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Dev Biol. 2019 Jun 21. pii: S0012-1606(19)30078-8. doi: 10.1016/j.ydbio.2019.06.016. [Epub ahead of print]

Fndc-1 contributes to paternal mitochondria elimination in C. elegans.

Author information

1
Department of Medicine, Nephrology Division, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, NY, 14642, USA.
2
Developmental Biology Laboratory, Sorbonne Université, CNRS, Institut de Biologie Paris Seine, IBPS, UMR7622, Paris, France.
3
Department of Biology, Middle Tennessee State University, 1301 E. Main Street, Murfreesboro, TN, 37132, USA.
4
Department of Anesthesiology, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, NY, 14642, USA; Department of Pharmacology and Physiology, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, NY, 14642, USA.
5
Developmental Biology Laboratory, Sorbonne Université, CNRS, Institut de Biologie Paris Seine, IBPS, UMR7622, Paris, France. Electronic address: vincent.galy@upmc.fr.
6
Department of Medicine, Nephrology Division, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, NY, 14642, USA; Department of Pharmacology and Physiology, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, NY, 14642, USA. Electronic address: keith_nehrke@urmc.rochester.edu.

Abstract

Paternal mitochondria are eliminated following fertilization by selective autophagy, but the mechanisms that restrict this process to sperm-derived organelles are not well understood. FUNDC1 (FUN14 domain containing 1) is a mammalian mitophagy receptor expressed on the mitochondrial outer membrane that contributes to mitochondrial quality control following hypoxic stress. Like FUNDC1, the C. elegans ortholog FNDC-1 is widely expressed in somatic tissues and mediates hypoxic mitophagy. Here, we report that FNDC-1 is strongly expressed in sperm but not oocytes and contributes to paternal mitochondria elimination. Paternal mitochondrial DNA is normally undetectable in wildtype larva, but can be detected in the cross-progeny of fndc-1 mutant males. Moreover, loss of fndc-1 retards the rate of paternal mitochondria degradation, but not that of membranous organelles, a nematode specific membrane compartment whose fusion is required for sperm motility. This is the first example of a ubiquitin-independent mitophagy receptor playing a role in the selective degradation of sperm mitochondria.

KEYWORDS:

Autophagy; C. elegans; Maternal inheritance; Mitochondria; Mitophagy

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