ETS1 acts as a regulator of human healthy aging via decreasing ribosomal activity

Fu Hui Xiao; Qin Yu; Zhi Li Deng; Ke Yang; Yunshuang Ye; Ming Xia Ge; Dongjing Yan; Hao Tian Wang; Xiao Qiong Chen; Li Qin Yang; Bin Yu Yang; Rong Lin; Wen Zhang; Xing Li Yang; Lei Dong; Yonghan He; Jumin Zhou; Wang Wei Cai; Ji Li; Qing Peng Kong

doi:10.1126/sciadv.abf2017

ETS1 acts as a regulator of human healthy aging via decreasing ribosomal activity

Fu Hui Xiao, Qin Yu, Zhi Li Deng, Ke Yang, Yunshuang Ye, Ming Xia Ge, Dongjing Yan, Hao Tian Wang, Xiao Qiong Chen, Li Qin Yang, Bin Yu Yang, Rong Lin, Wen Zhang, Xing Li Yang, Lei Dong, Yonghan He, Jumin Zhou, Wang Wei Cai, Ji Li, Qing Peng Kong

Research output: Contribution to journal › Article › peer-review

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Abstract

Adaptation to reduced energy production during aging is a fundamental issue for maintaining healthspan or prolonging life span. Currently, however, the underlying mechanism in long-lived people remains poorly understood. Here, we analyzed transcriptomes of 193 long-lived individuals (LLIs) and 86 spouses of their children from two independent Chinese longevity cohorts and found that the ribosome pathway was significantly down-regulated in LLIs. We found that the down-regulation is likely controlled by ETS1 (ETS proto-oncogene 1), a transcription factor down-regulated in LLIs and positively coexpressed with most ribosomal protein genes (RPGs). Functional assays showed that ETS1 can bind to RPG promoters, while ETS1 knockdown reduces RPG expression and alleviates cellular senescence in human dermal fibroblast (HDF) and embryonic lung fibroblast (IMR-90) cells. As protein synthesis/turnover in ribosomes is an energy-intensive cellular process, the decline in ribosomal biogenesis governed by ETS1 in certain female LLIs may serve as an alternative mechanism to achieve energy-saving and healthy aging.

Original language	English
Article number	eabf2017
Journal	Science advances
Volume	8
Issue number	17
DOIs	https://doi.org/10.1126/sciadv.abf2017
State	Published - Apr 2022
Externally published	Yes

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Xiao, F. H., Yu, Q., Deng, Z. L., Yang, K., Ye, Y., Ge, M. X., Yan, D., Wang, H. T., Chen, X. Q., Yang, L. Q., Yang, B. Y., Lin, R., Zhang, W., Yang, X. L., Dong, L., He, Y., Zhou, J., Cai, W. W., Li, J., & Kong, Q. P. (2022). ETS1 acts as a regulator of human healthy aging via decreasing ribosomal activity. Science advances, 8(17), Article eabf2017. https://doi.org/10.1126/sciadv.abf2017

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title = "ETS1 acts as a regulator of human healthy aging via decreasing ribosomal activity",

abstract = "Adaptation to reduced energy production during aging is a fundamental issue for maintaining healthspan or prolonging life span. Currently, however, the underlying mechanism in long-lived people remains poorly understood. Here, we analyzed transcriptomes of 193 long-lived individuals (LLIs) and 86 spouses of their children from two independent Chinese longevity cohorts and found that the ribosome pathway was significantly down-regulated in LLIs. We found that the down-regulation is likely controlled by ETS1 (ETS proto-oncogene 1), a transcription factor down-regulated in LLIs and positively coexpressed with most ribosomal protein genes (RPGs). Functional assays showed that ETS1 can bind to RPG promoters, while ETS1 knockdown reduces RPG expression and alleviates cellular senescence in human dermal fibroblast (HDF) and embryonic lung fibroblast (IMR-90) cells. As protein synthesis/turnover in ribosomes is an energy-intensive cellular process, the decline in ribosomal biogenesis governed by ETS1 in certain female LLIs may serve as an alternative mechanism to achieve energy-saving and healthy aging.",

