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A dozen questions about how tissue cells crawl.

A K Harris1

  • 1Department of Biology, University of North Carolina at Chapel Hill 27599-3280, USA.

Biochemical Society Symposium
|May 13, 1999
PubMed
Summary

This paper reviews unresolved questions about how tissue cells move and organize. It connects classical observations with recent molecular findings to reconsider longstanding hypotheses. The authors examine how actin assembly is localized to cell edges and inhibited at cell-cell contacts. They also explore the role of microtubules in controlling cell directionality and contractility. The paper highlights that adhesions concentrate at cell margins, possibly due to localized actin assembly inhibition. Stress fibers may nucleate at focal adhesions rather than assemble from lamellipodial actin. Fibroblasts may orient along ridges due to actin reorganization at bent edges. Traction forces may play a role in embryonic development and cell rounding, though the exact mechanism remains unclear. The authors suggest that these findings highlight the need for further integration of molecular and morphological data.

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Area of Science:

  • Cell motility in developmental biology
  • Cytoskeletal dynamics in cell biology
  • Tissue morphogenesis in biomedical research

Background:

A core challenge in cell biology involves understanding how tissue cells move and organize during development and repair. Prior research has shown that actin reorganization at cell edges drives locomotion, while cell-cell adhesions inhibit movement. However, many mechanisms remain unclear. For example, it was already known that microtubules influence cell directionality and contractility. Yet, the exact role of microtubules in regulating actin assembly remains uncertain. Additionally, the mechanisms behind adhesion focalization and stress fiber formation are not fully resolved. This uncertainty has driven recent efforts to integrate molecular insights with traditional observations. No prior work had resolved how traction forces contribute to embryonic development or cell rounding. That uncertainty motivated this review of unresolved questions in cell locomotion. This gap motivated the synthesis of existing molecular and morphological data to reconsider longstanding hypotheses.

Purpose Of The Study:

Keywords:
cell motility researchactin dynamics in biologytissue development mechanismscell adhesion regulation

Frequently Asked Questions

The authors suggest that contact inhibition may result from inhibition of actin assembly at cell-cell contacts or adhesions.

Microtubules may restrict actin assembly to certain cell regions, affecting directionality and contractility when inhibited.

Stress fibers may nucleate at focal adhesions rather than assemble from lamellipodial actin.

Fibroblasts may orient along ridges due to actin reorganization at bent cell edges.

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The study aims to reframe key questions about tissue cell locomotion in light of recent molecular discoveries. It addresses unresolved issues such as how actin assembly is restricted to certain cell regions and how microtubules influence cell directionality and contractility. The paper also explores whether actomyosin stress fibers form at focal adhesions or assemble from lamellipodial actin. Another goal is to clarify the role of traction forces in embryonic development and cell rounding. The authors propose that these questions remain unanswered due to a lack of integration between molecular and morphological data. This paper seeks to stimulate further investigation by highlighting these unresolved issues. The motivation stems from the need to reconcile classical observations with modern molecular findings. The study does not propose new experiments but synthesizes existing evidence to guide future research.

Main Methods:

The authors review a series of unresolved questions in cell locomotion, comparing classical observations with recent molecular data. They analyze how actin assembly is localized to cell edges and inhibited at cell-cell contacts. The paper examines the role of microtubules in controlling actin assembly and cell directionality. It also investigates how adhesions concentrate at cell margins and how stress fibers form. The authors compare alternative hypotheses for each question, such as whether stress fibers nucleate at focal adhesions or assemble from lamellipodial actin. They assess the role of traction forces in embryonic development and cell rounding. The approach relies on synthesizing existing literature rather than presenting new data. The paper emphasizes unresolved questions rather than definitive answers.

Main Results:

The strongest finding is that actin reassembly at cell edges is likely linked to contact inhibition of locomotion. The authors suggest that invasiveness may result from continued actin assembly at contacted cell margins. They propose that microtubules regulate actin assembly localization, influencing cell directionality and contractility. The paper highlights that adhesions concentrate at cell margins, possibly due to localized actin assembly inhibition. Stress fibers may nucleate at focal adhesions rather than assemble from lamellipodial actin. The authors suggest that fibroblasts orient along ridges due to actin reorganization at bent cell edges. Traction forces may play a role in embryonic development and cell rounding, though the exact mechanism remains unclear. The paper emphasizes that alternative answers exist for each question, based on current evidence.

Conclusions:

The authors synthesize evidence to suggest that actin assembly inhibition at cell-cell contacts may underlie contact inhibition of locomotion. They propose that invasiveness could result from continued actin assembly at contacted margins. Microtubules likely regulate actin assembly localization, affecting cell directionality and contractility. Adhesions may concentrate at cell margins due to localized actin inhibition. Stress fibers may nucleate at focal adhesions rather than assemble from lamellipodial actin. Fibroblast orientation along ridges may result from actin reorganization at bent edges. Traction forces may contribute to embryonic development and cell rounding, though the exact role remains unclear. The authors suggest that these findings highlight the need for further integration of molecular and morphological data.

Traction forces may contribute to embryonic development and cell rounding, though the exact mechanism is unclear.

Cell rounding may result from active contraction or adhesion maximization, as suggested by the authors.