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Cited by 66Peroxisome Proliferator-Activated ReceptorsGenomics and Chromatin DynamicsLipid metabolism and biosynthesis

Dynamic repression by BCL6 controls the genome-wide liver response to fasting and steatosis

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Sommars, Meredith A, Ramachandran, Krithika, Senagolage, Madhavi D, Futtner, Christopher R, Germain, Derrik M, Allred, Amanda L, Omura, Yasuhiro, Bederman, Ilya R +1 more·2019·eLife
DOI 10.7554/elife.43922PMC PMC6464608
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Abstract

Transcription is tightly regulated to maintain energy homeostasis during periods of feeding or fasting, but the molecular factors that control these alternating gene programs are incompletely understood. Here, we find that the B cell lymphoma 6 (BCL6) repressor is enriched in the fed state and converges genome-wide with PPARα to potently suppress the induction of fasting transcription. Deletion of hepatocyte Bcl6 enhances lipid catabolism and ameliorates high-fat-diet-induced steatosis. In Ppara -null mice, hepatocyte Bcl6 ablation restores enhancer activity at PPARα-dependent genes and overcomes defective fasting-induced fatty acid oxidation and lipid accumulation. Together, these findings identify BCL6 as a negative regulator of oxidative metabolism and reveal that alternating recruitment of repressive and activating transcription factors to shared cis-regulatory regions dictates hepatic lipid handling.

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  • Bcl6 is a transcriptional repressor that is enriched in the fed state and cooperates with PPARα to suppress the induction of fasting transcription, and Bcl6 loss has been shown to increase insulin sensitivity and repress NASH.

    “Bcl6 is a transcriptional repressor that is enriched in the fed state and cooperates with PPARα to suppress the induction of fasting transcription, and Bcl6 loss has been shown to increase insulin sensitivity and repress NASH36-38.”

    From Positive selection of somatically mutated clones identifies adaptive pathways in metabolic liver disease (2023) · cites this paper as [38]

    The Abstract describes BCL6 as a fed-state repressor that converges with PPARα to suppress fasting transcription; the Discussion clarifies that they bind independently and BCL6 opposes PPARα rather than cooperating with it. The Results ('Bcl6 ablation enhances hepatic lipid catabolism and reduces steatosis'; page not provided) report only a trend toward enhanced insulin responsiveness and protection from steatosis in mice. They do not establish increased insulin sensitivity or repression of NASH. (LLM, conf=0.89)

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References 71 · Cited by 66

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Authors
Sommars, M. A., Ramachandran, K., Senagolage, M. D., Futtner, C. R., Germain, D. M., Allred, A. L., Omura, Y., Bederman, I. R., & Barish, G. D.
Affiliations
  • Northwestern University (US)
  • Case Western Reserve University (US)
Corresponding author
Barish, Grant D
ORCID
Venue
eLife
Publisher
eLife Sciences Publications, Ltd
Published
2019-04-15
Volume
8
ISSN
2050-084X (ISSN-L)
DOI
10.7554/elife.43922
PMC
PMC6464608
OpenAlex
W2936708687
Cited by
66
References
71
Citations by year
2026: 6 · 2025: 7 · 2024: 13 · 2023: 9 · 2022: 10 · 2021: 9 · 2020: 11 · 2019: 1
FWCI
2.56
Type
journal article
Language
en
Open access
Licence
Locations
  • eLife (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Institutes of Health (R01DK108987, K08HL092298, T32GM008061)
  • American Diabetes Association (1-17-IBS-137)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
Keywords
BCL6, PPARα, fasting, hepatic steatosis, transcriptional repression, energy homeostasis, fatty acid oxidation, lipid degradation, enhancer activity, high-fat diet, hepatocytes, oxidative metabolism, cis-regulatory elements
MeSH terms
Animals, Fasting, Fatty Liver, Gene Expression Regulation, Liver, Gene Deletion, Lipid Metabolism, Mice, Proto-Oncogene Proteins c-bcl-6

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