Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

De novo DNA methylation suppresses aberrant fate trajectory during epiblast transition [RNA-seq]

ABSTRACT: De novo DNA methylation suppresses aberrant fate trajectory during epiblast transition [RNA-seq]

PROVIDER: PRJNA664787 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12683317.fastq.gz	Fastqsanger.gz
	SRR12683318.fastq.gz	Fastqsanger.gz
	SRR12683319.fastq.gz	Fastqsanger.gz
	SRR12683320.fastq.gz	Fastqsanger.gz
	SRR12683321.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 32

Similar Datasets

De novo DNA methylation suppresses aberrant fate trajectory during epiblast transition [ATAC-seq]

Project description:Genome remethylation is essential for mammalian development. Here we examined cell fate in the absence of de novo DNA methyltransferases. We found that embryonic stem (ES) cells deficient for Dnmt3a and Dnmt3b are rapidly eliminated from chimaeras. Pluripotency progression is derailed towards extra-embryonic trophoblast. This aberrant trajectory is propelled by failure to methylate and suppress expression of Ascl2 during formative transition. Ascl2 deletion rescues transition and improves contribution to chimaeric epiblast but mutant cells are progressively lost in later development. These findings indicate that methylation constrains transcriptome trajectories during developmental transitions by silencing potentially disruptive genes. This submission is ATAC-seq.

2021-09-01 | GSE158344 | GEO

De novo DNA methylation suppresses aberrant fate trajectory during epiblast transition [RNA-seq]

2021-09-01 | GSE158310 | GEO

De novo DNA methylation suppresses aberrant fate trajectory during epiblast transition [ATAC-seq]

Project description:De novo DNA methylation suppresses aberrant fate trajectory during epiblast transition [ATAC-seq]

| PRJNA664950 | ENA

De novo formation of apical-basal polarity by Rap1 regulates epiblast patterning

Project description:The epiblast is the first cell type that forms apical-basal polarity de novo as the mouse embryo implants into the maternal uterus, while the extraembryonic neighbours of the epiblast - trophectoderm and primitive endoderm - retain their pre-established polarity beyond implantation [1]; however, it is still unclear how the epiblast establishes apical-basal polarity de novo. Here, we focused on Rap1 signaling pathway, which is activated during the transition of the epiblast from the naïve to primed state of pluripotency during implantation [2]. Through the preestablished in vitro three-dimensional culture system [3], genetic knockouts and proximity-biotinylation analyses, we found that Rap1 integrates multiple signals that contribute to de novo formation of apical-basal polarity. Importantly, formation of apical-basal polarity in the epiblast is essential for its correct patterning and proper communication with the extraembryonic lineages. Altogether, these results not only dissect molecular details of de novo apical-basal polarity formation, but also have broader implications for epithelial polarity and development.

2022-06-14 | PXD028315 | Pride

Disabling de novo DNA methylation in embryonic stem cells allows an illegitimate fate trajectory

Project description:Genome remethylation is essential for mammalian development but specific reasons are unclear. Here we examined embryonic stem (ES) cell fate in the absence of de novo DNA methyltransferases. We observed that ES cells deficient for both Dnmt3a and Dnmt3b are rapidly eliminated from chimeras. On further investigation we found that in vivo and in vitro the formative pluripotency transition is derailed toward production of trophoblast. This aberrant trajectory is associated with failure to suppress activation of Ascl2. Ascl2 encodes a bHLH transcription factor expressed in the placenta. Misexpression of Ascl2 in ES cells provokes transdifferentiation to trophoblast-like cells. Conversely, Ascl2 deletion rescues formative transition of Dnmt3a/b mutants and improves contribution to chimeric epiblast. Thus, de novo DNA methylation safeguards against ectopic activation of Ascl2. However, Dnmt3a/b-deficient cells remain defective in ongoing embryogenesis. We surmise that multiple developmental transitions may be secured by DNA methylation silencing potentially disruptive genes. This SuperSeries is composed of the SubSeries listed below.

2021-08-31 | GSE158347 | GEO

Multi-Omic analyses reveal aberrant differentiation trajectory with WNT1 Loss-of-Function in type XV osteogenesis imperfecta

Project description:Osteogenesis imperfecta (OI) is a serious genetic bone disorder characterized by congenital low bone mass, deformity and frequent fractures. Type XV OI is a moderate to severe form of skeletal dysplasia caused by WNT1 mutations. In this cohort study from southern China, we summarized the clinical phenotypes of patients with WNT1 mutations and found the proportion of type XV patients was around 10.3% (25 out of 243) with diverse phenotypic spectrums. Functional assays indicated that mutations of WNT1 significantly impaired its secretion and effective activity, leading to moderate to severe clinical manifestations, porous bone structure and enhanced osteoclastic activities. Analysis of proteomic data from human skeleton indicated that the expression of SOST was dramatically reduced in type XV patients. Single-cell transcriptome data generated from human tibia samples revealed aberrant differentiation trajectory of skeletal progenitors and impaired maturation of osteocytes, resulting in excessive CXCL12+ progenitors and abnormal cell populations with adipogenic characteristics. The integration of multi-omics data from human skeleton delineates how WNT1 regulates the differentiation and maturation of skeletal progenitors, which will provide a new direction for the treatment strategy of type XV osteogenesis imperfecta and relative low bone mass diseases such as early onset osteoporosis.

2024-10-17 | PXD050841 | Pride

Microbial pattern recognition suppresses de novo organogenesis.

Project description:De novo root regeneration (DNRR) is a developmental process that regenerates adventitious roots from wounded tissues. Phytohormone signaling pathways involved in microbial resistance are mobilized after cutting and influence de novo root regeneration. Microbes may positively or negatively influence the development and stress responses of a plant. However, most studies on the molecular mechanisms of de novo organogenesis are performed in aseptic conditions. Thus, the potential crosstalk between organ regeneration and biotic stresses is underexplored. Here, we report the development of a versatile experimental system to study the impact of microbes on DNRR. Using this system, we found that bacteria inhibited root regeneration by activation of, but not limited to, pathogen-associated molecular pattern (PAMP)-triggered immunity. Sensing bacteria-derived flagellin 22 peptide (flg22) inhibited root regeneration by interfering with the formation of an auxin maximum at the wound site. This inhibition relies on the receptor complex that recognizes microbial patterns but may bypass the requirement of salicylic acid signaling.

| S-EPMC10259513 | biostudies-literature

Disabling de novo DNA methylation in embryonic stem cells allows an illegitimate fate trajectory

Project description:Disabling de novo DNA methylation in embryonic stem cells allows an illegitimate fate trajectory

| PRJNA664942 | ENA

Trancsriptomic analyses reveal aberrant differentiation trajectory with WNT1 Loss-of-Function in type XV osteogenesis imperfecta

Project description:Trancsriptomic analyses reveal aberrant differentiation trajectory with WNT1 Loss-of-Function in type XV osteogenesis imperfecta

| PRJNA1090225 | ENA

Multi-Omic analyses reveal aberrant differentiation trajectory with WNT1 Loss-of-Function in type XV osteogenesis imperfecta

Project description:Multi-Omic analyses reveal aberrant differentiation trajectory with WNT1 Loss-of-Function in type XV osteogenesis imperfecta

| PRJNA1090226 | ENA