Rupture-Repair Cycles in Regenerating Hydra Tissues
Oded Agam, Erez Braun

TL;DR
This study investigates how Hydra tissues repair ruptures through Ca2+-dependent mechanisms, revealing that weakening calcium responses leads to larger, more frequent ruptures and a transition from exponential to power-law rupture size distributions.
Contribution
It uncovers the role of mechanically evoked Ca2+ activity in controlling rupture statistics and introduces a model of rupture propagation akin to failure-front dynamics in disordered materials.
Findings
Ca2+ activity controls rupture size distribution tail.
Weakening Ca2+ response increases large rupture likelihood.
Rupture dynamics resemble stick-slip failure in disordered systems.
Abstract
Destructive mechanical breakdowns and fractures are ubiquitous events in driven physical matter; living tissues, by contrast, can rupture repeatedly while restoring integrity. Here we study rupture repair interplay in regenerating Hydra tissues, which cycle through osmotic inflation, pressure release by rupture, and resealing. We utilize bright field imaging of the tissue projected area as a readout of the rupture magnitude before it is arrested. Analyzing these event statistics, we find that the tail of the area-drop distribution is controlled by Ca2+-dependent repair efficiency. When the Ca2+ response is weakened, either by partially blocking gap-junctions mediating the intercellular communication, or by inhibiting stretch-activated Ca2+ channels, the actomyosin force that arrests the rupture process is delayed or reduced. Under these conditions, rare large pressure releases become…
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Taxonomy
TopicsMarine Invertebrate Physiology and Ecology · Cellular Mechanics and Interactions · Calcium Carbonate Crystallization and Inhibition
