Abstract
Morphogenetic epithelial movement occurs during embryogenesis and drives complex tissue formation. However, how epithelial cells coordinate their unidirectional movement while maintaining epithelial integrity is unclear. Here we propose a novel mechanism for collective epithelial cell movement based on Drosophila genitalia rotation, in which epithelial tissue rotates clockwise around the genitalia. We found that this cell movement occurs autonomously and requires myosin II. The moving cells exhibit repeated left–right-biased junction remodelling, while maintaining adhesion with their neighbours, in association with a polarized myosin II distribution. Reducing myosinID, known to cause counter-clockwise epithelial-tissue movement, reverses the myosin II distribution. Numerical simulations revealed that a left–right asymmetry in cell intercalation is sufficient to induce unidirectional cellular movement. The cellular movement direction is also associated with planar cell-shape chirality. These findings support a model in which left–right asymmetric cell intercalation within an epithelial sheet drives collective cellular movement in the same direction.
Highlights
Morphogenetic epithelial movement occurs during embryogenesis and drives complex tissue formation
The deformation of developing epithelial tissues along the body axis involves an epithelial cell rearrangement process that is induced by planar polarized junctional contractility elicited by myosin II (Myo-II), and junctional shortening caused by the endocytosis of E-cadherin[5,7,23,24]
We found that en-GAL4- and AbdBGAL4LDN-driven expressions did not overlap in the A8 segment (Supplementary Fig. 1a,b)
Summary
Morphogenetic epithelial movement occurs during embryogenesis and drives complex tissue formation. In Drosophila germ band elongation, cell junctions perpendicular to the anterior–posterior (AP) axis accumulate high levels of non-muscle myosin II (Myo-II), which increases the strength of the junctional tension, accompanied by a decrease in junctional length, whereas cell junctions parallel to the AP axis have low levels of Myo-II and tend to expand[5] This process is mediated by the polarized remodelling of the adherens junctions, protein complexes at cell–cell junctions that contain actomyosin cables and adhesion molecules such as E-cadherin[7,8,9,10]. There are examples of cell clusters lacking a leading edge that undergo collective movement while maintaining their epithelial characteristics, such as in tracheal invagination[11], mammary gland sprouting[11] and eyelid closure in mice[13], and in egg chamber rotation in Drosophila[14,15,16,17]. The conserved type ID unconventional myosin 31DF gene (myosinID: myoID) contributes to the clockwise direction of genitalia rotation[21] and is transcriptionally controlled by the Hox gene, AbdB22; the mechanism by which the rotation is achieved is unknown
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