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

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

PROVIDER: PRJNA1170193 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30911200_1.fastq.gz	Fastqsanger.gz
	SRR30911200_2.fastq.gz	Fastqsanger.gz
	SRR30911201_1.fastq.gz	Fastqsanger.gz
	SRR30911201_2.fastq.gz	Fastqsanger.gz
	SRR30911202_1.fastq.gz	Fastqsanger.gz

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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

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 [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 [ATAC-seq]

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 | GSE279031 | GEO

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

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

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.

2014-11-20 | GSE55416 | GEO

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.

2025-06-26 | GSE279036 | GEO

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

SUZ12 immunoprecipitation followed by protein indentification via mass spectrometry (SUZ12 IP-MS) in mESCs of SUZ12 WT, delta exon 4, KO, and KO rescues with SUZ12-L and SUZ12-S

Project description: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). We reasoned that exon 4 skipping might alter the structure of SUZ12 and, possibly, PRC2 composition. To explore this possibility, we generated ESCs that lack the Suz12 exon 4 via CRISPR-Cas9–induced deletion. In addition, to rule out any biases due to the expression levels and/or SUZ12 epitope masking, we generated Suz12 knockout (KO) ESCs (herein, KO) in which Suz12 expression was subsequently rescued by re-introducing either the Suz12-L or Suz12-S mouse isoform fused to a triple-Flag tag under the regulation of a CAG promoter (KO+L/S; Figures S2H–S2K). We performed SUZ12 immunoprecipitation coupled with mass spectrometry (IP-MS) in the WT and ∆ex4 clones to compare their interactomes and with a flag antibody in the KO and rescue cell lines. As expected, no peptides corresponding to exon 4 were retrieved in ∆ex4 samples, while the rest of the sequence displayed similar coverage. Comparison of interactors in the two conditions revealed that SUZ12 binding to AEBP2 and JARID2 was strongly reduced in ∆ex4 cells with respect to WT cells, whereas SUZ12 binding to most core components or to PRC2.1-specific factors was unchanged or only slightly increased . These observations were confirmed by SUZ12 IP followed by Western blot (WB). Flag IP-MS in rescue cells confirmed that, while the long isoform was able to correctly form comparable amounts of both PRC2.1 and PRC2.2 subtypes, interaction of the SUZ12-S with PRC2.2-specific factors was drastically reduced.

2024-03-18 | PXD046660 | Pride

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