Cited by 75Signaling Pathways in DiseaseGenomics and Chromatin DynamicsNF-κB Signaling Pathways

Nuclear factor of activated T cells 1 (NFAT1)-induced permissive chromatin modification facilitates nuclear factor-κB (NF-κB)-mediated interleukin-9 (IL-9) transactivation

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Jash, Arijita, Sahoo, Anupama, Kim, Gi-Cheon, Chae, Chang-Suk, Hwang, Ji-Sun, Kim, Jung-Eun, Im, Sin-Hyeog·2012·Journal of Biological Chemistry

Abstract

IL-9 regulates diverse inflammatory immune responses. Although the functional importance of IL-9 has been investigated in various pathophysiological conditions, molecular mechanisms by which TCR stimulation induced IL-9 gene expression are still unclear. In this study, we investigated the functional importance of the NFAT1 and NF-κB (p65) in IL-9 gene transcription in CD4(+) T cells. In vivo binding of NFAT1 and NF-κB (p65) to the IL-9 promoter was observed. NFAT1 binding induced a transcriptionally active chromatin configuration at the IL-9 promoter locus, whereas NF-κB (p65) binding transactivated the IL-9 promoter. Mouse deficient in NFAT1 shows a significant down-regulation of IL-9 expression that resulted from an inaccessible chromatin configuration at the IL-9 promoter. In parallel, knockdown of NF-κB (p65) also resulted in reduced IL-9 expression. In this process, NFAT1 plays a pivotal role as a core protein that creates an accessible platform for the assembly of transcription activators. The presence of NFAT1 correlates with recruitment of NF-κB (p65), p300, and active histone markers on the IL-9 promoter, resulting in a transcriptionally competent promoter. NFAT1 deficiency significantly reduced the recruitment of the above activation complex to the IL-9 promoter. In summary, our data suggest that functional cooperation of NFAT1 and NF-κB synergistically enhances IL-9 transcription in CD4(+) T cells.

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  • Gcn5-dependent histone acetylation probably increases binding of T cell receptor-induced factors such as NF-κB or NFAT that matter for Il9 expression after antigen receptor stimulation, or may help general transcription factors including RNA polymerase II.

    “Gcn5-dependent histone acetylation likely increases binding of T cell receptor-induced factors such as NF-κB or NFAT that are important for Il9 gene expression following antigen receptor stimulation (27) or may facilitate the function of general transcription factors including RNA polymerase II (49).”

    From Gcn5 Is Required for PU.1-Dependent IL-9 Induction in Th9 Cells (2012) · cites this paper as [27]

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  1. Elyaman, W., Bradshaw, E. M., Uyttenhove, C., Dardalhon, V., Awasthi, A., Imitola, J., Bettelli, E., Oukka, M., van Snick, J., Renauld, J. C., Kuchroo, V. K., and Khoury, S. J. (2009) IL-9 induces differentiation of TH17 cells and enhances function of FoxP3 ϩ natural regulatory T cells. Proc. Natl. Acad. Sci. U.S.A. 106, 12885-12890

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Authors
Jash, A., Sahoo, A., Kim, G.-C., Chae, C.-S., Hwang, J.-S., Kim, J.-E., & Im, S.-H.
Affiliations
  • Gwangju Institute of Science and Technology (KR)
  • The University of Texas MD Anderson Cancer Center (US)
Corresponding author
Im, Sin-Hyeog
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2012-05
Volume
287
Issue
19
Pages
15445-15457
ISSN
0021-9258 (ISSN-L)
OpenAlex
W1987528629
Cited by
75
References
81
Citations by year
2026: 1 · 2025: 8 · 2024: 1 · 2023: 5 · 2022: 6 · 2021: 7 · 2020: 7 · 2019: 4 · 2018: 7 · 2017: 7 · 2016: 9 · 2015: 4 · 2014: 2 · 2013: 3 · 2012: 4
FWCI
1.67
Type
journal article
Language
en
Open access
Locations
  • Journal of Biological Chemistry (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Research Foundation (2011-0028529)
  • Gwangju Institute of Science and Technology
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Keywords
NFAT1, NF-κB p65, IL-9, chromatin accessibility, CD4+ T cells, T cell receptor stimulation, transcription factor cooperation, P300, histone modifications
MeSH terms
Animals, Base Sequence, Binding Sites, Cells, Cultured, Chromatin, Humans, Mice, Inbred C57BL, Molecular Sequence Data, Mutation, Promoter Regions, Genetic, Protein Binding, Sequence Homology, Nucleic Acid, Immunoblotting, CD4-Positive T-Lymphocytes, Transcriptional Activation, Interleukin-9, Mice, Knockout, RNA Interference, Chromatin Immunoprecipitation, NFATC Transcription Factors, Mice, Transcription Factor RelA, HEK293 Cells

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