Evidence map›Paper›PMID 31233739›Full record

ArticleDevelopmental biology2019

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

Yunki Lim, Karinna Rubio-Peña, Peter J Sobraske, Paola A Molina, Paul S Brookes, Vincent Galy, Keith Nehrke

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Developmental biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

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  9. Mitochondrial curation for the next generation.Current opinion in genetics & development · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Yunki LimDepartment of Medicine, Nephrology Division, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, NY, 14642, USA.
Karinna Rubio-PeñaDevelopmental Biology Laboratory, Sorbonne Université, CNRS, Institut de Biologie Paris Seine, IBPS, UMR7622, Paris, France.
Peter J SobraskeDepartment of Medicine, Nephrology Division, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, NY, 14642, USA.
Paola A MolinaDepartment of Biology, Middle Tennessee State University, 1301 E. Main Street, Murfreesboro, TN, 37132, USA.
Paul S BrookesDepartment 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.
Vincent GalyDevelopmental Biology Laboratory, Sorbonne Université, CNRS, Institut de Biologie Paris Seine, IBPS, UMR7622, Paris, France. Electronic address: vincent.galy@upmc.fr.
Keith NehrkeDepartment 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.
University of Rochester Medical Center · USCentre National de la Recherche Scientifique · FRMiddle Tennessee State University · US

Funding

The Role of the Mitochondrial UPR in Ischemic ProtectionR01HL127891 · NHLBI · UNIVERSITY OF ROCHESTER · PI BROOKES, PAUL S, NEHRKE, KEITH · 2015 to 2018
$2.5M
Degradation of sperm organelles after fertilizationR15HD083882 · NICHD · MIDDLE TENNESSEE STATE UNIVERSITY · PI BOYD, LYNN · 2015 to 2015
$310k
NHLBI NIH HHS R01 HL127891NICHD NIH HHS R15 HD083882
6 · The paper itself

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.

Indexed as

AnimalsAutophagyCaenorhabditis elegansCaenorhabditis elegans ProteinsDNA, MitochondrialEmbryo, NonmammalianFertilizationHumansLysosomesMaleMembrane ProteinsMitochondriaMitochondrial MembranesMitochondrial ProteinsMitophagyOocytesCaenorhabditis elegans ProteinsDNA, MitochondrialFUNDC1 protein, humanMembrane ProteinsMitochondrial ProteinsUbiquitinAutophagyC. elegansMaternal inheritanceMitochondriaMitophagy

Identifiers

PMID31233739
PMCPMC6717525
OpenAlexW2951185153

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.