Evidence map›Paper›PMID 27852436›Full record

ArticleeLife2016

Elimination of paternal mitochondria in mouse embryos occurs through autophagic degradation dependent on PARKIN and MUL1.

Rebecca Rojansky, Moon-Yong Cha, David C Chan

Open access · goldAbstract read
In one paragraph

Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 202 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
202citing papers in PubMed, 1 pooled it
23.8field-weighted citation impact, top 1% 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

202 citing papers in PubMed, 1 synthesis or guideline pooled it, 328 citations in OpenAlex.

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  19. Top-Down Coercive Mechanisms and the Major Transitions in Evolution.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
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142 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Rebecca RojanskyDivision of Biology and Biological Engineering, California Institute of Technology, Pasadena, United States.
Moon-Yong ChaDivision of Biology and Biological Engineering, California Institute of Technology, Pasadena, United States.
David C ChanDivision of Biology and Biological Engineering, California Institute of Technology, Pasadena, United States.ORCID 0000-0002-0191-2154
California Institute of Technology · US

Funding

UCLA-Caltech Medical Scientist Training ProgramT32GM008042 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI AJIJOLA, OLUJIMI A, DAWSON, DAVID WAYNE · 1985 to 2023
$29.9M
Analysis of Fis1 in Mitophagy in MammalsR01GM119388 · NIGMS · CALIFORNIA INSTITUTE OF TECHNOLOGY · PI CHAN, DAVID C · 2016 to 2018
$1.5M
Structural and mechanistic studies of mitochondrial fissionR01GM083121 · NIGMS · CALIFORNIA INSTITUTE OF TECHNOLOGY · PI CHAN, DAVID C · 2007 to 2010
$1.4M
NIGMS NIH HHS R01 GM083121NIGMS NIH HHS R01 GM119388NIGMS NIH HHS T32 GM008042
6 · The paper itself

Abstract

A defining feature of mitochondria is their maternal mode of inheritance. However, little is understood about the cellular mechanism through which paternal mitochondria, delivered from sperm, are eliminated from early mammalian embryos. Autophagy has been implicated in nematodes, but whether this mechanism is conserved in mammals has been disputed. Here, we show that cultured mouse fibroblasts and pre-implantation embryos use a common pathway for elimination of mitochondria. Both situations utilize mitophagy, in which mitochondria are sequestered by autophagosomes and delivered to lysosomes for degradation. The E3 ubiquitin ligases PARKIN and MUL1 play redundant roles in elimination of paternal mitochondria. The process is associated with depolarization of paternal mitochondria and additionally requires the mitochondrial outer membrane protein FIS1, the autophagy adaptor P62, and PINK1 kinase. Our results indicate that strict maternal transmission of mitochondria relies on mitophagy and uncover a collaboration between MUL1 and PARKIN in this process.

Indexed as

AnimalsEmbryo, MammalianHumansMiceMitochondriaMitochondrial ProteinsMitophagyPaternal InheritanceProtein KinasesPTEN-Induced Putative KinaseTranscription FactorsTranscription Factor TFIIHUbiquitin-Protein LigasesFIS1 protein, mouseGtf2h1 protein, mouseMitochondrial ProteinsMUL1 protein, mouseparkin proteinProtein KinasesPTEN-Induced Putative KinaseTranscription FactorsTranscription Factor TFIIHUbiquitin-Protein Ligasesautophagycancer biologymitochondriamitophagymouse

Identifiers

PMID27852436
PMCPMC5127638
OpenAlexW2551880155

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.