Evidence map›Paper›PMID 35648791›Full record

ArticlePLoS genetics2022

Trim41 is required to regulate chromosome axis protein dynamics and meiosis in male mice.

Seiya Oura, Toshiaki Hino, Takashi Satoh, Taichi Noda, Takayuki Koyano, Ayako Isotani, Makoto Matsuyama, Shizuo Akira, Kei-Ichiro Ishiguro, Masahito Ikawa

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.1field-weighted citation impact, top 58% 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

2 citing papers in PubMed, 1 citations in OpenAlex.

  1. Article
  2. 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

10 authors at 7 institutions in 1 country.

Seiya OuraResearch Institute for Microbial Diseases, Osaka University, Osaka, Japan.ORCID 0000-0002-7606-732X
Toshiaki HinoDepartment of Biological Sciences, Asahikawa Medical University, Asahikawa, Japan.
Takashi SatohDepartment of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.ORCID 0000-0002-8868-5782
Taichi NodaResearch Institute for Microbial Diseases, Osaka University, Osaka, Japan.ORCID 0000-0003-0260-7861
Takayuki KoyanoDivision of Molecular Genetics, Shigei Medical Research Institute, Okayama, Japan.ORCID 0000-0003-1675-2525
Ayako IsotaniResearch Institute for Microbial Diseases, Osaka University, Osaka, Japan.ORCID 0000-0002-4720-2318
Makoto MatsuyamaDivision of Molecular Genetics, Shigei Medical Research Institute, Okayama, Japan.
Shizuo AkiraLaboratory of Host Defense, WPI Immunology Frontier Research Center, Osaka University, Osaka, Japan.
Kei-Ichiro IshiguroDepartment of Chromosome Biology, Institute of Molecular Embryology and Genetics (IMEG), Kumamoto University, Kumamoto, Japan.ORCID 0000-0002-7515-1511
Masahito IkawaResearch Institute for Microbial Diseases, Osaka University, Osaka, Japan.ORCID 0000-0001-9859-6217
Kumamoto University · JPShigei Medical Research Institute · JPTokyo Medical and Dental University · JPAsahikawa Medical University · JPNara Institute of Science and Technology · JPOsaka University of Pharmaceutical Sciences · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Meiosis is a hallmark event in germ cell development that accompanies sequential events executed by numerous molecules. Therefore, characterization of these factors is one of the best strategies to clarify the mechanism of meiosis. Here, we report tripartite motif-containing 41 (TRIM41), a ubiquitin ligase E3, as an essential factor for proper meiotic progression and fertility in male mice. Trim41 knockout (KO) spermatocytes exhibited synaptonemal complex protein 3 (SYCP3) overloading, especially on the X chromosome. Furthermore, mutant mice lacking the RING domain of TRIM41, required for the ubiquitin ligase E3 activity, phenocopied Trim41 KO mice. We then examined the behavior of mutant TRIM41 (ΔRING-TRIM41) and found that ΔRING-TRIM41 accumulated on the chromosome axes with overloaded SYCP3. This result suggested that TRIM41 exerts its function on the chromosome axes. Our study revealed that Trim41 is essential for preventing SYCP3 overloading, suggesting a TRIM41-mediated mechanism for regulating chromosome axis protein dynamics during male meiotic progression.

Indexed as

Nuclear ProteinsSynaptonemal ComplexAnimalsCell Cycle ProteinsMaleMeiosisMiceMice, KnockoutSpermatocytesUbiquitin-Protein LigasesCell Cycle ProteinsNuclear ProteinsTrim41 protein, mouseUbiquitin-Protein Ligases

Identifiers

PMID35648791
PMCPMC9191731
OpenAlexW4281966246

What OpenQuestion holds

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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.