Mettl14 is required for mouse postimplantation development by facilitating epiblast maturation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA683789 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13224331_1.fastq.gz | Fastqsanger.gz | |||
| SRR13224331_2.fastq.gz | Fastqsanger.gz | |||
| SRR13224332_1.fastq.gz | Fastqsanger.gz | |||
| SRR13224332_2.fastq.gz | Fastqsanger.gz | |||
| SRR13224333_1.fastq.gz | Fastqsanger.gz |
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Project description:N6-methyladenosine (m6A) is the most prevalent and reversible internal modification of mammalian messenger and noncoding RNAs mediated by specificm6A writer, reader, and eraser proteins. As an m6A writer, the methyltransferase-like 3-methyltransferase–like 14 (METTL14)–Wilms tumor 1–associated protein complex dynamically regulates m6A modification and plays important roles in diverse biologic processes. However, our knowledge about the complete functions of this RNA methyltransferase complex, the contributions of each componenttothemethylation, andtheir effects on different biologicpathways are still limited. By using both in vivo and in vitro models, we here report that METTL14 is indispensable for postimplantation embryonic development by facilitating the conversion from naive to primed state of the epiblast. Depletion of Mettl14 leads to conspicuous embryonic growth retardation from embryonic d 6.5, mainly as a result of resistanceto differentiation, which further leads to embryonic lethality early in gestation. Our data highlight the critical function of METTL14 as an m6A modification regulator in orchestrating early mouse embryogenesis.
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Project description:The early development of mouse embryos involves a tightly regulated series of lineage specification events. Following implantation, these events include maturation of the pluripotent epiblast and simultaneous establishment of the embryonic axes. Here we report that Zfp281, a transcription factor shown to be required for transitioning cells in culture from naïve to primed states of pluripotency, is essential for mouse embryonic development by regulating epiblast maturation. Transcriptomic analyses of Zfp281 mutant embryos revealed a failure in activating Nodal signaling in the epiblast leading to failure in establishing the anterior-posterior axis, and impaired epiblast maturation. Our study establishes Zfp281 as a critical factor that coordinates transcriptional and epigenetic control of pluripotent epiblast maturation.
2017-11-24 | GSE93043 | GEO
Project description:The early development of mouse embryos involves a tightly regulated series of lineage specification events. Following implantation, these events include maturation of the pluripotent epiblast and simultaneous establishment of the embryonic axes. Here we report that Zfp281, a transcription factor shown to be required for transitioning cells in culture from naïve to primed states of pluripotency, is essential for mouse embryonic development by regulating epiblast maturation. Transcriptomic analyses of Zfp281 mutant embryos revealed a failure in activating Nodal signaling in the epiblast leading to failure in establishing the anterior-posterior axis, and impaired epiblast maturation. Our study establishes Zfp281 as a critical factor that coordinates transcriptional and epigenetic control of pluripotent epiblast maturation.
2017-11-24 | GSE93042 | GEO
Project description:STAT3 has been studied extensively in the context of self-renewal of naïve pluripotent mouse embryonic stem cells (mESCs). Although STAT3 is required to maintain ICM lineages when maternally eliminated, the role of STAT3 during gastrulation is unclear as the conventional knockout of Stat3 develops until E6.5. In this study, we observed that zygotic loss of Stat3 on CD1 genetic background leads to consistent developmental retardation from implantation to mid-gestation, beginning with a significant reduction in the number of epiblast cells by the time of implantation. Remarkably, mutants appear to scale normally and resemble non-affected embryos from the previous day at all postimplantation stages examined. Bulk RNA-seq analysis using isolated epiblast cells revealeed that E6.5 null epiblasts were intermediate between WT E5.5 and E6.5; E7.5 null epiblasts grouped more closely with WT E6.5 than E7.5 epiblasts. Gene ontology analysis revealed lipid metabolism was compromised in Stat3 null embryos as early as E6.5. Interestingly, Socs3, downstream target of STAT3, was not induced in WT rpiblast cells until E7.5. We found Y705 phospholylated STAT3 was not exist postimplantation epiblast, but S727 phoshorylated STAT3 was abundant over the time, suggesting postimplantation specific roles of S727 phosphorylated STAT3 in growth and differentiation. Our study revealed that while Stat3 null epiblast cells progress along a near normal differentiation trajectory, Stat3 deletion compromises lipid metabolism as early as E6.5.
