Cited by 198

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Mitochondrial endonuclease G mediates breakdown of paternal mitochondria upon fertilization

Zhou, Qinghua, Li, Haimin, Li, Hanzeng, Nakagawa, Akihisa, Lin, Jason L. J., Lee, Eui-Seung, Harry, Brian L., Skeen-Gaar, Riley Robert, Suehiro, Yuji, William, Donna, Mitani, Shohei, Yuan, Hanna S., Kang, Byung-Ho, Xue, Ding·2016·Science

Abstract

Eliminating paternal mitochondria: During fertilization, the oocyte and sperm each bring their mitochondria to the union. Shortly afterward, the paternal mitochondria are degraded, and only the maternal mitochondria are conveyed to the progeny. Zhou et al. observed that the integrity of the inner membrane of paternal mitochondria is compromised, which apparently marks them for degradation (see the Perspective by van der Bliek). Autophagy commences by mitochondrial endonuclease G relocating from the intermembrane space into the matrix and subsequently degrading the paternal mitochondrial DNA. Any delay in this process increases embryonic lethality. Science , this issue p. 394 ; see also p. 351

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  • After this reaction, the probe can be fixed and remains in the mitochondria independent of subsequent alterations in mitochondrial function or mitochondrial membrane potential.

    “After this reaction, the probe can be fixed and remains in the mitochondria independent of subsequent alterations in mitochondrial function or mitochondrial membrane potential [1115,1117,1118].”

    From Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1 (2021) · cites this paper as [1118]

    The passage labeled Abstract (page unavailable) reports that potential-insensitive MitoTracker Red staining persisted in paternal mitochondria after potential-sensitive TMRE staining was lost. This supports retention despite a change in membrane potential, but our copy does not say the probe can be fixed or that retention is independent of subsequent changes in mitochondrial function generally. (LLM, conf=0.85)

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Metadata

Authors
Zhou, Q., Li, H., Li, H., Nakagawa, A., Lin, J. L. J., Lee, E.-S., Harry, B. L., Skeen-Gaar, R. R., Suehiro, Y., William, D., Mitani, S., Yuan, H. S., Kang, B.-H., & Xue, D.
Affiliations
  • Department of Molecular, Cellular, and Developmental Biology, University of Colorado, Boulder, CO 80309, USA.
  • Institute of Molecular Biology, Academia Sinica, Taipei 11529, Taiwan.
  • Department of Physiology, Tokyo Women’s Medical University, School of Medicine and CREST, Japan Science and Technology Agency, Tokyo 162-8666, Japan.
  • Department of Microbiology and Cell Science, University of Florida, Gainesville, FL 32611, USA.
  • School of Life Sciences, Centre for Cell and Developmental Biology and State Key Laboratory of Agrobiotechnology, Chinese University of Hong Kong, Hong Kong, China.
Venue
Science
Published
2016-07-22
Volume
353
Issue
6297
Pages
394-399
ISSN
  • 0036-8075
  • 1095-9203
Cited by
198
References
0
Language
en
Funders
  • March of Dimes (1-FY14-300)
  • NIH (GM59083, GM79097, GM118188)
  • Research Grants Council of Hong Kong (AoE/M-05/12)

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