ArticleProceedings of the National Academy of Sciences of the United States of America2004
Context-dependent regulation of GATA-1 by friend of GATA-1.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
82 citing papers in PubMed, 127 citations in OpenAlex.
- The SAMD1 transcription factor coordinates hematopoietic lineage differentiation and H3K4 methylation status.Blood advances · 2025Article
- Epigenetic Regulation of Erythropoiesis: From Developmental Programs to Therapeutic Targets.International journal of molecular sciences · 2025Review
- Pioneering new enhancers by GATA3: role of facilitating transcription factors and chromatin remodeling.Nucleic acids research · 2025Article
- A novel role for Friend of GATA1 (FOG-1) in regulating cholesterol transport in murine erythropoiesis.PLoS genetics · 2025Article
- Multidimensional profiling reveals GATA1-modulated stage-specific chromatin states and functional associations during human erythropoiesis.Nucleic acids research · 2023Article
- Gene silencing dynamics are modulated by transiently active regulatory elements.Molecular cell · 2023Article
- HDAC1 is required for GATA-1 transcription activity, global chromatin occupancy and hematopoiesis.Nucleic acids research · 2021Article
- Distinct properties and functions of CTCF revealed by a rapidly inducible degron system.Cell reports · 2021Article
- Human GATA2 mutations and hematologic disease: how many paths to pathogenesis?Blood advances · 2020Review
- Article
- Interrogating Histone Acetylation and BRD4 as Mitotic Bookmarks of Transcription.Cell reports · 2019Article
- Transcriptional Burst Initiation and Polymerase Pause Release Are Key Control Points of Transcriptional Regulation.Molecular cell · 2019Article
- Exploiting genetic variation to uncover rules of transcription factor binding and chromatin accessibility.Nature communications · 2018Article
- Fitting structure to function in gene regulatory networks.History and philosophy of the life sciences · 2017Article
- The GATA factor revolution in hematology.Blood · 2017Review
- GATA1 Binding Kinetics on Conformation-Specific Binding Sites Elicit Differential Transcriptional Regulation.Molecular and cellular biology · 2016Article
- O-Linked N-Acetylglucosamine (O-GlcNAc) Transferase and O-GlcNAcase Interact with Mi2β Protein at the Aγ-Globin Promoter.The Journal of biological chemistry · 2016Article
- NetDecoder: a network biology platform that decodes context-specific biological networks and gene activities.Nucleic acids research · 2016Article
- Enhancer Regulation of Transcriptional Bursting Parameters Revealed by Forced Chromatin Looping.Molecular cell · 2016Article
- The Hematopoietic Stem and Progenitor Cell Cistrome: GATA Factor-Dependent cis-Regulatory Mechanisms.Current topics in developmental biology · 2016Review
22 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The transcription factor GATA-1 and its cofactor, friend of GATA-1 (FOG-1), are essential for normal erythroid development. FOG-1 physically interacts with GATA-1 to augment or inhibit its activity. The mechanisms by which FOG-1 regulates GATA-1 function are unknown. By using an assay that is based on the phenotypic rescue of a GATA-1-null erythroid cell line, we found that a conditional form of GATA-1 (GATA-1-ER) strongly induced histone acetylation at the beta-major globin promoter in vivo, consistent with previous results. In contrast, GATA-1 bearing a point mutation that impairs FOG-1 binding [GATA-1(V205M)-ER] failed to induce high levels of histone acetylation at this site. However, at DNase I-hypersensitive site (HS)3 of the beta-globin locus control region, GATA-1-induced histone acetylation was FOG-1-independent. Because the V205M mutation does not disrupt GATA-1 binding to DNA templates in vitro, we were surprised to find that in vivo GATA-1(V205M)-ER fails to bind the beta-globin promoter. However, at HS3, DNA binding by GATA-1 was FOG-1-independent, thus correlating histone acetylation with GATA-1 occupancy. Examination of additional GATA-1-dependent regulatory elements showed that the interaction with FOG-1 is required for GATA-1 occupancy at select sites, such as HS2, but is dispensable at others, including the FOG-1-independent GATA-1 target gene EKLF. Remarkably, at the GATA-2 gene, which is repressed by GATA-1, interaction with FOG-1 was dispensable for GATA-1 occupancy and was required for transcriptional inhibition and histone deacetylation. These results indicate that FOG-1 employs distinct mechanisms when cooperating with GATA-1 during transcriptional activation and repression.
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Registered trials
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.