Evidence map›Paper›PMID 40376928›Full record

ArticleFEBS open bio2025

Knockout of the mitoribosome rescue factors Ict1 or Mtrfr is viable in zebrafish but not mice: compensatory mechanisms underlying each factor's loss.

Nobukazu Nameki, Chika Tomisawa, Soichiro Hoshino, Hidehiko Shimizu, Masashi Abe, Sho Arai, Kanako Kuwasako, Naoki Asakawa, Yusuke Inoue, Takuro Horii and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in FEBS open bio, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Nobukazu NamekiDivision of Molecular Science, Graduate School of Science and Technology, Gunma University, Kiryu-shi, Japan.ORCID https://orcid.org/0000-0002-6222-4451
Chika TomisawaDivision of Molecular Science, Graduate School of Science and Technology, Gunma University, Kiryu-shi, Japan.ORCID https://orcid.org/0009-0004-5189-3504
Soichiro HoshinoDivision of Molecular Science, Graduate School of Science and Technology, Gunma University, Kiryu-shi, Japan.ORCID https://orcid.org/0009-0005-1397-5055
Hidehiko ShimizuDivision of Molecular Science, Graduate School of Science and Technology, Gunma University, Kiryu-shi, Japan.ORCID https://orcid.org/0009-0009-7001-9579
Masashi AbeDivision of Molecular Science, Graduate School of Science and Technology, Gunma University, Kiryu-shi, Japan.
Sho AraiDivision of Molecular Science, Graduate School of Science and Technology, Gunma University, Kiryu-shi, Japan.
Kanako KuwasakoFaculty of Pharmacy and Research Institute of Pharmaceutical Sciences, Musashino University, Nishitokyo-shi, Japan.ORCID https://orcid.org/0000-0003-3758-0814
Naoki AsakawaDivision of Molecular Science, Graduate School of Science and Technology, Gunma University, Kiryu-shi, Japan.ORCID https://orcid.org/0000-0002-3633-1624
Yusuke InoueDivision of Molecular Science, Graduate School of Science and Technology, Gunma University, Kiryu-shi, Japan.ORCID https://orcid.org/0000-0002-9710-7482
Takuro HoriiLaboratory of Genome Science, Biosignal Genome Resource Center, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Japan.
Izuho HatadaLaboratory of Genome Science, Biosignal Genome Resource Center, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Japan.
Masakatsu WatanabeGraduate School of Frontier Biosciences, Osaka University, Suita, Japan.ORCID https://orcid.org/0000-0002-5744-197X

Funding

Ministry of Education, Culture, Sports, Science, and Technology of Japan 23K05677Naito Foundation
6 · The paper itself

Abstract

The mitochondrial translation system contains two ribosome rescue factors, ICT1 and MTRFR (C12orf65), which hydrolyze peptidyl-tRNA in stalled ribosomes. ICT1 also functions as a ribosomal protein of the mitochondrial large ribosomal subunit (mtLSU) in mice and humans, and its deletion is lethal. In contrast, MTRFR does not share this role. Although loss-of-function mutations in MTRFR have been linked to human mitochondrial diseases, data on this association in other vertebrates are lacking. Here, attempts to generate Mtrfr knockout mice were unsuccessful. However, knockout zebrafish lines were successfully generated for both ict1 and mtrfr (ict1

Indexed as

MitochondriaMitochondrial ProteinsRibosomal ProteinsZebrafish ProteinsAnimalsGene Knockout TechniquesHumansMiceMice, KnockoutRibosomesZebrafishMitochondrial ProteinsRibosomal ProteinsZebrafish ProteinsCOXPD7micemitochondrial morphologymitochondrial ribosome rescuethe YSLDK motifzebrafish

Identifiers

PMID40376928
PMCPMC12319706

What Socratic 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 Socratic graph.