Abstract
The phenomenon of tissue fluidity—cells’ ability to rearrange relative to each other in confluent tissues—has been linked to several morphogenetic processes and diseases, yet few molecular regulators of tissue fluidity are known. Ommatidial rotation (OR), directed by planar cell polarity signaling, occurs during Drosophila eye morphogenesis and shares many features with polarized cellular migration in vertebrates. We utilize in vivo live imaging analysis tools to quantify dynamic cellular morphologies during OR, revealing that OR is driven autonomously by ommatidial cell clusters rotating in successive pulses within a permissive substrate. Through analysis of a rotation-specific nemo mutant, we demonstrate that precise regulation of junctional E-cadherin levels is critical for modulating the mechanical properties of the tissue to allow rotation to progress. Our study defines Nemo as a molecular tool to induce a transition from solid-like tissues to more viscoelastic tissues broadening our molecular understanding of tissue fluidity.
Highlights
The phenomenon of tissue fluidity—cells’ ability to rearrange relative to each other in confluent tissues—has been linked to several morphogenetic processes and diseases, yet few molecular regulators of tissue fluidity are known
Planar cell polarity (PCP)-signaling induces the differential specification of R3 and R4, which breaks the symmetry of the pre-cluster and is followed by the rotation process with the direction of rotation being governed by the R3/R4 positioning, clockwise dorsally or counterclockwise ventrally[16]
This work defines a role for Nmo kinase in modulating tissue fluidity, which is essential for proper tissue morphogenesis
Summary
The phenomenon of tissue fluidity—cells’ ability to rearrange relative to each other in confluent tissues—has been linked to several morphogenetic processes and diseases, yet few molecular regulators of tissue fluidity are known. Planar cell polarity (PCP)-signaling induces the differential specification of R3 and R4, which breaks the symmetry of the pre-cluster and is followed by the rotation process with the direction of rotation being governed by the R3/R4 positioning (in the R3 to R4 direction), clockwise dorsally or counterclockwise ventrally[16]. This creates a line of mirror-symmetry along the D/V midline, the equator (Fig. 1a and Supplementary Fig. 1a–c). Mutations in any of these components lead to rotation defects, with clusters either rotating asynchronously, or too little or too much (reviewed in[17], refs. 20–24)
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