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Loss of mpv17 affected early embryonic development via mitochondria dysfunction in zebrafish

文献类型：期刊论文

作者Bian, Wan-Ping1; Pu, Shi-Ya1,2; Xie, Shao-Lin1; Wang, Chao1; Deng, Shun1; Strauss, Phyllis R.3; Pei, De-Sheng2
刊名CELL DEATH DISCOVERY
出版日期2021-09-18
卷号7期号:1页码:10
DOI10.1038/s41420-021-00630-w
通讯作者Pei, De-Sheng(deshengpei@gmail.com)
英文摘要MVP17 encodes a mitochondrial inner-membrane protein, and mutation of human MVP17 can cause mitochondria DNA depletion syndrome (MDDS). However, the underlying function of mpv17 is still elusive. Here, we developed a new mutant with mpv17 knockout by using the CRISPR/Cas9 system. The mpv17(-/-) zebrafish showed developmental defects in muscles, liver, and energy supply. The mpv17(-/-) larvae hardly survived beyond a month, and they showed abnormal growth during the development stage. Abnormal swimming ability was also found in the mpv17(-/-) zebrafish. The transmission electron microscope (TEM) observation indicated that the mpv17(-/-) zebrafish underwent severe mitochondria dysfunction and the disorder of mitochondrial cristae. As an energy producer, the defects of mitochondria significantly reduced ATP content in mpv17(-/-) zebrafish, compared to wild-type zebrafish. We hypothesized that the disorder of mitochondria cristae was contributed to the dysfunction of muscle and liver in the mpv17(-/-) zebrafish. Moreover, the content of major energy depot triglycerides (TAG) was decreased dramatically. Interestingly, after rescued with normal exogenous mitochondria by microinjection, the genes involved in the TAG metabolism pathway were recovered to a normal level. Taken together, this is the first report of developmental defects in muscles, liver, and energy supply via mitochondria dysfunction, and reveals the functional mechanism of mpv17 in zebrafish.
资助项目CAS Team Project of the Belt and Road ; Research Program of Chongqing Science and Technology Commission[cstc2019jcyj-zdxmX0035] ; Research Program of Chongqing Science and Technology Commission[cstc2019jcyj-msxm0700] ; Research Program of Chongqing Science and Technology Commission[CSTCCXLJRC201714] ; Research Program of Chongqing Science and Technology Commission[2019-04 Beibei] ; Program of China-Sri Lanka Joint Center for Water Technology Research and Demonstration by Chinese Academy of Sciences (CAS)/China-Sri Lanka Joint Center for Education and Research by CAS ; International Partnership Program of CAS[121311kysb20190071]
WOS研究方向Cell Biology
语种英语
WOS记录号WOS:000739834300003
出版者SPRINGERNATURE
源URL[http://119.78.100.138/handle/2HOD01W0/15013]  
专题中国科学院重庆绿色智能技术研究院
通讯作者Pei, De-Sheng
作者单位1.Chinese Acad Sci, Chongqing Inst Green & Intelligent Technol, Chongqing 400714, Peoples R China
2.Chongqing Med Univ, Sch Publ Hlth & Management, Chongqing 400016, Peoples R China
3.Northeastern Univ, Coll Sci, Dept Biol, Boston, MA 02115 USA
推荐引用方式
GB/T 7714		 Bian, Wan-Ping,Pu, Shi-Ya,Xie, Shao-Lin,et al. Loss of mpv17 affected early embryonic development via mitochondria dysfunction in zebrafish[J]. CELL DEATH DISCOVERY,2021,7(1):10.
APA Bian, Wan-Ping.,Pu, Shi-Ya.,Xie, Shao-Lin.,Wang, Chao.,Deng, Shun.,...&Pei, De-Sheng.(2021).Loss of mpv17 affected early embryonic development via mitochondria dysfunction in zebrafish.CELL DEATH DISCOVERY,7(1),10.
MLA Bian, Wan-Ping,et al."Loss of mpv17 affected early embryonic development via mitochondria dysfunction in zebrafish".CELL DEATH DISCOVERY 7.1(2021):10.

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来源：重庆绿色智能技术研究院

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