Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Biomodal role of H3.3 in safe-guarding and establishing cell identities during reprogramming

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE99592 | GEO | 2018/02/28

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Biomodal role of H3.3 in safe-guarding and establishing cell identities during reprogramming [ChIP-Seq]

Project description:Identification of the genome-wide enrichment of H3.3, H3K4me3 and H3K36me3 during cellular reprogramming using ChIP-Seq

2018-02-28 | GSE99591 | GEO

Biomodal role of H3.3 in safe-guarding and establishing cell identities during reprogramming [RNA-Seq]

Project description:Determination of transcriptome rewiring during cellular reprogramming using RNA-Seq

2018-02-28 | GSE99548 | GEO

Biomodal role of H3.3 in safe-guarding and establishing cell identities during reprogramming [ATAC-Seq]

Project description:Determination of chromatin accessibility changes during cellular reprogramming using RNA-Seq

2018-02-28 | GSE99547 | GEO

Biomodal role of H3.3 in safe-guarding and establishing cell identities during reprogramming [RNA-Seq H3.3 KD]

Project description:Determination of transcriptome rewiring during cellular reprogramming in cells in which H3.3 had been depleted.

2018-02-28 | GSE107050 | GEO

Biomodal role of H3.3 in safe-guarding and establishing cell identities during reprogramming

Project description:Biomodal role of H3.3 in safe-guarding and establishing cell identities during reprogramming

| PRJNA388875 | ENA

Biomodal role of H3.3 in safe-guarding and establishing cell identities during reprogramming [RNA-Seq H3.3 KD]

Project description:Biomodal role of H3.3 in safe-guarding and establishing cell identities during reprogramming [RNA-Seq H3.3 KD]

| PRJNA418916 | ENA

Maternal H3.3-Mediated Reprogramming of Parental Genomes during Minor Zygotic Genome Activation

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-09-12 | GSE242960 | GEO

Establishing the pre-placodal region and breaking it into placodes with distinct identities.

Project description:Specialized sensory organs in the vertebrate head originate from thickenings in the embryonic ectoderm called cranial sensory placodes. These placodes, as well as the neural crest, arise from a zone of ectoderm that borders the neural plate. This zone separates into a precursor field for the neural crest that lies adjacent to the neural plate, and a precursor field for the placodes, called the pre-placodal region (PPR), that lies lateral to the neural crest. The neural crest domain and the PPR are established in response to signaling events mediated by BMPs, FGFs and Wnts, which differentially activate transcription factors in these territories. In the PPR, members of the Six and Eya families, act in part to repress neural crest specific transcription factors, thus solidifying a placode developmental program. Subsequently, in response to environmental cues the PPR is further subdivided into placodal territories with distinct characteristics, each expressing a specific repertoire of transcription factors that provide the necessary information for their progression to mature sensory organs. In this review we summarize recent advances in the characterization of the signaling molecules and transcriptional effectors that regulate PPR specification and its subdivision into placodal domains with distinct identities.

| S-EPMC3985045 | biostudies-literature

Histone variant H3.3 is an essential maternal factor for oocyte reprogramming.

Project description:Mature oocyte cytoplasm can reprogram somatic cell nuclei to the pluripotent state through a series of sequential events including protein exchange between the donor nucleus and ooplasm, chromatin remodeling, and pluripotency gene reactivation. Maternal factors that are responsible for this reprogramming process remain largely unidentified. Here, we demonstrate that knockdown of histone variant H3.3 in mouse oocytes results in compromised reprogramming and down-regulation of key pluripotency genes; and this compromised reprogramming for developmental potentials and transcription of pluripotency genes can be rescued by injecting exogenous H3.3 mRNA, but not H3.2 mRNA, into oocytes in somatic cell nuclear transfer embryos. We show that maternal H3.3, and not H3.3 in the donor nucleus, is essential for successful reprogramming of somatic cell nucleus into the pluripotent state. Furthermore, H3.3 is involved in this reprogramming process by remodeling the donor nuclear chromatin through replacement of donor nucleus-derived H3 with de novo synthesized maternal H3.3 protein. Our study shows that H3.3 is a crucial maternal factor for oocyte reprogramming and provides a practical model to directly dissect the oocyte for its reprogramming capacity.

| S-EPMC4034224 | biostudies-literature

Critical role of transient activation of human endogenous retroviruses during reprogramming toward pluripotency

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-08-04 | E-GEOD-56569 | biostudies-arrayexpress