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Sidekick dynamically rebalances contractile and protrusive forces to control tissue morphogenesis.

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Summary

Sidekick (Sdk) protein dynamically balances cell contraction and expansion in developing fly retinas. It recruits proteins to promote actin branching and protrusion, controlling epithelial organization.

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Area of Science:

  • Developmental biology
  • Cell biology
  • Biochemistry

Background:

  • Epithelial development involves dynamic cell shape changes.
  • Actin networks drive cell contraction and protrusion.
  • Sidekick (Sdk) protein was previously linked to epithelial contraction.

Purpose of the Study:

  • To investigate the role of Sidekick (Sdk) in balancing epithelial contraction and protrusion.
  • To elucidate the molecular mechanism by which Sdk regulates actin dynamics.

Main Methods:

  • Immunofluorescence microscopy to visualize protein localization.
  • Analysis of protein-protein interactions at cellular vertices.
  • Genetic manipulation to study protein function in vivo.

Main Results:

  • Sidekick (Sdk) accumulates at vertices during increased tension and recruits the WAVE regulatory complex (WRC) to promote actin branching.
  • Sdk uses the same C-terminal motif to interact with both WRC and Polychaetoid (Pyd).
  • Sdk and WRC levels decrease as Pyd levels increase during protrusion, preceding another contraction phase.

Conclusions:

  • Sidekick (Sdk) acts as a central regulator of the balance between contraction and expansion in the developing fly retina epithelium.
  • Sdk's dynamic vertex association and interchangeable interactions with contractile (Pyd) and protrusive (WRC) factors are key to epithelial organization.