Mechanisms governing the pioneering and redistribution capabilities of the non-classical pioneer PU.1
Open accessAbstract
Establishing gene regulatory networks during differentiation or reprogramming requires master or pioneer transcription factors (TFs) such as PU.1, a prototype master TF of hematopoietic lineage differentiation. To systematically determine molecular features that control its activity, here we analyze DNA-binding in vitro and genome-wide in vivo across different cell types with native or ectopic PU.1 expression. Although PU.1, in contrast to classical pioneer factors, is unable to access nucleosomal target sites in vitro, ectopic induction of PU.1 leads to the extensive remodeling of chromatin and redistribution of partner TFs. De novo chromatin access, stable binding, and redistribution of partner TFs both require PU.1's N-terminal acidic activation domain and its ability to recruit SWI/SNF remodeling complexes, suggesting that the latter may collect and distribute co-associated TFs in conjunction with the non-classical pioneer TF PU.1.
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PU.1 binds specific DNA sequences known as ETS motifs, which are located predominantly in enhancers but also in promoters of target genes.
“PU.1, as an ETS family transcription factor, binds specific DNA sequences known as ETS motifs, which are located predominantly in the enhancers but also in the promoters of target genes [30, 31].”
From Targeting Microglial Transcriptional Reprogramming as a Therapy Strategy for Alzheimer's Disease (2026) · cites this paper as [31]
The Results sections on PU.1 binding and ETS-family interactions show that PU.1 binds sequence-specific motifs and that PU.1-binding sites can occur in promoters. The Discussion links PU.1 to enhancer establishment, but the passages do not establish that its binding sites are predominantly in enhancers rather than promoters. Page numbers are unavailable in our copy. (LLM, conf=0.83)
Experimental — accuracy not yet measuredPU.1, IRF8, and BHLHE40/41 regulate multiple downstream targets that orchestrate microglial immune response functions, including phagocytosis, cytokine production, and inflammatory signaling.
“PU.1, IRF8, and BHLHE40/41 regulates multiple downstream targets that orchestrate microglial immune response functions, including phagocytosis, cytokine production, and inflammatory signaling”
From Targeting Microglial Transcriptional Reprogramming as a Therapy Strategy for Alzheimer's Disease (2026) · cites this paper as [31]
The Results section, “Immediate consequences of de novo PU.1 expression” (page unavailable), reports that PU.1 induces genes associated with myeloid activation and differentiation. The Introduction identifies IRF8 as a PU.1 interaction partner. Our copy does not establish that PU.1, IRF8, and BHLHE40/41 jointly regulate downstream targets in microglia, or link them to the specified functions of phagocytosis, cytokine production, and inflammatory signaling. (LLM, conf=0.87)
Experimental — accuracy not yet measuredPU.1 is a non-canonical pioneer transcription factor that functions as a master regulator of myeloid and lymphoid lineage differentiation.
“PU.1, a non-canonical pioneer transcription factor that functions as a master regulator of myeloid and lymphoid lineage differentiation18–20.”
From Lymphoid gene expression supports neuroprotective microglia function (2025) · cites this paper as [20]
This suggests compromised differentiation-relevant chromatin rearrangement.
“suggesting a compromised differentiation-relevant chromatin rearrangement, in line with recent reports (41).”
From PU.1-Dependent Enhancer Inhibition Separates <i>Tet2</i> -Deficient Hematopoiesis from Malignant Transformation (2022) · cites this paper as [41]
Exceptions to the rule that PU.1 binding is largely unperturbed by DNA methylation have been reported.
“exceptions have been reported in the past (41).”
From PU.1-Dependent Enhancer Inhibition Separates <i>Tet2</i> -Deficient Hematopoiesis from Malignant Transformation (2022) · cites this paper as [41]
The study identified a set of highly enriched and similar ETS motifs harboring a core PU-box motif and 5′ flanking cytosines that have been shown to exhibit reduced binding affinity for PU.1 when methylated (methETS).
“We identified a set of highly enriched and similar ETS motifs harboring a core PU-box motif and 5′ flanking cytosines that have been shown to exhibit a reduced binding affinity for PU.1 when methylated (referred to as methETS; ref. 41).”
