Evidence map›Paper›PMID 40265983›Full record

ArticleAndrology2026

The absence of both RIBC1 and RIBC2 induces decreased sperm motility and litter size in male mice.

Kento Katsuma, Keisuke Shimada, Shingo Tonai, Daisuke Mashiko, Rie Iida-Norita, Yuki Kaneda, Haruhiko Miyata, Masahito Ikawa

Abstract read
In one paragraph

Article in Andrology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

8 authors.

Kento KatsumaThe Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Keisuke ShimadaResearch Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.ORCID 0000-0003-3739-7163
Shingo TonaiResearch Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.
Daisuke MashikoImmunology Frontier Research Center, Osaka University, Suita, Osaka, Japan.
Rie Iida-NoritaResearch Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.ORCID 0000-0003-0104-1974
Yuki KanedaResearch Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.ORCID 0000-0001-6300-4234
Haruhiko MiyataResearch Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.ORCID 0000-0003-4758-5803
Masahito IkawaThe Institute of Medical Science, The University of Tokyo, Tokyo, Japan.ORCID 0000-0001-9859-6217

Funding

Functional analysis of novel testis-expressed secreted and transmembrane proteinsR01HD088412 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI MARTIN M. MATZUK · 2016 to 2026
$4.5M
Eunice Kennedy Shriver National Institute of Child Health and Human Development R01HD088412Japan Society for the Promotion of Science (JSPS) KAKENHI JP21H05033Japan Society for the Promotion of Science (JSPS) KAKENHI JP22H03214Japan Society for the Promotion of Science (JSPS) KAKENHI JP23K05831Japan Society for the Promotion of Science (JSPS) KAKENHI JP23K18328NICHD NIH HHS R01 HD088412Takeda Science Foundation
6 · The paper itself

Abstract

backgroundRIBC1 (RIB43A domain with coiled-coils 1) and RIBC2 (RIB43A domain with coiled-coils 2) are homolog proteins of RIB43a which is localized to microtubules in the cilia and flagella of unicellular organisms. Cryo-electron microscopy and artificial intelligence studies showed that RIBC1 and RIBC2 are microtubule inner proteins (MIPs) localized in the inner lumen of the doublet microtubules (DMTs) in mouse sperm flagella. However, the function of RIBC1 and RIBC2 in mammalian reproduction and sperm flagella is still unknown.

objectiveTo clarify the function of RIBC1 and RIBC2 in mouse spermatozoa. MATERIALS AND

methodsWe generated Ribc1 knockout (KO), Ribc2 KO, and Ribc1 and Ribc2 double-knockout (Ribc1/2 DKO) mice using the CRISPR/Cas9 system and analyzed their phenotypes.

resultsWe revealed that the loss of either RIBC1 or RIBC2 alone did not affect male fertility, but the absence of both caused a decrease in pup numbers. Sperm motility analysis showed that Ribc1 KO spermatozoa had reduced velocity, but Ribc2 KO sperm velocities were comparable with WT mice. However, Ribc1/2 DKO sperm velocities were significantly lower than those from Ribc1 KO mice. No structural abnormalities in the axonemal structure at the transmission electron microscope (TEM) level and no abnormalities in the flagellar waveform pattern were observed in Ribc1/2 DKO spermatozoa. DISCUSSION AND

conclusionBoth RIBC1 and RIBC2 are not significant for maintaining the axonemal structure in mouse spermatozoa, but both proteins function cooperatively in sperm motility. This result may indicate that minor structural changes due to RIBC protein absence are not detected at the TEM level, and RIBC2 function depends on RIBC1 in sperm motility. We think that reduced litter size in Ribc1/2 DKO mice is caused by reduced sperm motility due to minor structural abnormalities caused by the loss of two RIBC proteins.

Indexed as

Litter SizeMicrotubule ProteinsSpermatozoaSperm MotilityAnimalsFemaleFertilityMaleMiceMice, KnockoutSperm TailMicrotubule Proteinsdoublet microtubulesmicrotubule inner proteinsRIBC1RIBC2sperm motility

Identifiers

PMID40265983
PMCPMC12842877

What Socratic holds

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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 Socratic graph.