Evidence map›Paper›PMID 31125351›Full record

ArticlePLoS genetics2019

Drosophila ADCK1 is critical for maintaining mitochondrial structures and functions in the muscle.

Woongchang Yoon, Sun-Hong Hwang, Sang-Hee Lee, Jongkyeong Chung

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

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  13. Aging mechanisms-A perspective mostly fromAdvanced genetics (Hoboken, N.J.) · 2020
    Article
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  15. Review
  16. Functional analysis of Aarf domain-containing kinase 1 in Drosophila melanogaster.Developmental dynamics : an official publication of the American Association of Anatomists · 2019
    Article
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

4 authors at 1 institution in 1 country.

Woongchang YoonNational Creative Research Initiatives Center for Energy Homeostasis Regulation, Institute of Molecular Biology and Genetics, Seoul National University, Gwanak-Gu, Seoul, Republic of Korea.ORCID 0000-0003-0544-1553
Sun-Hong HwangNational Creative Research Initiatives Center for Energy Homeostasis Regulation, Institute of Molecular Biology and Genetics, Seoul National University, Gwanak-Gu, Seoul, Republic of Korea.
Sang-Hee LeeInstitute of Molecular Biology and Genetics, Seoul National University, Gwanak-Gu, Seoul, Republic of Korea.
Jongkyeong ChungNational Creative Research Initiatives Center for Energy Homeostasis Regulation, Institute of Molecular Biology and Genetics, Seoul National University, Gwanak-Gu, Seoul, Republic of Korea.ORCID 0000-0001-5894-7537
Seoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The function of AarF domain-containing kinase 1 (ADCK1) has not been thoroughly revealed. Here we identified that ADCK1 utilizes YME1-like 1 ATPase (YME1L1) to control optic atrophy 1 (OPA1) and inner membrane mitochondrial protein (IMMT) in regulating mitochondrial dynamics and cristae structure. We firstly observed that a serious developmental impairment occurred in Drosophila ADCK1 (dADCK1) deletion mutant, resulting in premature death before adulthood. By using temperature sensitive ubiquitously expression driver tub-Gal80ts/tub-Gal4 or muscle-specific expression driver mhc-Gal4, we observed severely defective locomotive activities and structural abnormality in the muscle along with increased mitochondrial fusion in the dADCK1 knockdown flies. Moreover, decreased mitochondrial membrane potential, ATP production and survival rate along with increased ROS and apoptosis in the flies further demonstrated that the structural abnormalities of mitochondria induced by dADCK1 knockdown led to their functional abnormalities. Consistent with the ADCK1 loss-of-function data in Drosophila, ADCK1 over-expression induced mitochondrial fission and clustering in addition to destruction of the cristae structure in Drosophila and mammalian cells. Interestingly, knockdown of YME1L1 rescued the phenotypes of ADCK1 over-expression. Furthermore, genetic epistasis from fly genetics and mammalian cell biology experiments led us to discover the interactions among IMMT, OPA1 and ADCK1. Collectively, these results established a mitochondrial signaling pathway composed of ADCK1, YME1L1, OPA1 and IMMT, which has essential roles in maintaining mitochondrial morphologies and functions in the muscle.

Indexed as

AnimalsAnimals, Genetically ModifiedApoptosisATPases Associated with Diverse Cellular ActivitiesDrosophila melanogasterDrosophila ProteinsHumansMembrane Potential, MitochondrialMembrane ProteinsMetalloendopeptidasesMitochondriaMitochondrial DynamicsMitochondrial MembranesMitochondrial ProteinsMuscle ProteinsProtein KinasesADCK1 protein, humanATPases Associated with Diverse Cellular ActivitiesDrosophila ProteinsIMMT protein, humanMembrane ProteinsMetalloendopeptidasesMitochondrial ProteinsMuscle ProteinsOPA1 protein, DrosophilaProtein KinasesYME1L1 protein, human

Identifiers

PMID31125351
PMCPMC6553794
OpenAlexW2945942504

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LicenceCC BY
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Registered trials

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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.