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Cited by 86Genomics and Chromatin DynamicsChromatin Remodeling and CancerDevelopmental Biology and Gene Regulation

PU.1 can participate in an active enhancer complex without its transcriptional activation domain

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Pongubala, Jagan M. R., Atchison, Michael L.·1997·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.94.1.127PMC PMC19254
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Abstract

The transcription factor PU.1 is necessary for the development of multiple hematopoietic lineages and contributes to the activity of the immunoglobulin κ 3′ enhancer. A variety of proteins bind to the 3′ enhancer (PU.1, PIP, ATF1, CREM, c-Fos, c-Jun, and E2A), but the mechanism of 3′-enhancer activity and the proteins necessary for its activity are presently unclear. We show here that PU.1 participates with other transcription factors in forming a higher-order complex with 3′-enhancer DNA sequences. Each protein is necessary for formation of this complex. Individually, transcription factors that bind to the 3′ enhancer do not appreciably stimulate transcription in a cell type in which the 3′ enhancer is normally silent (NIH 3T3). However, mixture of multiple transcription factors (PU.1, PIP, c-Fos, and c-Jun) can greatly activate the enhancer. PU.1 is necessary for maximal enhancer activity, but mutants of PU.1 that lack the transcriptional activation domain are nearly as efficient at stimulating enhancer activity as the wild-type PU.1 protein. PU.1 apparently can activate transcription by playing an architectural role in interactions with other transcription factors.

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Crossref · 10.1073/pnas.94.1.127

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  • Mutants of PU.1 that lack the transcriptional activation domain are as efficient at stimulating enhancer activity as the wild-type PU.1 protein.

    “In this context, mutants of PU.1 that lack the transcriptional activation domain are as efficient at stimulating enhancer activity as the wild-type PU.1 protein (60).”

    From c-Jun Is a JNK-independent Coactivator of the PU.1 Transcription Factor (1999) · cites this paper as [60]

    The Results (Fig. 3E) report that PU.1 mutants lacking the transcriptional activation domain stimulated enhancer activity, but describe them as “nearly as efficient” as wild-type PU.1. The claim omits that qualification and states equal efficiency. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • Prior studies report that physical interaction between transcription factors can enhance DNA binding, which may explain synergy when two factors are present.

    “In several studies, the physical interaction between transcription factors increases DNA-binding ability, providing an explanation for synergistic activation in the presence of two factors (11,18,56,58,67).”

    From Multiple Functional Domains of AML1: PU.1 and C/EBPα Synergize with Different Regions of AML1 (1998) · cites this paper as [56]

  • PU.1 nucleates a multi-transcription factor complex on Eκ3'.

    “recent work has shown that PU.1 nucleates a multi-transcription factor complex on the E κ3Ј”

    From Assembly requirements of PU.1–Pip (IRF‐4) activator complexes: inhibiting function in vivo using fused dimers (1999) · cites this paper as Pongubala and Atchison, 1997

  • The immunoglobulin 3' enhancer is activated by PU.1, c-Jun, PIP, and c-Fos and contains respective DNA binding sites for these factors.

    “The immunoglobulin 3Ј enhancer is activated by PU.1, c-Jun, PIP, and c-Fos and contains respective DNA binding sites for these factors (60).”

    From c-Jun Is a JNK-independent Coactivator of the PU.1 Transcription Factor (1999) · cites this paper as [60]

  • The PEST domain interacts with IRFs including Pip/NF-EM5 and ICSBP.

    “This domain interacts with interferon regulatory factors (IRFs), including Pip/NF-EM5 and interferon consensus sequence binding protein (ICSBP) [44–46].”

    From PU.1 and partners: regulation of haematopoietic stem cell fate in normal and malignant haematopoiesis (2009) · cites this paper as [45]

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Research works printed but not linked: 2

  1. [10]Hagemeier, C., Bannister, A. J., Cook, A. & Kouzarides, T. (1993) Proc. Natl. Acad. Sci. USA 90, 1580-1584.
  2. [31]Delmas, V., Laoide, B. M., Masquilier, D., deGroot, R. P., Foulkes, N. S. & Sassone-Corsi, P. (1992) Proc. Natl. Acad. Sci. USA 89, 4226-4230.

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Authors
Pongubala, J. M. R., & Atchison, M. L.
Affiliations
University of Pennsylvania (US)
Corresponding author
Atchison, Michael L.
ORCID
Pongubala, Jagan M. R.
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
1997-01-07
Volume
94
Issue
1
Pages
127-132
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
DOI
10.1073/pnas.94.1.127
PMC
PMC19254
OpenAlex
W2017956702
Cited by
86
References
39
Citations by year
2025: 1 · 2024: 1 · 2023: 1 · 2021: 3 · 2019: 2 · 2017: 1 · 2014: 1 · 2012: 4
FWCI
3.56
Type
journal article
Language
en
Open access
Locations
  • Proceedings of the National Academy of Sciences (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Institute of General Medical Sciences (GM-42415, R01GM042415)
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 › Developmental Biology and Gene Regulation
Keywords
PU.1, transactivation domain, transcriptional activation, Pip, c-fos, c-Jun, E2A, ATF1, CREM, transcription factor interaction, enhancer architecture, hematopoietic development, NIH3T3 cells
MeSH terms
Interferon Regulatory Factor-4, Proto-Oncogene Protein Spi-1, DNA-Binding Proteins, Drug Synergism, Enhancer Elements, Genetic, Immunoglobulin kappa-Chains, Models, Genetic, Nucleoproteins, Protein Binding, Proto-Oncogene Proteins, Transcription Factors, Transcription, Genetic, Trans-Activators, Interferon Regulatory Factors

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