ArticleThe Journal of experimental medicine2020
Constructing and deconstructing GATA2-regulated cell fate programs to establish developmental trajectories.
Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed.
- ZEB1 drives terminal erythroid maturation by controlling the GATA2-KLF1 regulatory switch.Nucleic acids research · 2026Article
- Epigenetic programming by H3K23ac defines lineage fate of Meg3Nature cell biology · 2026Article
- Article
- Oncogenic DEAD-box ATPase DDX41 establishes transcript ensembles via CLK3-dependent and -independent mechanisms.Nature communications · 2025Article
- A unified multimodal single-cell framework reveals a discrete state model of hematopoiesis in mice.Nature immunology · 2025Article
- GATA2 decommissioning of enhancers: A mechanism to constrain inflammatory signaling.Cell reports · 2025Article
- Identifying lncRNA-Protein Interactions in Hematopoietic Progenitor Cells by Hybridization Capture and Mass Spectrometry.Journal of proteome research · 2025Article
- Systemic Identification of Functionally Conserved Long Noncoding RNA Metabolic Regulators in Human and Mouse Livers.Gastroenterology · 2025Article
- Dual mechanism of inflammation sensing by the hematopoietic progenitor genome.Science advances · 2025Article
- BmNPV interacts with super-enhancer regions of the host chromatin to hijack cellular transcription machinery.Nucleic acids research · 2025Article
- The co-receptor Neuropilin-1 enhances proliferation in inv(16) acute myeloid leukemia via VEGF signaling.Leukemia · 2025Article
- Systemic identification of functionally conserved lncRNA metabolic regulators in human and mouse livers.bioRxiv : the preprint server for biology · 2024Article
- An intricate regulatory circuit between FLI1 and GATA1/GATA2/LDB1/ERG dictates erythroid vs. megakaryocytic differentiation.Molecular medicine reports · 2024Article
- Pathogenic GATA2 genetic variants utilize an obligate enhancer mechanism to distort a multilineage differentiation program.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Linking GATA2 to myeloid dysplasia and complex cytogenetics in adult myelodysplastic neoplasm and acute myeloid leukemia.Blood advances · 2024Article
- A gain-of-function p53 mutant synergizes with oncogenic NRAS to promote acute myeloid leukemia in mice.The Journal of clinical investigation · 2023Article
- A transcriptional network governing ceramide homeostasis establishes a cytokine-dependent developmental process.Nature communications · 2023Article
- Secondary bile acids function through the vitamin D receptor in myeloid progenitors to promote myelopoiesis.Blood advances · 2023Article
- Multidimensional profiling reveals GATA1-modulated stage-specific chromatin states and functional associations during human erythropoiesis.Nucleic acids research · 2023Article
- Restricting genomic actions of innate immune mediators on fetal hematopoietic progenitor cells.iScience · 2023Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Stem and progenitor cell fate transitions constitute key decision points in organismal development that enable access to a developmental path or actively preclude others. Using the hematopoietic system, we analyzed the relative importance of cell fate-promoting mechanisms versus negating fate-suppressing mechanisms to engineer progenitor cells with multilineage differentiation potential. Deletion of the murine Gata2-77 enhancer, with a human equivalent that causes leukemia, downregulates the transcription factor GATA2 and blocks progenitor differentiation into erythrocytes, megakaryocytes, basophils, and granulocytes, but not macrophages. Using multiomics and single-cell analyses, we demonstrated that the enhancer orchestrates a balance between pro- and anti-fate circuitry in single cells. By increasing GATA2 expression, the enhancer instigates a fate-promoting mechanism while abrogating an innate immunity-linked, fate-suppressing mechanism. During embryogenesis, the suppressing mechanism dominated in enhancer mutant progenitors, thus yielding progenitors with a predominant monocytic differentiation potential. Coordinating fate-promoting and -suppressing circuits therefore averts deconstruction of a multifate system into a monopotent system and maintains critical progenitor heterogeneity and functionality.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.