한빛사논문
- 조회363
Myeong-Gyun Kang,1# Hwa-Ryeon Kim,2# Hee Yong Lee,1# Chulhwan Kwak1,3, Hyewon Koh1, Byoung Heon Kang4, Jae-Seok Roe,2* and Hyun-Woo Rhee5*
1Department of Chemistry, Seoul National University, Seoul 08826, Korea
2Department of Biochemistry, Yonsei University, Seoul 03722, Korea
3Present Address: Department of Neurosurgery, Stanford University, Stanford, CA, 94305, USA
4Department of Biological Sciences, Ulsan National Institute of Science and Technology(UNIST), Ulsan 44919, Korea
5Department of Chemistry and School of Biological Sciences, Seoul National University, Seoul 08826, Korea
#M.-G.K., H.-R.K., and H.Y.L. contributed equally to this work.
*Corresponding Authors : Jae-Seok Roe, Hyun-Woo Rhee
Abstract
Mitochondrial thermogenesis is a process in which heat is generated by mitochondrial respiration. In living organisms, the thermogenic mechanisms that maintain body temperature have been studied extensively in fat cells with little knowledge on how mitochondrial heat may act beyond energy expenditure. Here, we highlight that the exothermic oxygen reduction reaction (ΔHf° = −286 kJ/mol) is the main source of the protonophore-induced mitochondrial thermogenesis, and this heat is conducted to other cellular organelles, including the nucleus. As a result, mitochondrial heat that reached the nucleus initiated the classical heat shock response, including the formation of nuclear stress granules and the localization of heat shock factor 1 (HSF1) to chromatin. Consequently, activated HSF1 increases the level of gene expression associated with the response to thermal stress in mammalian cells. Our results illustrate heat generated within the cells as a potential source of mitochondria-nucleus communication and expand our understanding of the biological functions of mitochondria in cell physiology.
논문정보
- Research article
- 2024년 06월 (BRIC 등록일 2024-06-12)
- 국내 연구진
- 생명과학 > 세포생물학
관련 보도자료
- Bio통신원
- 2024. 06. 17
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