Interface Contractility between Differently Fated Cells Drives Cell Elimination and Cyst Formation

Area of Science:

• Developmental Biology
• Cell Biology
• Tissue Homeostasis

Background:

• Cellular tumor suppression is well-studied, but tissue-level mechanisms preventing aberrant cells in epithelia are less understood.
• Ectopic expression of cell fate transcription factors can disrupt epithelial organization.

Purpose of the Study:

• To investigate tissue-level mechanisms suppressing aberrant cells in epithelia.
• To understand how cell-fate heterogeneities influence epithelial morphogenesis and homeostasis.

Main Methods:

• Utilized Drosophila imaginal discs to study epithelial cyst formation.
• Employed 3D vertex model simulations and experimental validation.
• Investigated actomyosin enrichment and interface contractility.

Main Results:

• Juxtaposition of cells with divergent fates induces actomyosin enrichment and increased interface contractility.
• Enhanced contractility drives various morphogenetic behaviors, including cyst formation and cell segregation.
• Single aberrant cells are eliminated via apoptosis due to lateral interface contractility; failure leads to cyst formation.

Conclusions:

• Increased interface contractility serves as a crucial error correction mechanism at the tissue level.
• Failure of this mechanism, particularly with aberrant cell proliferation, results in cyst formation, potentially promoting disease.
• Cell-fate heterogeneity can drive morphogenetic events that maintain or disrupt epithelial homeostasis.