Abstract
Convergence and extension movements elongate tissues during development. Drosophila germ-band extension (GBE) is one example, which requires active cell rearrangements driven by Myosin II planar polarisation. Here, we develop novel computational methods to analyse the spatiotemporal dynamics of Myosin II during GBE, at the scale of the tissue. We show that initial Myosin II bipolar cell polarization gives way to unipolar enrichment at parasegmental boundaries and two further boundaries within each parasegment, concomitant with a doubling of cell number as the tissue elongates. These boundaries are the primary sites of cell intercalation, behaving as mechanical barriers and providing a mechanism for how cells remain ordered during GBE. Enrichment at parasegment boundaries during GBE is independent of Wingless signaling, suggesting pair-rule gene control. Our results are consistent with recent work showing that a combinatorial code of Toll-like receptors downstream of pair-rule genes contributes to Myosin II polarization via local cell-cell interactions. We propose an updated cell-cell interaction model for Myosin II polarization that we tested in a vertex-based simulation.
Highlights
Polarised cell rearrangements drive the simultaneous elongation and narrowing of cell sheets during development
Because the polarity is essentially aligned along the AP embryonic axis, the polarity amplitude can be projected onto the AP axis and quantified using a Gaussian fit which allows a better separation between bidirectional and unidirectional polarity signals, compared to the Fourier method (Figure 1—figure supplement 2). (C”) Amplitude of Myosin II bidirectional polarity along the AP axis and over time, calculated using the Gaussian method. (D) Fourier quantification of Myosin II unidirectional polarity, shown on a movie frame 39 min after germband extension (GBE) onset
We find that parasegmental boundary (PSB) interfaces are more DV-oriented compared to flanking -1 and +1 interfaces, throughout most of GBE
Summary
Polarised cell rearrangements drive the simultaneous elongation and narrowing of cell sheets (convergence and extension) during development. The first molecular mechanism for convergence and extension was found in Drosophila, where planar polarisation of actomyosin was shown to underlie the polarised cell rearrangements of germband extension (GBE) (Zallen and Wieschaus, 2004; Bertet et al, 2004). This discovery paved the way for in-depth studies of how the planar polarisation of actomyosin and other components such as Bazooka (Par-3) and E-Cadherin drives the selective shortening of cell-cell junctions during active intercalation of epithelial cells (Zallen and Wieschaus, 2004; Rauzi et al, 2008; 2010; Levayer et al, 2011; Levayer and Lecuit, 2013; Blankenship et al, 2006; FernandezGonzalez et al, 2009; Simoes et al, 2010; 2014; Tamada et al, 2012). Actomyosin planar polarisation was found to be required during convergence and extension in vertebrate
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