Evidence map›Paper›PMID 41134626›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2025

A steady-state pool of calcium-dependent actin is maintained by Homer and controls epithelial mechanosensation.

Kenji Matsuzawa, Makoto Suzuki, Yuma Cho, Ryoya Fujinaga, Junichi Ikenouchi

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. 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. Homer condensates orchestrate YAP-Wnt signaling crosstalk downstream of the Crumbs polarity complex.Proceedings of the National Academy of Sciences of the United States of America · 2026
    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

5 authors.

Kenji Matsuzawa *Department of Biochemistry, Kyushu University Graduate School of Medical Sciences, Fukuoka 812-8582, Japan.
Makoto Suzuki *Amphibian Research Center, Program of Biomedical Science, Graduate School of Integrated Sciences for Life, Hiroshima University, Hiroshima 739-8526, Japan.ORCID 0000-0002-5494-6593
Yuma ChoDepartment of Biochemistry, Kyushu University Graduate School of Medical Sciences, Fukuoka 812-8582, Japan.ORCID 0009-0008-6847-8947
Ryoya FujinagaDepartment of Biochemistry, Kyushu University Graduate School of Medical Sciences, Fukuoka 812-8582, Japan.
Junichi IkenouchiDepartment of Biochemistry, Kyushu University Graduate School of Medical Sciences, Fukuoka 812-8582, Japan.ORCID 0000-0002-2936-3548

Funding

MEXT | Japan Society for the Promotion of Science (JSPS) JP22K06225MEXT | Japan Society for the Promotion of Science (JSPS) JP23KJ1689MEXT | Japan Society for the Promotion of Science (JSPS) JP25H00994MEXT | Japan Society for the Promotion of Science (JSPS) JP25H01325MEXT | JST | Fusion Oriented REsearch for disruptive Science and Technology (FOREST) JPMJFR204LTakeda Science Foundation (TSF) no reference numberToyota Physical and Chemical Research Institute (TPCRI) no reference number
6 · The paper itself

Abstract

Epithelial cells are inherently contractile and in homeostasis, tissue integrity is maintained by balancing the uneven contractile forces in neighboring cells at the cell-cell interface. By contrast, epithelial cells can utilize an imbalance in contractile force to communicate various information to induce tissue-wide response as in wound healing. Contractility is generated and processed at the apical junctional complex (AJC) by the dynamic behavior of the actin cytoskeleton. Calcium signaling can pattern cellular responses based on its reach and amplitude and the actin cytoskeleton is supported by its wide ranging effects on actin regulators. Calcium transients regulate various cell behaviors associated with actin remodeling, such as in damage response and developmental morphogenesis. Here, we report that calcium maintains an adaptive pool of AJC-associated actin that is sensitive to tension and encoded by calcium dynamics. For this, the recently identified epithelial polarity module Homer-MUPP1/PatJ is required. Homer regulates calcium signaling in various tissue contexts through interaction with numerous components of the endoplasmic reticulum (ER) and plasma membrane (PM) calcium signal toolkit. Knockout of either Homer or MUPP1/PatJ attenuated tension-induced calcium response and severely disrupted wound healing migration, which is dependent on guidance input through AJC tension. We also show that Homer is integral to early embryonic neurodevelopment as its suppression causes failure of neural tube closure. Our findings highlight the critical role of localized calcium dynamics on AJC actin remodeling and cellular behavior, elucidating the means of tissue coordination through intercellular tension.

Indexed as

ActinsCalciumEpithelial CellsHomer Scaffolding ProteinsMechanotransduction, CellularActin CytoskeletonAnimalsCalcium SignalingEndoplasmic ReticulumHumansMiceMice, KnockoutWound HealingActinsCalciumHomer Scaffolding ProteinsactincalciumHomerMUPP1PatJ

Identifiers

PMID41134626
PMCPMC12582288

What OpenQuestion holds

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LicenceCC BY-NC-ND
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 OpenQuestion graph.