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

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

PROVIDER: PRJNA1170206 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30911200_1.fastq.gz	Fastqsanger.gz
	SRR30911200_2.fastq.gz	Fastqsanger.gz
	SRR30911300_1.fastq.gz	Fastqsanger.gz
	SRR30911300_2.fastq.gz	Fastqsanger.gz
	SRR30911400_1.fastq.gz	Fastqsanger.gz

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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]

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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]

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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]

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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]

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Replication timing in Suz12 knockout ESCs

Project description:We profiled replication timing in Suz12 knockout ESCs and observed no differences relative to wild-type controls.

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

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

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CRISPR screen for NMD regulators

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SUZ12 immunoprecipitation followed by PRM of SUZ12 peptides to identify alternatively spliced isoforms of SUZ12 at the protein level.

Project description:Alternative splicing of SUZ12 exon 4 is predicted to generate two alternative isoforms differing by the inclusion or exclusion of 69 nucleotides in exon 4, which we named SUZ12-long (SUZ12-L) and SUZ12-short (SUZ12-S) respectively. At the protein level SUZ12 exon 4 encodes 23 amino acids (aa 129–152 in SUZ12-L) that partially overlap with the WD-binding domain 1 (WDB1, 110–145). To detect the existance of SUZ12-S at the protein levels we performed SUZ12 immunoprecipitation coupled with mass spectrometry (IP-MS) in the WT and ∆ex4 clones to identify SUZ12-S unique peptides. We identified a SUZ12-S specific peptide in both WT #2 and ∆ex4 #1. These observations were confirmed by SUZ12 IP followed by Western blot (WB) (size shift).

2024-03-18 | PXD046742 | Pride

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