From PU.1-Dependent Enhancer Inhibition Separates <i>Tet2</i> -Deficient Hematopoiesis from Malignant Transformation (2022) · cites this paper as [41]
The HAF1 complex activates a range of genes associated with microglial activation, including iNOS, COX-2, TNF-α, IL-12α, IL-12β, CXCL9, CCL5, and C1qc.
“The HAF1 complex activates a range of genes associated with microglial activation, including inducible nitric oxide synthase (iNOS), Cyclooxygenase‐2 (COX‐2), TNF‐α, IL‐12α, IL‐12β, CXCL9, CCL5, and complement components such as the complement C1q C chain (C1qc) (Figure 1) [31, 35, 39, 61].”
From Targeting Microglial Transcriptional Reprogramming as a Therapy Strategy for Alzheimer's Disease (2026) · cites this paper as [31]
The Introduction and Results passages discuss PU.1 binding and its interaction with the SWI/SNF chromatin-remodeling complex, not HAF1-driven microglial gene activation. Searches for HAF1, microglia, iNOS, and C1qc found no passage in our copy addressing the attributed claim. No page numbers are available in the indexed passages. (LLM, conf=0.76)
Experimental — accuracy not yet measuredMEF2C functions as a counterbalance by suppressing excessive pro-inflammatory responses.
“MEF2C functions as a counterbalance by suppressing excessive pro‐inflammatory responses”
From Targeting Microglial Transcriptional Reprogramming as a Therapy Strategy for Alzheimer's Disease (2026) · cites this paper as [31]
The Introduction and Results passages discuss PU.1 binding and redistribution of other transcription factors, but do not describe MEF2C suppressing pro-inflammatory responses. Searches for “MEF2C” and the claimed counterbalancing function found no passage addressing that point in our copy; page numbers were not provided. (LLM, conf=0.72)
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- Authors
- Minderjahn, J., Schmidt, A., Fuchs, A., Schill, R., Raithel, J., Babina, M., Schmidl, C., Gebhard, C., Schmidhofer, S., Mendes, K., Ratermann, A., Glatz, D., Nützel, M., Edinger, M., Hoffmann, P., Spang, R., Längst, G., Imhof, A., & Rehli, M.
- Affiliations
- University Hospital Regensburg (DE)
- Ludwig-Maximilians-Universität München (DE)
- University of Regensburg (DE)
- Charité – Universitätsmedizin Berlin (DE)
- Hôpital Maisonneuve-Rosemont (CA)
- Corresponding author
- Rehli, Michael
- ORCID
- Venue
- Nature Communications
- Published
- 2020-01-21
- Volume
- 11
- Issue
- 1
- Pages
- 402-402
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC6972792
- OpenAlex
- W3000851240
- Cited by
- 136
- References
- 56
- Citations by year
- 2026: 19 · 2025: 16 · 2024: 36 · 2023: 18 · 2022: 16 · 2021: 18 · 2020: 13
- FWCI
- 5.27
- Type
- journal article
- Language
- en
- Update notices
- correction (2020-02-25)
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- University of Regensburg Publication Server (University of Regensburg) (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Open access LMU (Ludwid Maxmilian's Universitat Munchen) (submittedVersion, cc-by)
- University of Regensburg Publication Server (University of Regensburg)
- Funders
- Deutsche Forschungsgemeinschaft (RE 1310/17)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Keywords
- PU.1, pioneer transcription factors, hematopoietic differentiation, chromatin remodeling, SWI/SNF complex, nucleosome accessibility, transcription factor-DNA binding, gene regulatory networks, transcriptional reprogramming
- MeSH terms
- Protein Domains, RNA-Seq, Proto-Oncogene Protein Spi-1, Binding Sites, Cell Differentiation, Chromosomal Proteins, Non-Histone, DNA, Hematopoiesis, Hematopoietic Stem Cells, Humans, Leukapheresis, Nucleosomes, Proto-Oncogene Proteins, Trans-Activators, Chromatin Assembly and Disassembly, Cell Line, Tumor, Gene Regulatory Networks, Healthy Volunteers
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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