sorting. Data from three embryonic time points (E12.5, E13.5, and E14.5) was integrated and compared to obtain a better understanding of the dynamics of early skin development.

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Mammalian copper chaperone Cox17p has an essential role in activation of cytochrome C oxidase and embryonic development.

Project description:Cox17p is essential for the assembly of functional cytochrome c oxidase (CCO) and for delivery of copper ions to the mitochondrion for insertion into the enzyme in yeast. Although this small protein has already been cloned or purified from humans, mice, and pigs, the function of Cox17p in the mammalian system has not yet been elucidated. In vitro biochemical data for mammalian Cox17p indicate that the copper binds to the sequence -KPCCAC-. Although mouse embryos homozygous for COX17 disruption die between embryonic days E8.5 and E10, they develop normally until E6.5. This phenotype is strikingly similar to embryos of Ctr1(-/-), a cell surface copper transporter, in its lethality around the time of gastrulation. COX17-deficient embryos exhibit severe reductions in CCO activity at E6.5. Succinate dehydrogenase activity and immunoreactivities for anti-COX subunit antibodies were normal in the COX17(-/-) embryos, indicating that this defect was not caused by the deficiency of other complexes and/or subunits but was caused by impaired CCO activation by Cox17p. Since other copper chaperone (Atox1 and CCS)-deficient mice show a more moderate defect, the disruption of the COX17 locus causes the expression of only the phenotype of Ctr1(-/-). We found that the activity of lactate dehydrogenase was also normal in E6.5 embryos, implying that the activation of CCO by Cox17p may not be essential to the progress of embryogenesis before gastrulation.

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scRNA-Seq analysis of differentiation to primitive streak fate of mouse embryonic stem cells

Project description:scRNA-Seq analysis of differentiation to primitive streak fate of mouse embryonic stem cells

2022-01-20 | E-MTAB-10243 | biostudies-arrayexpress