TAp63 contributes to sexual dimorphism in POMC neuron functions and energy homeostasis

Chunmei Wang, Yanlin He, Pingwen Xu, Yongjie Yang, Kenji Saito, Yan Xia, Xiaofeng Yan, Antentor Hinton, Chunling Yan, Hongfang Ding, Likai Yu, Gang Shu, Rajat Gupta, Qi Wu, Qingchun Tong, William R. Lagor, Elsa R. Flores and Yong Xu ()
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Chunmei Wang: Baylor College of Medicine
Yanlin He: Baylor College of Medicine
Pingwen Xu: Baylor College of Medicine
Yongjie Yang: Baylor College of Medicine
Kenji Saito: Baylor College of Medicine
Yan Xia: Baylor College of Medicine
Xiaofeng Yan: Baylor College of Medicine
Antentor Hinton: Baylor College of Medicine
Chunling Yan: Baylor College of Medicine
Hongfang Ding: Baylor College of Medicine
Likai Yu: Baylor College of Medicine
Gang Shu: Baylor College of Medicine
Rajat Gupta: Baylor College of Medicine
Qi Wu: Baylor College of Medicine
Qingchun Tong: University of Texas Health Science Center at Houston
William R. Lagor: Baylor College of Medicine
Elsa R. Flores: H. Lee Moffitt Cancer Center
Yong Xu: Baylor College of Medicine

Nature Communications, 2018, vol. 9, issue 1, 1-11

Abstract: Abstract Sexual dimorphism exists in energy balance, but the underlying mechanisms remain unclear. Here we show that the female mice have more pro-opiomelanocortin (POMC) neurons in the arcuate nucleus of hypothalamus than males, and female POMC neurons display higher neural activities, compared to male counterparts. Strikingly, deletion of the transcription factor, TAp63, in POMC neurons confers “male-like” diet-induced obesity (DIO) in female mice associated with decreased POMC neural activities; but the same deletion does not affect male mice. Our results indicate that TAp63 in female POMC neurons contributes to the enhanced POMC neuron functions and resistance to obesity in females. Thus, TAp63 in POMC neurons is one key molecular driver for the sexual dimorphism in energy homeostasis.

Date: 2018
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DOI: 10.1038/s41467-018-03796-7

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