Abstract
In convergent-extension (CE), a planar-polarized epithelial tissue elongates (extends) in-plane in one direction while shortening (converging) in the perpendicular in-plane direction, with the cells both elongating and intercalating along the converging axis. CE occurs during the development of most multicellular organisms. Current CE models assume cell or tissue asymmetry, but neglect the preferential filopodial activity along the convergent axis observed in many tissues. We propose a cell-based CE model based on asymmetric filopodial tension forces between cells and investigate how cell-level filopodial interactions drive tissue-level CE. The final tissue geometry depends on the balance between external rounding forces and cell-intercalation traction. Filopodial-tension CE is robust to relatively high levels of planar cell polarity misalignment and to the presence of non-active cells. Addition of a simple mechanical feedback between cells fully rescues and even improves CE of tissues with high levels of polarity misalignments. Our model extends easily to three dimensions, with either one converging and two extending axes, or two converging and one extending axes, producing distinct tissue morphologies, as observed in vivo.
Highlights
Embryonic development requires numerous changes in tissue morphology
We propose a filopodial-tension model that shows how tension from oriented cell protrusions leads to observed patterns of tissue CE
We explicitly model the number of cell-cell connections, their range, angular distribution, strength, and frequency of formation and breakage
Summary
Embryonic development requires numerous changes in tissue morphology. Convergent-extension (CE) is a basic tissue shape change [1,2,3,4,5,6,7,8,9], during which cells in an epithelial sheet rearrange to narrow (converge) the tissue along one planar axis while lengthening (extending) it along the perpendicular planar axis (Fig 1). CE has been observed in the development of many organisms [1,2,3,4,5,6,7,8], the specific cellular mechanisms that drive such movements are still subject of investigation [10]. Both asymmetric external forces on a tissue (passive CE) and asymmetric forces generated by the cells within a tissue (active CE) can lead to CE (Fig 1) [10]. Existing models of CE, neglect the experimentally observed prevalence of filopodial extension parallel to the direction of tissue convergence [3,9,19,20,21,22,23,24], which could produce anisotropic traction forces between cells or between cells and the extracellular matrix [25,26,27,28]
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