Lipids Reprogram Metabolism to Become a Major Carbon Source for Histone Acetylation

Institut for Lægemiddeldesign og Farmakologi

Lipids Reprogram Metabolism to Become a Major Carbon Source for Histone Acetylation

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Standard

Lipids Reprogram Metabolism to Become a Major Carbon Source for Histone Acetylation. / McDonnell, Eoin; Crown, Scott B; Fox, Douglas B; Kitir, Betül; Ilkayeva, Olga R; Olsen, Christian A; Grimsrud, Paul A; Hirschey, Matthew D.

I: Cell Reports, Bind 17, Nr. 6, 01.11.2016, s. 1463-1472.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

McDonnell, E, Crown, SB, Fox, DB, Kitir, B, Ilkayeva, OR, Olsen, CA, Grimsrud, PA & Hirschey, MD 2016, 'Lipids Reprogram Metabolism to Become a Major Carbon Source for Histone Acetylation', Cell Reports, bind 17, nr. 6, s. 1463-1472. https://doi.org/10.1016/j.celrep.2016.10.012

APA

McDonnell, E., Crown, S. B., Fox, D. B., Kitir, B., Ilkayeva, O. R., Olsen, C. A., Grimsrud, P. A., & Hirschey, M. D. (2016). Lipids Reprogram Metabolism to Become a Major Carbon Source for Histone Acetylation. Cell Reports, 17(6), 1463-1472. https://doi.org/10.1016/j.celrep.2016.10.012

Vancouver

McDonnell E, Crown SB, Fox DB, Kitir B, Ilkayeva OR, Olsen CA o.a. Lipids Reprogram Metabolism to Become a Major Carbon Source for Histone Acetylation. Cell Reports. 2016 nov. 1;17(6):1463-1472. https://doi.org/10.1016/j.celrep.2016.10.012

Author

McDonnell, Eoin ; Crown, Scott B ; Fox, Douglas B ; Kitir, Betül ; Ilkayeva, Olga R ; Olsen, Christian A ; Grimsrud, Paul A ; Hirschey, Matthew D. / Lipids Reprogram Metabolism to Become a Major Carbon Source for Histone Acetylation. I: Cell Reports. 2016 ; Bind 17, Nr. 6. s. 1463-1472.

Bibtex

@article{a99a572a29ef434389915fe488479a46,

title = "Lipids Reprogram Metabolism to Become a Major Carbon Source for Histone Acetylation",

abstract = "Cells integrate nutrient sensing and metabolism to coordinate proper cellular responses to a particular nutrient source. For example, glucose drives a gene expression program characterized by activating genes involved in its metabolism, in part by increasing glucose-derived histone acetylation. Here, we find that lipid-derived acetyl-CoA is a major source of carbon for histone acetylation. Using (13)C-carbon tracing combined with acetyl-proteomics, we show that up to 90% of acetylation on certain histone lysines can be derived from fatty acid carbon, even in the presence of excess glucose. By repressing both glucose and glutamine metabolism, fatty acid oxidation reprograms cellular metabolism, leading to increased lipid-derived acetyl-CoA. Gene expression profiling of octanoate-treated hepatocytes shows a pattern of upregulated lipid metabolic genes, demonstrating a specific transcriptional response to lipid. These studies expand the landscape of nutrient sensing and uncover how lipids and metabolism are integrated by epigenetic events that control gene expression.",

author = "Eoin McDonnell and Crown, {Scott B} and Fox, {Douglas B} and Bet{\"u}l Kitir and Ilkayeva, {Olga R} and Olsen, {Christian A} and Grimsrud, {Paul A} and Hirschey, {Matthew D}",

year = "2016",

month = nov,

day = "1",

doi = "10.1016/j.celrep.2016.10.012",

language = "English",

volume = "17",

pages = "1463--1472",

journal = "Cell Reports",

issn = "2211-1247",

publisher = "Cell Press",

number = "6",

}

RIS

TY - JOUR

T1 - Lipids Reprogram Metabolism to Become a Major Carbon Source for Histone Acetylation

AU - McDonnell, Eoin

AU - Crown, Scott B

AU - Fox, Douglas B

AU - Kitir, Betül

AU - Ilkayeva, Olga R

AU - Olsen, Christian A

AU - Grimsrud, Paul A

AU - Hirschey, Matthew D

PY - 2016/11/1

Y1 - 2016/11/1

N2 - Cells integrate nutrient sensing and metabolism to coordinate proper cellular responses to a particular nutrient source. For example, glucose drives a gene expression program characterized by activating genes involved in its metabolism, in part by increasing glucose-derived histone acetylation. Here, we find that lipid-derived acetyl-CoA is a major source of carbon for histone acetylation. Using (13)C-carbon tracing combined with acetyl-proteomics, we show that up to 90% of acetylation on certain histone lysines can be derived from fatty acid carbon, even in the presence of excess glucose. By repressing both glucose and glutamine metabolism, fatty acid oxidation reprograms cellular metabolism, leading to increased lipid-derived acetyl-CoA. Gene expression profiling of octanoate-treated hepatocytes shows a pattern of upregulated lipid metabolic genes, demonstrating a specific transcriptional response to lipid. These studies expand the landscape of nutrient sensing and uncover how lipids and metabolism are integrated by epigenetic events that control gene expression.

AB - Cells integrate nutrient sensing and metabolism to coordinate proper cellular responses to a particular nutrient source. For example, glucose drives a gene expression program characterized by activating genes involved in its metabolism, in part by increasing glucose-derived histone acetylation. Here, we find that lipid-derived acetyl-CoA is a major source of carbon for histone acetylation. Using (13)C-carbon tracing combined with acetyl-proteomics, we show that up to 90% of acetylation on certain histone lysines can be derived from fatty acid carbon, even in the presence of excess glucose. By repressing both glucose and glutamine metabolism, fatty acid oxidation reprograms cellular metabolism, leading to increased lipid-derived acetyl-CoA. Gene expression profiling of octanoate-treated hepatocytes shows a pattern of upregulated lipid metabolic genes, demonstrating a specific transcriptional response to lipid. These studies expand the landscape of nutrient sensing and uncover how lipids and metabolism are integrated by epigenetic events that control gene expression.

U2 - 10.1016/j.celrep.2016.10.012

DO - 10.1016/j.celrep.2016.10.012

M3 - Journal article

C2 - 27806287

VL - 17

SP - 1463

EP - 1472

JO - Cell Reports

JF - Cell Reports

SN - 2211-1247

IS - 6

ER -

ID: 169436094