期刊
MOLECULAR CELL
卷 62, 期 2, 页码 194-206出版社
CELL PRESS
DOI: 10.1016/j.molcel.2016.03.036
关键词
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资金
- NIH [DK089098, P01 DK057751, CT DPH 2014-0139, DK71900, R01GM101171, R21CA177925, GM59507, R01AG030593, R01AG023166]
- Ellison Medical Foundation
- Starr Foundation Tri-Institutional Stem Cell Initiative [2014-021]
- National Natural Science Foundation of China [81125023]
- Shanghai Commission of Science and Technology [14431902800]
- National Basic Research Program of China (973 Program) [2014CBA02004]
- Shanghai Municipal Science and Technology Commission [15410723100]
- Nancy and Leonard Florsheim Family Fund
- National Research Foundation of Korea [22A20154413076] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Here we report the identification and verification of a beta-hydroxybutyrate-derived protein modification, lysine beta-hydroxybutyrylation (Kbhb), as a new type of histone mark. Histone Kbhb marks are dramatically induced in response to elevated beta-hydroxybutyrate levels in cultured cells and in livers from mice subjected to prolonged fasting or streptozotocin-induced diabetic ketoacidosis. In total, we identified 44 histone Kbhb sites, a figure comparable to the known number of histone acetylation sites. By ChIP-seq and RNA-seq analysis, we demonstrate that histone Kbhb is a mark enriched in active gene promoters and that the increased H3K9bhb levels that occur during starvation are associated with genes upregulated in starvation-responsive metabolic pathways. Histone beta-hydroxybutyrylation thus represents a new epigenetic regulatory mark that couples metabolism to gene expression, offering a new avenue to study chromatin regulation and diverse functions of beta-hydroxybutyrate in the context of important human pathophysiological states, including diabetes, epilepsy, and neoplasia.
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