Kinetics and specificity of paternal mitochondrial elimination in Caenorhabditis elegans

Yang Wang, Yi Zhang, Lianwan Chen, Qian Liang, Xiao-Ming Yin, Long Miao, Byung-Ho Kang () and Ding Xue ()
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Yang Wang: School of Life Sciences and Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Tsinghua University
Yi Zhang: School of Life Sciences and Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Tsinghua University
Lianwan Chen: Institute of Biophysics, Chinese Academic of Sciences
Qian Liang: School of Life Sciences and Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Tsinghua University
Xiao-Ming Yin: Indiana University School of Medicine
Long Miao: Institute of Biophysics, Chinese Academic of Sciences
Byung-Ho Kang: State Key Laboratory of Agrobiotechnology, Cellular and Molecular Biology Program, School of Life Sciences, The Chinese University of Hong Kong
Ding Xue: School of Life Sciences and Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Tsinghua University

Nature Communications, 2016, vol. 7, issue 1, 1-15

Abstract: Abstract In most eukaryotes, mitochondria are inherited maternally. The autophagy process is critical for paternal mitochondrial elimination (PME) in Caenorhabditis elegans, but how paternal mitochondria, but not maternal mitochondria, are selectively targeted for degradation is poorly understood. Here we report that mitochondrial dynamics have a profound effect on PME. A defect in fission of paternal mitochondria delays PME, whereas a defect in fusion of paternal mitochondria accelerates PME. Surprisingly, a defect in maternal mitochondrial fusion delays PME, which is reversed by a fission defect in maternal mitochondria or by increasing maternal mitochondrial membrane potential using oligomycin. Electron microscopy and tomography analyses reveal that a proportion of maternal mitochondria are compromised when they fail to fuse normally, leading to their competition for the autophagy machinery with damaged paternal mitochondria and delayed PME. Our study indicates that mitochondrial dynamics play a critical role in regulating both the kinetics and the specificity of PME.

Date: 2016
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DOI: 10.1038/ncomms12569

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