10.5061/DRYAD.3H061
Covarrubias, Anthony J.
Department of Genetics and Complex Diseases, Harvard T.H. Chan School of
Public Health, Boston, United States
Aksoylar, Halil Ibrahim
Department of Genetics and Complex Diseases, Harvard T.H. Chan School of
Public Health, Boston, United States
Yu, Jiujiu
Department of Genetics and Complex Diseases, Harvard T.H. Chan School of
Public Health, Boston, United States
Snyder, Nathaniel W.
University of Pennsylvania
Worth, Andrew J.
University of Pennsylvania
Iyer, Shankar S.
Brigham and Women's Hospital
Wang, Jiawei
Chinese Academy of Sciences
Ben-Sahra, Issam
Department of Genetics and Complex Diseases, Harvard T.H. Chan School of
Public Health, Boston, United States
Byles, Vanessa
Department of Genetics and Complex Diseases, Harvard T.H. Chan School of
Public Health, Boston, United States
Polynne-Stapornkul, Tiffany
Department of Genetics and Complex Diseases, Harvard T.H. Chan School of
Public Health, Boston, United States
Espinosa, Erika C.
Department of Genetics and Complex Diseases, Harvard T.H. Chan School of
Public Health, Boston, United States
Lamming, Dudley
University of Wisconsin-Madison
Manning, Brendan D.
Department of Genetics and Complex Diseases, Harvard T.H. Chan School of
Public Health, Boston, United States
Zhang, Yijing
Chinese Academy of Sciences
Blair, Ian A.
University of Pennsylvania
Horng, Tiffany
Department of Genetics and Complex Diseases, Harvard T.H. Chan School of
Public Health, Boston, United States
Data from: Akt-mTORC1 signaling regulates Acly to integrate metabolic
input to control of macrophage activation
Dryad
dataset
2016
mouse
2016-03-18T04:26:26Z
2016-03-18T04:26:26Z
en
https://doi.org/10.7554/eLife.11612
12378638590 bytes
1
CC0 1.0 Universal (CC0 1.0) Public Domain Dedication
Macrophage activation/polarization to distinct functional states is
critically supported by metabolic shifts. How polarizing signals
coordinate metabolic and functional reprogramming, and the potential
implications for control of macrophage activation, remains poorly
understood. Here we show that IL-4 signaling co-opts the Akt-mTORC1
pathway to regulate Acly, a key enzyme in Ac-CoA synthesis, leading to
increased histone acetylation and M2 gene induction. Only a subset of M2
genes is controlled in this way, including those regulating cellular
proliferation and chemokine production. Moreover, metabolic signals
impinge on the Akt-mTORC1 axis for such control of M2 activation. We
propose that Akt-mTORC1 signaling calibrates metabolic state to
energetically demanding aspects of M2 activation, which may define a new
role for metabolism in supporting macrophage activation.
20150422-AC1-AC1809_S1_R1Mock rep120150422-AC2-AC1809_S2_R1Mock
rep220150422-AC4-AC1809_S3_R1AKTinh rep120150422-AC5-AC1809_S4_R1AKTinh
rep220150422-AC7-AC1809_S5_R1ACLYinh rep120150422-AC8-AC1809_S6_R1ACLYinh
rep220150422-AC13-AC1809_S9_R1IL-4 rep120150422-AC14-AC1809_S10_R1IL-4
rep220150422-AC16-AC1809_S11_R1IL-4 AKTinh
rep120150422-AC17-AC1809_S12_R1IL-4 AKTinh
rep220150422-AC19-AC1809_S13_R1IL-4 ACLYinh
rep120150422-AC20-AC1809_S14_R1IL-4 ACLYinh rep2