Cell polarity triggered by cell-cell adhesion via E-cadherin

Area of Science:

• Cell Biology
• Developmental Biology

Background:

• Cell polarity is crucial for various biological processes like cell migration, division, and tissue repair.
• Extracellular signals typically guide cell polarization, influencing events such as chemotaxis and wound healing.

Purpose of the Study:

• To investigate the role of cell-cell adhesion in inducing cell polarity.
• To understand how engineered cell-cell adhesion asymmetries influence cell organization and behavior.

Main Methods:

• Utilized micropatterned substrates to create controlled cell-cell adhesion asymmetries in kidney epithelial cells.
• Observed nuclear displacement, centrosomal reorientation, and lamellipodial ruffling in response to cell-cell contact.
• Disrupted E-cadherin engagement to assess its role in polarity establishment.
• Investigated the involvement of the actin cytoskeleton and specific signaling pathways (Cdc42, RhoA, Rac).

Main Results:

• Engineered cell-cell contact induced nucleus displacement towards the contact zone.
• Cell-cell contact led to centrosomal reorientation and distal lamellipodial ruffling.
• Disruption of E-cadherin abolished polarity induction in patterned cells and scrape-wound assays.
• Polarity induction required an intact actin cytoskeleton and Cdc42 activity, but not RhoA or Rac.

Conclusions:

• Cell-cell adhesion is a novel and significant factor in inducing cell polarity, independent of external cues.
• Asymmetric cell-cell adhesions can direct nuclear positioning, cytoskeletal organization, and cell migration.
• Findings have implications for understanding developmental patterning and the mechanisms of wound healing.