author = "Xiao, {Fu Hui} and Qin Yu and Deng, {Zhi Li} and Ke Yang and Yunshuang Ye and Ge, {Ming Xia} and Dongjing Yan and Wang, {Hao Tian} and Chen, {Xiao Qiong} and Yang, {Li Qin} and Yang, {Bin Yu} and Rong Lin and Wen Zhang and Yang, {Xing Li} and Lei Dong and Yonghan He and Jumin Zhou and Cai, {Wang Wei} and Ji Li and Kong, {Qing Peng}",

note = "Publisher Copyright: Copyright {\textcopyright} 2022 The Authors, some rights reserved;",

year = "2022",

month = apr,

doi = "10.1126/sciadv.abf2017",

language = "English",

volume = "8",

journal = "Science advances",

issn = "2375-2548",

publisher = "American Association for the Advancement of Science",

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AU - Xiao, Fu Hui

AU - Yu, Qin

AU - Deng, Zhi Li

AU - Yang, Ke

AU - Ye, Yunshuang

AU - Ge, Ming Xia

AU - Yan, Dongjing

AU - Wang, Hao Tian

AU - Chen, Xiao Qiong

AU - Yang, Li Qin

AU - Yang, Bin Yu

AU - Lin, Rong

AU - Zhang, Wen

AU - Yang, Xing Li

AU - Dong, Lei

AU - He, Yonghan

AU - Zhou, Jumin

AU - Cai, Wang Wei

AU - Li, Ji

AU - Kong, Qing Peng

PY - 2022/4

Y1 - 2022/4

N2 - Adaptation to reduced energy production during aging is a fundamental issue for maintaining healthspan or prolonging life span. Currently, however, the underlying mechanism in long-lived people remains poorly understood. Here, we analyzed transcriptomes of 193 long-lived individuals (LLIs) and 86 spouses of their children from two independent Chinese longevity cohorts and found that the ribosome pathway was significantly down-regulated in LLIs. We found that the down-regulation is likely controlled by ETS1 (ETS proto-oncogene 1), a transcription factor down-regulated in LLIs and positively coexpressed with most ribosomal protein genes (RPGs). Functional assays showed that ETS1 can bind to RPG promoters, while ETS1 knockdown reduces RPG expression and alleviates cellular senescence in human dermal fibroblast (HDF) and embryonic lung fibroblast (IMR-90) cells. As protein synthesis/turnover in ribosomes is an energy-intensive cellular process, the decline in ribosomal biogenesis governed by ETS1 in certain female LLIs may serve as an alternative mechanism to achieve energy-saving and healthy aging.

AB - Adaptation to reduced energy production during aging is a fundamental issue for maintaining healthspan or prolonging life span. Currently, however, the underlying mechanism in long-lived people remains poorly understood. Here, we analyzed transcriptomes of 193 long-lived individuals (LLIs) and 86 spouses of their children from two independent Chinese longevity cohorts and found that the ribosome pathway was significantly down-regulated in LLIs. We found that the down-regulation is likely controlled by ETS1 (ETS proto-oncogene 1), a transcription factor down-regulated in LLIs and positively coexpressed with most ribosomal protein genes (RPGs). Functional assays showed that ETS1 can bind to RPG promoters, while ETS1 knockdown reduces RPG expression and alleviates cellular senescence in human dermal fibroblast (HDF) and embryonic lung fibroblast (IMR-90) cells. As protein synthesis/turnover in ribosomes is an energy-intensive cellular process, the decline in ribosomal biogenesis governed by ETS1 in certain female LLIs may serve as an alternative mechanism to achieve energy-saving and healthy aging.

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JO - Science advances

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ETS1 acts as a regulator of human healthy aging via decreasing ribosomal activity

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