Elongated Cells Drive Morphogenesis in a Surface-Wrapped Finite-Element Model of Germband Retraction

Area of Science:

• Developmental Biology
• Biophysics
• Computational Biology

Background:

• Drosophila germband extension involves ventral furrow formation and cell neighbor exchanges.
• Germband retraction differs from extension, involving cell shape changes rather than neighbor exchanges.
• Understanding the interplay of cell shape, tissue organization, and forces in germband retraction is crucial.

Purpose of the Study:

• To investigate the mechanisms driving Drosophila germband retraction.
• To elucidate the roles of cell shape, tissue organization, and cellular forces in this process.
• To model germband retraction using a finite-element approach.

Main Methods:

• Developed a whole-embryo, surface-wrapped cellular finite-element model.
• Modeled the amnioserosa and germband as 2D cellular sheets on an ellipsoidal embryo approximation.
• Fitted model parameters using in vivo retraction kinematics and experimental observations of cellular forces.

Main Results:

• The model accurately reproduced germband retraction kinematics by adjusting only amnioserosa cell interface tension.
• Model predictions aligned with experimental data on mechanical stress and retraction failures.
• Retraction robustness was critically dependent on pre-elongated amnioserosa cells, not just cellular force magnitudes.

Conclusions:

• Drosophila germband retraction is primarily driven by the reversed morphogenesis of highly elongated amnioserosa cells.
• Cellular force strengths are less critical than the precisely established cell shapes that direct these forces.
• The amnioserosa tissue's shape reversal is key to coordinating forces that return the germband to its original state.