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SUMMARY:Adhesion-regulated junction slippage controls cell intercalation d
 ynamics in an Apposed-Cortex Adhesion Model  - Alexander Nestor-Bergmann (
 PDN\, University of Cambridge)
DTSTART:20220207T143000Z
DTEND:20220207T153000Z
UID:TALK168980@talks.cam.ac.uk
CONTACT:Elena Scarpa
DESCRIPTION:Cell intercalation is a key cell behaviour of morphogenesis an
 d wound healing\, where local cell neighbour exchanges can cause dramatic 
 tissue deformations such as body axis extension.  While substantial experi
 mental work has identified the key molecular players facilitating intercal
 ation\, there remains a lack of consensus and understanding of their physi
 cal roles. Existing biophysical models that represent cell-cell contacts w
 ith single edges cannot study neighbour exchange as a continuous process\,
  where neighbouring cell cortices must uncouple. I will present an Apposed
 -Cortex Adhesion Model (ACAM) to understand active cell intercalation beha
 viours in the context of a 2D epithelial tissue. The junctional actomyosin
  cortex of every cell is modelled as a continuous viscoelastic rope-loop\,
  explicitly representing cortices facing each other at bicellular junction
 s and the adhesion molecules that couple them. The model parameters relate
  directly to the physical properties of the key subcellular players that d
 rive dynamics (actin\, myosin and adhesion)\, providing a multi-scale unde
 rstanding of cell behaviours. The ACAM predicts that active junctional con
 tractility and cortical turnover are sufficient to shrink and remove a jun
 ction\, while the growth of a new\, orthogonal junction follows passively.
  The model reveals how the turnover of adhesion molecules specifies a fric
 tion that regulates tissue dynamics and tension transmission by controllin
 g slippage between apposed cell cortices. Increasing the friction from adh
 esion in an actively intercalating tissue can lead to the formation of ros
 ette structures\, where vertices become common to many cells. \n
LOCATION:Online
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