Competing adhesions rigidify the vertebrate body axis
ORAL
Abstract
Solidification of the presomitic mesoderm (PSM), an axial tissue of developing vertebrate embryos, is required for
healthy vertebrate body axis elongation. Failure of the PSM to solidify in zebrafish leads to delayed development and
bilateral asymmetry, such as curved tails. It has been found that in cadherin loss-of-function mutants, where cells do
not form cadherin-based cell-cell adhesions, the PSM has reduced cell packing fraction and yield stress. Despite the
reduced tissue integrity in cadherin mutants, we show that the PSM can still solidify in the absence of cell-cell
adhesion. We propose that the cadherin mutants experience increased integrin-based interactions between cells and
the extracellular matrix (ECM) that partially rescues tissue integrity. We develop numerical simulations using the
deformable particle model to investigate the relative contributions of cell-cell and cell-ECM adhesions to tissue
integrity. Our work shows that both cell-cell and cell-ECM adhesion are sufficient for tissue solidification, although
their molecular and physical mechanisms are different.
healthy vertebrate body axis elongation. Failure of the PSM to solidify in zebrafish leads to delayed development and
bilateral asymmetry, such as curved tails. It has been found that in cadherin loss-of-function mutants, where cells do
not form cadherin-based cell-cell adhesions, the PSM has reduced cell packing fraction and yield stress. Despite the
reduced tissue integrity in cadherin mutants, we show that the PSM can still solidify in the absence of cell-cell
adhesion. We propose that the cadherin mutants experience increased integrin-based interactions between cells and
the extracellular matrix (ECM) that partially rescues tissue integrity. We develop numerical simulations using the
deformable particle model to investigate the relative contributions of cell-cell and cell-ECM adhesions to tissue
integrity. Our work shows that both cell-cell and cell-ECM adhesion are sufficient for tissue solidification, although
their molecular and physical mechanisms are different.
* NSF 2102789
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Presenters
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Andrew Ton
Yale University
Authors
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Andrew Ton
Yale University