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Genome-Wide CRISPR Screen Identifies an NF2-adheren junction mechanistic dependency for cardiac lineage

GSE244362 Homo sapiens (human) RNA-seq (gene expression) 41 samples Submitted 2024/04/30 Platform GPL20301
At a glance

RNA-seq (gene expression) · human · 41 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Homo sapiens (human)
Samples
41 samples: 16 conditions, mostly in triplicateGroups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper
Genome-Wide CRISPR Screen Identifies an NF2-Adherens Junction Mechanistic Dependency for Cardiac LineageCirculation · 2024
Summary (written by the submitters)
Cardiac differentiation involves a stepwise clearance of repressors and fate-restricting regulators through the modulation of BMP/Wnt-signaling pathways. However, the mechanisms and how regulatory roadblocks are removed with specific developmental signaling pathways remain unclear. Here, we performed a genome-wide CRISPR screen to uncover essential regulators of cardiomyocyte specification in human embryonic stem cells (hESCs) and identify NF2, a Moesin-Ezrin-Radixin Like (MERLIN) Tumor Suppressor, as an upstream driver of cardiomyocyte specification.
Read the full summary ↓
Transcriptional regulation and trajectory inference from NF2-null cells reveal the loss of cardiomyocyte identity and the acquisition of non-mesodermal identity. Sustained elevation of early mesoderm lineage repressor SOX2 and upregulation of late anti-cardiac regulators CDX2, MSX1 in NF2 knockout cells reflect a necessary role for NF2 in removing regulatory roadblocks. Since YAP is a known repressor of mesendoderm genes, we found that NF2 and AMOT cooperatively bind to YAP during mesendoderm formation, thereby preventing YAP activation independent on canonical MST-LATS1 kinase activity. Mechanistically, cardiomyocyte lineage identity was rescued by wild-type and NF2 Serine-518 phospho-mutants, but not NF2 FERM-domain blue-box mutants, showing that the critical FERM domain-dependent formation of the AMOT-NF2-YAP scaffold complex at the adherens junction is required for cardiomyocyte lineage differentiation. These results provide mechanistic insight into the essential role of NF2 for cardiomyocyte lineage specification by sequestering the repressive effect of YAP and relieving regulatory roadblocks en route to cardiomyocytes.
Published in
Genome-Wide CRISPR Screen Identifies an NF2-Adherens Junction Mechanistic Dependency for Cardiac Lineage
Lee CJM, Autio MI, Zheng W et al. · Circulation 2024 · PMID 38752370 · doi:10.1161/CIRCULATIONAHA.122.061335
This dataset
Open GSE244362 in finder → Find more human RNA-seq datasets →
Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓
2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE244362_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓
3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA841051 and SRA study SRP376385. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 38752370) ↗
Study design
16 conditions, mostly in triplicate
H1-hESC, NF2 WT2, Day 1, ×3 H1-hESC, NF2 WT2, Day 5, ×3 H1-hESC, NF2 WT2, Day 14, ×3 H1-hESC, NF2 KO1, Day 1, ×3 H1-hESC, NF2 KO1, Day 5, ×3 H1-hESC, NF2 KO1, Day 14, ×3 H1-hESC, NF2 KO2, Day 1, ×3 H1-hESC, NF2 KO2, Day 5, ×3 +8 more

Supports a between-group comparison across 41 samples.

How we read this: 16 replicated groups read from 41 sample titles; they account for 41 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study

+ 1 more — browse all 41 samples with per-sample file links →

Datasets on a similar topic

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