Abstract
Recent studies have revealed that intrinsic, individual cell behavior can provide the driving force for deforming a two-dimensional cell sheet to a three-dimensional tissue without the need for external regulatory elements. However, whether intrinsic, individual cell behavior could actually generate the force to induce tissue deformation was unclear, because there was no experimental method with which to verify it in vivo. In such cases, mathematical modeling can be effective for verifying whether a locally generated force can propagate through an entire tissue and induce deformation. Moreover, the mathematical model sometimes provides potential mechanistic insight beyond the information obtained from biological experimental results. Here, we present two examples of modeling tissue morphogenesis driven by cell deformation or cell interaction. In the first example, a mathematical study on tissue-autonomous folding based on a two-dimensional vertex model revealed that active modulations of cell mechanics along the basal–lateral surface, in addition to the apical side, can induce tissue-fold formation. In the second example, by applying a two-dimensional vertex model in an apical plane, a novel mechanism of tissue flow caused by asymmetric cell interactions was discovered, which explained the mechanics behind the collective cellular movement observed during epithelial morphogenesis.
Highlights
IntroductionMorphogenetic epithelial movement drives the formation of complex tissues
During embryogenesis, morphogenetic epithelial movement drives the formation of complex tissues
We found that individual epithelial cells surrounding the genitalia adopt a left–right (LR) asymmetric polarity within their apical plane [10], termed planar cell-shape chirality (PCC), which was found to be an intrinsic cellular process [11,24,25]
Summary
Morphogenetic epithelial movement drives the formation of complex tissues. The junctions contract in the manner of a drawstring purse, resulting in a “wedge-shaped” cell morphology with a smaller apical surface and larger basal surface [18,19] This wedge-shaped deformation was proposed to be the driving force of tissue bending by causing the cell sheet to fold [20], it was difficult to prove in vivo whether an entire epithelial tissue could be folded just by deforming the cells located along a line. The LR asymmetric distribution of Myosin-II is reversed in flies expressing MyoID dsRNA [10] Despite these detailed observations, it was still unclear whether the diagonal cell intercalation of these individual cells could generate the force to induce the collective cellular movement, because there is no experimental method with which to verify this point in vivo. We present a mathematical model showing that the direction of the collective movement of epithelial cells is regulated by PCC, further demonstrating that PCC-associated LR asymmetric cell intercalation is sufficient to drive unidirectional tissue flow
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