ArticleNature communications2025
A genome-wide screen identifies genes required for erythroid differentiation.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Molecular and therapeutic frontiers in anemia therapy.The Journal of clinical investigation · 2026Review
- ReducedInternational journal of molecular sciences · 2026Article
- LSD1 inhibition ameliorates congenital dyserythropoietic anemia type II.Science translational medicine · 2026Article
- p27Kip1 regulates γ-globin production.Blood · 2026Article
- UBE2O as a key regulator of drug-induced erythropoiesis in the context of myelodysplastic syndromes.Blood advances · 2026Article
- A scalable computational framework for predicting gene expression from candidateGenome research · 2026Article
- Trimodal Single-Cell Gene Regulatory Networks Reveal Principles of Stemness Loss and Cell Fate Acquisition in Human Hematopoiesis.bioRxiv : the preprint server for biology · 2025Article
- Altered behaviour and immune response in mice with NHLRC2 p.Asp148Tyr variant.Brain, behavior, & immunity - health · 2025Article
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Authors and funding
28 authors.
Funding
Abstract
The complete array of genes required for terminal erythroid differentiation remains unknown. To address this knowledge gap, we perform a genome-scale CRISPR knock-out screen in the human erythroid progenitor cell line HUDEP-2 and validate candidate regulators of erythroid differentiation in a custom secondary screen. Comparison of sgRNA abundance in the CRISPR library, proerythroblasts, and orthochromatic erythroblasts, resulted in the identification of genes that are essential for proerythroblast survival and genes that are required for terminal erythroid differentiation. Among the top genes identified are known regulators of erythropoiesis, underscoring the validity of this screen. Notably, using a Log2 fold change of <-1 and false discovery rate of <0.01, the screen identified 277 genes that are required for terminal erythroid differentiation, including multiple genes not previously nominated through GWAS. NHLRC2, which was previously implicated in hemolytic anemia, was a highly ranked gene. We suggest that anemia due to NHLRC2 mutation results at least in part from a defect in erythroid differentiation. Another highly ranked gene in the screen is VAC14, which we validated for its requirement in erythropoiesis in vitro and in vivo. Thus, data from this CRISPR screen may help classify the underlying mechanisms that contribute to erythroid disorders.
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Registered trials
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