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Zie Craig1, Torey R Arnold1, Kelsey Walworth1

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Anillin protein is crucial for repairing cell barrier leaks by regulating RhoA activity and actomyosin contraction at tight junctions. Its absence impairs junction repair and barrier maintenance.

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Area of Science:

  • Cell Biology
  • Biochemistry
  • Physiology

Background:

  • Cell-cell junctions, particularly tight junctions, require dynamic remodeling to maintain barrier function during cellular shape changes.
  • A rapid tight junction repair pathway involving localized, transient RhoA activations (Rho flares) has been identified, promoting actomyosin-mediated junction remodeling to fix leaks.
  • Junction elongation acts as a mechanical trigger for RhoA activation via calcium influx and p115RhoGEF recruitment, but regulatory mechanisms for RhoA activity and Myosin II contractility remain unclear.

Purpose of the Study:

  • To investigate the role of the scaffolding protein Anillin in regulating RhoA activity and actomyosin contractility during tight junction repair.
  • To elucidate how Anillin influences the dynamics of Rho flares and their impact on junction integrity and barrier function.

Main Methods:

  • Utilized knockdown models to assess the effects of Anillin depletion on Rho flare characteristics and downstream signaling.
  • Quantified Anillin localization to Rho flares and measured RhoA activity, F-actin, and Myosin II accumulation.
  • Assessed the functional consequences of Anillin knockdown on tight junction repair efficiency and barrier integrity under stress.

Main Results:

  • Anillin localizes to Rho flares and modulates RhoA activity and actomyosin contraction.
  • Anillin knockdown leads to more intense but shorter Rho flares, with reduced F-actin and Myosin II accumulation.
  • This results in decreased junction contraction, impaired reinforcement of tight junction breaks, and compromised barrier protection against damage.

Conclusions:

  • Anillin plays a novel regulatory role in tight junction repair by tuning RhoA signaling and actomyosin contractility.
  • Anillin-dependent regulation of RhoA is essential for effective repair of tight junction leaks and maintenance of epithelial barrier function.
  • These findings highlight Anillin as a key mediator in cellular responses to barrier damage and remodeling.