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作 者:Ying Wang Hua-Min Wang Yan Zhou Ling-Hong Hu Jing-Ming Wan Ji-Hui Yang Hong-Bo Niu Xiu-Ping Hong Peng Hu Liang-Biao Chen
机构地区:[1]International Research Center for Marine Biosciences,Ministry of Science and Technology,Shanghai Ocean University,Shanghai 200120,China [2]Key Laboratory of Exploration and Utilization of Aquatic Genetic Resources,Ministry of Education,Shanghai Ocean University,Shanghai 200120,China [3]Shanghai Collaborative Innovation for Aquatic Animal Genetics and Breeding,Shanghai Ocean University,Shanghai 200120,China
出 处:《Zoological Research》2023年第1期126-141,共16页动物学研究(英文)
基 金:supported by the National Key Research and Development Program of China(2018YFD0900601);National Natural Science Foundation of China(32130109)。
摘 要:Temperature tolerance restricts the distribution of a species. However, the molecular and cellular mechanisms that set the thermal tolerance limits of an organism are poorly understood. Here, we report on the function of dual-specificity phosphatase 1(DUSP1) in thermal tolerance regulation. Notably, we found that dusp1-/- zebrafish grew normally but survived within a narrowed temperature range. The higher susceptibility of these mutant fish to both cold and heat challenges was attributed to accelerated cell death caused by aggravated mitochondrial dysfunction and over-production of reactive oxygen species in the gills. The DUSP1-MAPK-DRP1 axis was identified as a key pathway regulating these processes in both fish and human cells. These observations suggest that DUSP1 may play a role in maintaining mitochondrial integrity and redox homeostasis. We therefore propose that maintenance of cellular redox homeostasis may be a key mechanism for coping with cellular thermal stress and that the interplay between signaling pathways regulating redox homeostasis in the most thermosensitive tissue(i.e., gills) may play an important role in setting the thermal tolerance limit of zebrafish.
关 键 词:Redox homeostasis ZEBRAFISH Ectothermal Mitochondrial fission Thermal stress MAPK
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