Prdm16 is required for the maintenance of brown adipocyte identity and function in adult mice
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Prdm16 is required for the maintenance of brown adipocyte identity and function in adult mice. / Harms, Matthew J; Ishibashi, Jeff; Wang, Wenshan; Lim, Hee-Woong; Goyama, Susumu; Sato, Tomohiko; Kurokawa, Mineo; Won, Kyoung-Jae; Seale, Patrick.
I: Cell Metabolism, Bind 19, Nr. 4, 01.04.2014, s. 593-604.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Prdm16 is required for the maintenance of brown adipocyte identity and function in adult mice
AU - Harms, Matthew J
AU - Ishibashi, Jeff
AU - Wang, Wenshan
AU - Lim, Hee-Woong
AU - Goyama, Susumu
AU - Sato, Tomohiko
AU - Kurokawa, Mineo
AU - Won, Kyoung-Jae
AU - Seale, Patrick
N1 - Copyright © 2014 Elsevier Inc. All rights reserved.
PY - 2014/4/1
Y1 - 2014/4/1
N2 - Prdm16 is a transcription factor that regulates the thermogenic gene program in brown and beige adipocytes. However, whether Prdm16 is required for the development or physiological function of brown adipose tissue (BAT) in vivo has been unclear. By analyzing mice that selectively lacked Prdm16 in the brown adipose lineage, we found that Prdm16 was dispensable for embryonic BAT development. However, Prdm16 was required in young mice to suppress the expression of white-fat-selective genes in BAT through recruitment of the histone methyltransferase Ehmt1. Additionally, Prdm16 deficiency caused a severe adult-onset decline in the thermogenic character of interscapular BAT. This resulted in BAT dysfunction and cold sensitivity but did not predispose the animals to obesity. Interestingly, the loss of brown fat identity due to ablation of Prdm16 was accelerated by concurrent deletion of the closely related Prdm3 gene. Together, these results show that Prdm16 and Prdm3 control postnatal BAT identity and function.
AB - Prdm16 is a transcription factor that regulates the thermogenic gene program in brown and beige adipocytes. However, whether Prdm16 is required for the development or physiological function of brown adipose tissue (BAT) in vivo has been unclear. By analyzing mice that selectively lacked Prdm16 in the brown adipose lineage, we found that Prdm16 was dispensable for embryonic BAT development. However, Prdm16 was required in young mice to suppress the expression of white-fat-selective genes in BAT through recruitment of the histone methyltransferase Ehmt1. Additionally, Prdm16 deficiency caused a severe adult-onset decline in the thermogenic character of interscapular BAT. This resulted in BAT dysfunction and cold sensitivity but did not predispose the animals to obesity. Interestingly, the loss of brown fat identity due to ablation of Prdm16 was accelerated by concurrent deletion of the closely related Prdm3 gene. Together, these results show that Prdm16 and Prdm3 control postnatal BAT identity and function.
KW - Adipocytes, Brown/metabolism
KW - Aging/physiology
KW - Analysis of Variance
KW - Animals
KW - Blotting, Western
KW - Chromatin Immunoprecipitation
KW - DNA-Binding Proteins/genetics
KW - Flow Cytometry
KW - Gene Expression Regulation, Developmental/genetics
KW - Histological Techniques
KW - Histone-Lysine N-Methyltransferase/metabolism
KW - Mice
KW - Mice, Knockout
KW - Microarray Analysis
KW - Real-Time Polymerase Chain Reaction
KW - Transcription Factors/genetics
U2 - 10.1016/j.cmet.2014.03.007
DO - 10.1016/j.cmet.2014.03.007
M3 - Journal article
C2 - 24703692
VL - 19
SP - 593
EP - 604
JO - Cell Metabolism
JF - Cell Metabolism
SN - 1550-4131
IS - 4
ER -
ID: 199332305