Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide CRISPR screen identifies Menin and SUZ12 as regulators of human developmental timing.

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE279036 | GEO | 2025/06/26

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Genome-wide CRISPR screen identifies Menin and SUZ12 as regulators of human developmental timing [CUT&RUN]

Project description:Embryonic development follows a sequence of events that is broadly conserved across species, yet the pace of development is highly variable. Compared to most other species, humans exhibit a slower pace that is largely recapitulated in in vitro stem cell models, suggesting a cell-intrinsic clock that tracks time. Using the directed differentiation of human embryonic stem cells (hESCs) into neuroectoderm as a proxy for developmental timing, we performed a whole-genome CRISPR-Cas9 screen and found that epigenetic factors MEN1 and SUZ12 modulate the speed of hESC neural differentiation. Genetic and pharmacological loss-of-function of MEN1 or SUZ12 accelerates the acquisition of neural fate by altering the balance of activating H3K4me3 and repressive H3K27me3 chromatin modifications at bivalent promoters and thereby priming a faster activation of developmental genes upon differentiation. The acceleration effect is also observed in definitive endoderm, cardiomyocyte, and neuronal differentiations. These results indicate that chromatin bivalency acts a general driver of human-specific timing across all major germ layers and developmental stages. Furthermore, our study uncovers a novel functional cooperation between MEN1 and SUZ12 as a key mechanism for the temporal regulation of developmental programs.

2025-06-26 | GSE279033 | GEO

Genome-wide CRISPR screen identifies Menin and SUZ12 as regulators of human developmental timing [RNA-seq]

2025-06-26 | GSE279032 | GEO

Genome-wide CRISPR screen identifies Menin and SUZ12 as regulators of human developmental timing [ATAC-seq]

2025-06-26 | GSE279031 | GEO

Genome-wide CRISPR screen identifies Menin and SUZ12 as regulators of human developmental timing.

Project description:Genome-wide CRISPR screen identifies Menin and SUZ12 as regulators of human developmental timing.

| PRJNA1170206 | ENA

A Drosophila Genome-Wide Screen Identifies Regulators of Steroid Hormone Production and Developmental Timing.

Project description:Steroid hormones control important developmental processes and are linked to many diseases. To systematically identify genes and pathways required for steroid production, we performed a Drosophila genome-wide in vivo RNAi screen and identified 1,906 genes with potential roles in steroidogenesis and developmental timing. Here, we use our screen as a resource to identify mechanisms regulating intracellular levels of cholesterol, a substrate for steroidogenesis. We identify a conserved fatty acid elongase that underlies a mechanism that adjusts cholesterol trafficking and steroidogenesis with nutrition and developmental programs. In addition, we demonstrate the existence of an autophagosomal cholesterol mobilization mechanism and show that activation of this system rescues Niemann-Pick type C1 deficiency that causes a disorder characterized by cholesterol accumulation. These cholesterol-trafficking mechanisms are regulated by TOR and feedback signaling that couples steroidogenesis with growth and ensures proper maturation timing. These results reveal genes regulating steroidogenesis during development that likely modulate disease mechanisms.

| S-EPMC4918455 | biostudies-literature

Genome-wide CRISPR screen identifies Menin and SUZ12 as regulators of human developmental timing [RNA-seq]

Project description:Genome-wide CRISPR screen identifies Menin and SUZ12 as regulators of human developmental timing [RNA-seq]

| PRJNA1170191 | ENA

Genome-wide CRISPR screen identifies Menin and SUZ12 as regulators of human developmental timing [ATAC-seq]

Project description:Genome-wide CRISPR screen identifies Menin and SUZ12 as regulators of human developmental timing [ATAC-seq]

| PRJNA1170192 | ENA

Genome-wide CRISPR screen identifies Menin and SUZ12 as regulators of human developmental timing [CUT&RUN]

Project description:Genome-wide CRISPR screen identifies Menin and SUZ12 as regulators of human developmental timing [CUT&RUN]

| PRJNA1170193 | ENA

Genome-wide CRISPR/Cas9 screen identifies regulators of BCMA expression on multiple myeloma cells.

Project description: Not available

| S-EPMC10811322 | biostudies-literature

Genome-Wide RNAi Screen Identifies Regulators of Cardiomyocyte Necrosis.

Project description:Regulation of cellular death is central to nearly all physiological routines and is dysregulated in virtually all diseases. Cell death occurs by two major processes, necrosis which culminates in a pervasive inflammatory response and apoptosis which is largely immunologically inert. As necrosis has long been considered an accidental, unregulated form of cellular death that occurred in response to a harsh environmental stimulus, it was largely ignored as a clinical target. However, recent elegant studies suggest that certain forms of necrosis can be reprogrammed. However, scant little is known about the molecules and pathways that orchestrate calcium-overload-induced necrosis, a main mediator of ischemia/reperfusion (IR)-induced cardiomyocyte cell death. To rectify this critical gap in our knowledge, we performed a novel genome-wide siRNA screen to identify modulators of calcium-induced necrosis in human muscle cells. Our screen identified multiple molecular circuitries that either enhance or inhibit this process, including lysosomal calcium channel TPCN1, mitophagy mediatorTOMM7, Ran-binding protein RanBP9, Histone deacetylase HDAC2, chemokine CCL11, and the Arp2/3 complex regulator glia maturation factor-γ (GMFG). Notably, a number of druggable enzymes were identified, including the proteasome β5 subunit (encoded by PSMB5 gene), which controls the proteasomal chymotrypsin-like peptidase activity. Such findings open up the possibility for the discovery of pharmacological interventions that could provide therapeutic benefits to patients affected by myriad disorders characterized by excessive (or too little) necrotic cell loss, including but not limited to IR injury in the heart and kidney, chronic neurodegenerative disorders, muscular dystrophies, sepsis, and cancers.

| S-EPMC7088983 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data