The DOI matches its Crossref record; 55 of the 57 references it cites were found in a registry or an index.
Genome-wide analysis of transcriptional regulators in human HSPCs reveals a densely interconnected network of coding and noncoding genes
Abstract
Genome-wide combinatorial binding patterns for key transcription factors (TFs) have not been reported for primary human hematopoietic stem and progenitor cells (HSPCs), and have constrained analysis of the global architecture of molecular circuits controlling these cells. Here we provide high-resolution genome-wide binding maps for a heptad of key TFs (FLI1, ERG, GATA2, RUNX1, SCL, LYL1, and LMO2) in human CD34(+) HSPCs, together with quantitative RNA and microRNA expression profiles. We catalog binding of TFs at coding genes and microRNA promoters, and report that combinatorial binding of all 7 TFs is favored and associated with differential expression of genes and microRNA in HSPCs. We also uncover a previously unrecognized association between FLI1 and RUNX1 pairing in HSPCs, we establish a correlation between the density of histone modifications that mark active enhancers and the number of overlapping TFs at a peak, we demonstrate bivalent histone marks at promoters of heptad target genes in CD34(+) cells that are poised for later expression, and we identify complex relationships between specific microRNAs and coding genes regulated by the heptad. Taken together, these data reveal the power of integrating multifactor sequencing of chromatin immunoprecipitates with coding and noncoding gene expression to identify regulatory circuits controlling cell identity.
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“For instance, the combinatorial occupancy of chromatin by multiple master TFs has revealed regulatory networks that are important for hematopoiesis (Beck et al., 2013; Schütte et al., 2016), as well as key regulatory elements necessary for HSC self-renewal (Bahr et al., 2018).”
From Unraveling Hematopoiesis through the Lens of Genomics (2020) · cites this paper as Beck et al., 2013
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Giustacchini, A., Thongjuea, S., Barkas, N., Woll, P. S., Povinelli, B. J., Booth, C. A. G., Sopp, P., Norfo, R., Rodriguez-Meira, A., Ashley, N., et al. (2017) · Nature Medicine · doi:10.1038/nm.4336 · Cited by 403
Global transcriptome analyses of human and murine terminal erythroid differentiation
An, X., Schulz, V., Li, J., Wu, K., Liu, J., Xue, F., Hu, J., Mohandas, N., & Gallagher, P. G. (2014) · Blood · doi:10.1182/blood-2014-01-548305 · Cited by 361
Huang, J., Liu, X., Li, D., Shao, Z., Cao, H., Zhang, Y., Trompouki, E., Bowman, T. V., Zon, L. I., Yuan, G., et al. (2016) · Developmental Cell · doi:10.1016/j.devcel.2015.12.014 · Cited by 247
“We also re-analyzed 45 previously published ChIP-seq datasets of TFs and chromatin regulators obtained in the same cell populations (Abraham et al., 2013; Beck et al., 2013; Dogan Figure 3.”
MethodHaematopoietic and immune defects associated with GATA2 mutation
Collin, M. P., Dickinson, R. E., & Bigley, V. (2015) · British Journal of Haematology · doi:10.1111/bjh.13317 · Cited by 237
“…adult haematopoiesis, GATA2 is required for HSC survival and self-renewal, interacting with a complex network of transcription factors that specify early lineage commitment, including SPI1 (PU.1), FLI1, TAL1 (SCL), LMO2 and RUNX1, among others (Dore et al, 2012; Beck et al, 2013; May et al, 2013).”
BackgroundCai, X., Gao, L., Teng, L., Ge, J., Oo, Z. M., Kumar, A. R., Gilliland, D. G., Mason, P. J., Tan, K., & Speck, N. A. (2015) · Cell stem cell · doi:10.1016/j.stem.2015.06.002 · Cited by 237
“We analyzed the genome-wide occupancy of RUNX1 using previously published chromatin immunoprecipitation sequencing (ChIP-seq) data generated in human CD34+ HSPCs (Beck et al., 2013).”
Influential
Metadata
- Authors
- Beck, D., Thoms, J. A. I., Perera, D., Schütte, J., Unnikrishnan, A., Knezevic, K., Kinston, S. J., Wilson, N. K., O’Brien, T. A., Göttgens, B., Wong, J. W. H., & Pimanda, J. E.
- Affiliations
- UNSW Sydney (AU)
- University of Cambridge (GB)
- Centre for Children’s Cancer & Blood Disorders, Sydney Children’s Hospital, Sydney, Australia;
- Wellcome/MRC Cambridge Stem Cell Institute (GB)
- ORCID
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2013-10-03
- Volume
- 122
- Issue
- 14
- Pages
- e12-e22
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W1976712740
- Cited by
- 133
- References
- 57
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 9 · 2023: 12 · 2022: 6 · 2021: 15 · 2020: 16 · 2019: 12 · 2018: 7 · 2017: 12 · 2016: 15 · 2015: 10 · 2014: 14 · 2013: 1
- FWCI
- 5.98
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Blood (publishedVersion)
- PubMed (publishedVersion)
- The HKU Scholars Hub (University of Hong Kong) (submittedVersion)
- UTS ePRESS (University of Technology Sydney) (submittedVersion)
- Funders
- University of California, Santa Cruz
- Wellcome Trust (079249, 100140)
- Cancer Research UK (12765)
- National Centre for the Replacement, Refinement and Reduction of Animals in Research (G0900729/1)
- University of New South Wales
- Medical Research Council (MC_PC_12009)
- Biotechnology and Biological Sciences Research Council (BB/I00050X/1)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Keywords
- hematopoietic stem and progenitor cells, transcription factors, FLI1, RUNX1, GATA2, ERG, SCL, LYL1, LMO2, microRNA promoters, CD34+ cells, gene regulatory networks, cell identity, chromatin immunoprecipitation
- MeSH terms
- Cell Differentiation, Flow Cytometry, Hematopoiesis, Hematopoietic Stem Cells, Humans, Transcription Factors, Transcription, Genetic, Cluster Analysis, RNA, Untranslated, Chromatin Immunoprecipitation, Genome-Wide Association Study
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