# Stress fiber contraction induces cell body rotation in single keratocytes

**Authors:** Chika Okimura

PMC · DOI: 10.2142/biophysico.bppb-v22.0023 · 2025-10-04

## TL;DR

This review explains how stress fiber contraction causes cell body rotation in fish keratocytes, a unique mechanism not seen in man-made machines.

## Contribution

The paper introduces a novel conversion mechanism from linear motion to rotation in cell migration using stress fibers and soft cell deformation.

## Key findings

- Stress fiber contraction drives rotation of the keratocyte cell body during migration.
- Fish keratocytes are ideal for studying both single and collective cell migration due to their high speed and ease of culture.
- Robot models have been developed to demonstrate the mechanics of this unique cell movement.

## Abstract

Single epidermal keratocytes, which are responsible for wound repair in fish, migrate while maintaining their characteristic shape: a frontal crescent-shaped lamellipodium and a posterior rugby-ball-shaped cell body. These cells are widely used in cell migration studies, especially to examine the role of actin polymerization at the leading edge of the cell. In the posterior part of the cell, stress fibers, which are bundles of actomyosin, are aligned along the seam of the ‘rugby ball.’ The ball rotates with the stress fibers during migration. The linear contraction of stress fibers appears to drive the rotation of the cell body. This review describes a conversion mechanism from linear motion to rotation driven by stress fiber contraction and soft cell body deformation, which is not found in man-made machines. We also describe a unique research method that is able to demonstrate this machinery by creating robot models. Due to their high migration rate and ease of culturing, fish keratocytes appear to be one of the best materials for studying both single cell and collective cell migration. In this review, we will also give some recent research examples of collective migration using keratocytes.

## Linked entities

- **Proteins:** Act5C (Actin 5C)

## Full-text entities

- **Genes:** TMSB4X (thymosin beta 4 X-linked) [NCBI Gene 7114] {aka FX, PTMB4, TB4X, TMSB4}, PIK3R1 (phosphoinositide-3-kinase regulatory subunit 1) [NCBI Gene 5295] {aka AGM7, GRB1, IMD36, p85, p85-ALPHA, p85alpha}, VCL (vinculin) [NCBI Gene 479252]
- **Chemicals:** silicone (MESH:D012828), CO2 (MESH:D002245), LY-294002 (MESH:C085911), cytochalasin B (MESH:D003571), Alexa Fluor  Phalloidin (-), blebbistatin (MESH:C472645)
- **Species:** Actinopterygii (fishes, superclass) [taxon 7898], Homo sapiens (human, species) [taxon 9606]
- **Cell lines:** HL-60 — Homo sapiens (Human), Adult acute myeloid leukemia with maturation, Cancer cell line (CVCL_0002), fibroblasts — Mus musculus (Mouse), Spontaneously immortalized cell line (CVCL_0594)

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12582641/full.md

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Source: https://tomesphere.com/paper/PMC12582641