bioRxiv Science⌕ Search

Biology subjects

Piscitello-Gomez, R.

Publications and source records attributed to Piscitello-Gomez, R..

3 recordsLinked to original sources

Sensitivity of the timing of Drosophila pupal wing morphogenesis to external perturbations

The morphogenesis of the pupal wing of Drosophila melanogaster is a powerful model for understanding the physical mechanisms of tissue morphogenesis. During this process, the wing undergoes a dramatic reshaping where the hinge region contracts and pulls on the blade region, triggering a dynamic pattern of cell elongation changes, cell divisions, and cell neighborhood changes Etournay et al. (2015). Over our several year study of this process, we noticed that sometime after the year 2016, the onset of morphogenesis became consistently delayed by [~]6 h compared to previous years. Thus, the peak of cell elongation was now observed at 28 hours after puparium formation (hAPF) rather than at 20-22 hAPF. We show here that this delay is independent of genetic background and that the speed of the overall process is relatively unchanged, implying that an environmental factor causes a shift in the onset of the process relative to the start of pupariation. We then investigated how various environmental factors influence the timing of pupal wing morphogenesis, using the dynamics of cell elongation as a proxy. We find that imaging conditions, temperature, diet, Wolbachia infection, and the light/dark cycle have relatively little effect. Preliminary data show that the spectra of light used to rear the flies affects cell elongation dynamics, although the delay was not completely reverted and more experiments are needed to know precisely how this variable affects morphogenesis. In sum, our work suggests the presence of a gate controlling the onset of pupal wing morphogenesis that is influenced by a specific, yet unclear, environmental factor. Once the gate is released, pupal wing morphogenesis occurs at a fairly constant rate, remarkably robust to many environmental variables.

developmental biology↗

Core PCP mutations affect short time mechanical properties but not tissue morphogenesis in the Drosophila pupal wing

How morphogenetic movements are robustly coordinated in space and time is a fundamental open question in biology. We study this question using the wing of Drosophila melanogaster, an epithelial tissue that undergoes large-scale tissue flows during pupal stages. We showed previously (Etournay et al., 2015) that pupal wing morphogenesis involves both cellular behaviors that allow relaxation of mechanical tissue stress, as well as cellular behaviors that appear to be actively patterned. The core planar cell polarity (PCP) pathway influences morphogenetic cell movements in many other contexts, which suggests that it could globally pattern active cellular behaviors during pupal wing morphogenesis. We show here, however, that this is not the case: there is no significant phenotype on the cellular dynamics underlying pupal morphogenesis in mutants of core PCP. Furthermore, using laser ablation experiments, coupled with a rheological model to describe the dynamics of the response to laser ablation, we conclude that while core PCP mutations affect the fast timescale response to laser ablation, they do not affect overall tissue mechanics. In conclusion, our work shows that cellular dynamics and tissue shape changes during Drosophila pupal wing morphogenesis are independent of one potential chemical guiding cue, core PCP.

developmental biology↗

Mechanosensitive binding of p120-Catenin at cell junctions regulates E-Cadherin turnover and epithelial viscoelasticity

Studying how epithelia respond to mechanical stresses is key to understanding tissue shape changes during morphogenesis. Here, we study the viscoelastic deformation of the Drosophila pupal wing epithelium in response to mechanical stress that evolves during morphogenesis. We show that wing epithelial tissue viscoelasticity depends on endocytic turnover of E-Cadherin. The fraction of ECadherin undergoing turnover depends on mechanical stress in the epithelium. We identified mechanosensitive binding of the endocytic regulator p120-Catenin (p120) as a mechanism to regulate E-Cadherin turnover. Under high stress, p120 is released into the cytoplasm, destabilizing E-Cadherin complexes and increasing its turnover. In p120 mutants, E-Cadherin turnover is insensitive to mechanical stress. Furthermore, we show that p120 is crucial for the viscoelastic deformation of the wing epithelium. Taken together, our findings reveal that mechanosensitive binding of p120-Catenin tunes epithelial tissue viscoelasticity during morphogenesis.

biophysics↗