ArticleProceedings of the National Academy of Sciences of the United States of America2022
A synthetic lethality screen reveals ING5 as a genetic dependency of catalytically dead Set1A/COMPASS in mouse embryonic stem cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 13 citations in OpenAlex.
- OverlappING and DivergING roles of ING4 and ING5 in cancer, differentiation and development.Frontiers in cell and developmental biology · 2026Review
- ING5: multifaceted roles beyond tumor suppression in cellular physiology and disease.Epigenetics & chromatin · 2025Review
- BRPF1 in cancer epigenetics: a key regulator of histone acetylation and a promising therapeutic target.Cell death discovery · 2025Review
- Non-catalytic role of SETD1A promotes gastric cancer cell proliferation through the E2F4-TAF6 axis in the cell cycle.Cell death & disease · 2025Article
- Inhibitor of Growth Proteins: Epigenetic Regulators Shaping Neurobiology.Biomolecules · 2025Review
- Knockout of the ING5 epigenetic regulator confirms roles in stem cell maintenance and tumor suppression in vivo.PloS one · 2025Article
- TurboCas: A method for locus-specific labeling of genomic regions and isolating their associated protein interactome.Molecular cell · 2024Article
- Genome-scale CRISPR-Cas9 screening in stem cells: theories, applications and challenges.Stem cell research & therapy · 2024Review
- Epigenetic control ofHeliyon · 2024Article
- KMT2 Family of H3K4 Methyltransferases: Enzymatic Activity-dependent and -independent Functions.Journal of molecular biology · 2024Review
- Functional Roles of H3K4 Methylation in Transcriptional Regulation.Molecular and cellular biology · 2024Review
- Epigenetic moonlighting: Catalytic-independent functions of histone modifiers in regulating transcription.Science advances · 2023Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Embryonic stem cells (ESCs) are defined by their ability to self-renew and the potential to differentiate into all tissues of the developing organism. We previously demonstrated that deleting the catalytic SET domain of the Set1A/complex of proteins associated with SET1 histone methyltransferase (Set1A/COMPASS) in mouse ESCs does not impair their viability or ability to self-renew; however, it leads to defects in differentiation. The precise mechanisms by which Set1A executes these functions remain to be elucidated. In this study, we demonstrate that mice lacking the SET domain of Set1A are embryonic lethal at a stage that is unique from null alleles. To gain insight into Set1A function in regulating pluripotency, we conducted a CRISPR/Cas9-mediated dropout screen and identified the MOZ/MORF (monocytic leukaemia zinc finger protein/monocytic leukaemia zinc finger protein-related factor) and HBO1 (HAT bound to ORC1) acetyltransferase complex member ING5 as a synthetic perturbation to Set1A. The loss of Ing5 in Set1AΔSET mouse ESCs decreases the fitness of these cells, and the simultaneous loss of ING5 and in Set1AΔSET leads to up-regulation of differentiation-associated genes. Taken together, our results point toward Set1A/COMPASS and ING5 as potential coregulators of the self-renewal and differentiation status of ESCs.
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