Evidence map›Paper›PMID 41935076›Full record

ArticleNature communications2026

An in vivo fitness gene of Toxoplasma, MIC11, is essential for PLP1-mediated egress from host cells.

Yuta Tachibana, Xue Gu, Miwa Sasai, Hidetaka Kosako, Eizo Takashima, Daron M Standley, Vern B Carruthers, Dominique Soldati-Favre, Masahiro Yamamoto

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 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

9 authors.

Yuta TachibanaDepartment of Immunoparasitology, Research Institute for Microbial Diseases, The University of Osaka, Osaka, Japan.ORCID http://orcid.org/0000-0001-9683-7072
Xue GuDepartment of Immunoparasitology, Research Institute for Microbial Diseases, The University of Osaka, Osaka, Japan.
Miwa SasaiDepartment of Immunoparasitology, Research Institute for Microbial Diseases, The University of Osaka, Osaka, Japan.ORCID http://orcid.org/0000-0001-6440-3958
Hidetaka KosakoDivision of Cell Signaling, Institute of Advanced Medical Sciences, Tokushima University, Tokushima, Japan.ORCID http://orcid.org/0000-0003-3228-6368
Eizo TakashimaDivision of Malaria Research, Proteo-Science Center, Ehime University, Matsuyama, Ehime, Japan.ORCID http://orcid.org/0000-0001-9070-8499
Daron M StandleyDepartment of Genome Informatics, Research Institute for Microbial Diseases, The University of Osaka, Osaka, Japan.ORCID http://orcid.org/0000-0003-4078-0817
Vern B CarruthersDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI, USA.ORCID http://orcid.org/0000-0001-6859-8895
Dominique Soldati-FavreDepartment of Microbiology and Molecular Medicine, Faculty of Medicine, University of Geneva, Geneva, Switzerland.ORCID http://orcid.org/0000-0003-4156-2109
Masahiro YamamotoDepartment of Immunoparasitology, Research Institute for Microbial Diseases, The University of Osaka, Osaka, Japan. myamamoto@biken.osaka-u.ac.jp.ORCID http://orcid.org/0000-0002-6821-2785

Funding

Japan Agency for Medical Research and Development (AMED) JP223fa627002Japan Agency for Medical Research and Development (AMED) JP25fk0108682MEXT | Japan Science and Technology Agency (JST) JPMJFR206DMEXT | Japan Science and Technology Agency (JST) JPMJMS2025Ministry of Education, Culture, Sports, Science and Technology (MEXT) 23KJ1469Ministry of Education, Culture, Sports, Science and Technology (MEXT) 25K23812
6 · The paper itself

Abstract

After invasion and replication, intracellular pathogens must egress from infected host cells. Toxoplasma gondii facilitates this process by permeabilizing host cells through induced secretion of perforin-like protein 1 (PLP1). However, the precise mechanism of host cell permeabilization remains enigmatic. Here, we identify the secretory microneme protein MIC11 as a key factor for membrane disruption. A CRISPR-based in vivo screen identifies MIC11 as the top in vivo fitness-conferring gene. Deletion of MIC11 results in severe defects in membrane rupture and egress. Scanning mutagenesis identifies functional motifs in MIC11, and mechanistic analyses support an association between MIC11 and PLP1, suggesting that MIC11 is involved in PLP1-dependent membrane disruption. Moreover, the merozoite-specific paralogue MIC22 functionally complements MIC11 deletion, suggesting a conserved mechanism of egress in the feline-restricted stages of T. gondii. Collectively, the discovery of MIC11 advances our understanding of how parasites disrupt host cells to facilitate rapid egress and successful dissemination.

Indexed as

PerforinProtozoan ProteinsToxoplasmaAnimalsCatsCell MembraneHost-Parasite InteractionsHumansPerforinperforin-like protein 1, Toxoplasma gondiiProtozoan Proteins

Identifiers

PMID41935076
PMCPMC13230962

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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.