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Project description:STAT3 has been studied extensively in the context of self-renewal of naïve pluripotent mouse embryonic stem cells (mESCs). Although STAT3 is required to maintain ICM lineages when maternally eliminated, the role of STAT3 during gastrulation is unclear as the conventional knockout of Stat3 develops until E6.5. In this study, we observed that zygotic loss of Stat3 on CD1 genetic background leads to consistent developmental retardation from implantation to mid-gestation, beginning with a significant reduction in the number of epiblast cells by the time of implantation. Remarkably, mutants appear to scale normally and resemble non-affected embryos from the previous day at all postimplantation stages examined. Bulk RNA-seq analysis using isolated epiblast cells revealeed that E6.5 null epiblasts were intermediate between WT E5.5 and E6.5; E7.5 null epiblasts grouped more closely with WT E6.5 than E7.5 epiblasts. Gene ontology analysis revealed lipid metabolism was compromised in Stat3 null embryos as early as E6.5. Interestingly, Socs3, downstream target of STAT3, was not induced in WT rpiblast cells until E7.5. We found Y705 phospholylated STAT3 was not exist postimplantation epiblast, but S727 phoshorylated STAT3 was abundant over the time, suggesting postimplantation specific roles of S727 phosphorylated STAT3 in growth and differentiation. Our study revealed that while Stat3 null epiblast cells progress along a near normal differentiation trajectory, Stat3 deletion compromises lipid metabolism as early as E6.5.
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Project description:We encapsulated common marmoset pluripotent stem cells (cmPSCs) in agarose microgels and optimised culture conditions to generate epiblast and amnion spheroids. Using this system, we investigate the effects of signalling perturbations on epiblast and amnion spheroids as a model for early lineage specification
2022-07-06 | E-MTAB-10639 | biostudies-arrayexpress
Project description:Primitive ectoderm cells (PE) in blastocysts represent the foundation of the pluripotent state, which is lost progressively during development. For example, development of epiblast cells from PE in postimplantation embryos is accompanied by transcriptional and epigenetic changes, including DNA methylation and X inactivation (Refs); these changes alter the nature of epiblast cells fundamentally, affecting their responsiveness to signaling molecules, and constitute a robust boundary that prevents their reversion to a PE-like state. Notably, epiblast cells unlike PE, are refractory to leukaemia inhibitory factor (LIF)/STAT3 signalling in vitro; instead, they respond to FGF/Activin to form self-renewing epiblast stem cells (EpiSCs) that are like human ES cells, which differ significantly from mouse embryonic stem cells (ES) derived from PE. However, here we show that under appropriate conditions, epiblast cells from postimplantation embryos can respond to LIF/STAT3/fetal calf serum (FCS), and undergo reprogramming to form embryonic stem cell -like cells (repiES: reprogrammed epiblast ES-like cells). Reprogramming of epiblast cells occurs progressively. First, they form colonies that retain key properties of epiblast cells (cEpi: cultured epiblast), which subsequently show erasure of epigenetic modifications, including DNA demethylation and X-reactivation to generate repiES. Analysis also revealed that repiES progressively acquire a transcriptome profile of ES cells that is distinct from cEpi and EpiSCs. In chimeras, repiES contributed to all the tissues, including germ cells. Thus, we show for the first time that reversion of epiblast cells to repiES phenotype entails progressive loss of phenotypic and epigenetic memory of epiblast cells. Our study provides insights into underlying mechanisms, and a tractable model for how signaling molecules induce epigenetic reprogramming of cells leading to an elemental pluripotent state.
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Project description:m6A regulates virtually every step in RNA metabolism. However, its toles in limb development remains largely unknown. To understand the roles, we created a limb bud-specific conditional knockout (cKO) mice and control heterozygous (cHet) mice of the Mettl14 gene, which encodes an essential subunit in the m6A methyltransferase complex METTL3/METTL14. We harvested limb buds from the mice on E12.5 and applied the proteins to quantitative mass spectrometry to understand how the depletion of Mettl14 affected the proteomes.
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Project description:The pluripotency factor Zfp281 coordinates transcriptional and epigenetic control of epiblast maturation
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