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Berbee, N.

Publications and source records attributed to Berbee, N..

2 recordsLinked to original sources

Developmental growth rates adapt to enable self-correction of organ morphology after injury.

Proportional organ growth requires tissue-level control of cell behavior. Yet the cues that adapt growth rates, especially after organ injury, remain unclear. Here, we uncover that developing organs are robust to extensive damage, triggering injury-specific mechanisms sufficient to override genetically-encoded size defects. Using precision microsurgery in developing zebrafish pectoral fins, we find that injury drives growth asynchronously across tissues and fin axes, by increasing proliferation and extracellular spacing. Growth compensation scales with the amount of tissue lost, restoring size and structure without compromising developmental timing. A feedback-control model captures these dynamics, suggesting that growth rates are regulated toward an organ-specific target area. At the molecular scale, injury signals bypass developmentally-regulated BMP gradient scaling. Injury instead activates de novo BMP signaling, which supports growth adaptation and rescues wildtype fin size in developmentally small mutants. Our findings identify an injury-dependent compensatory growth mechanism that resets developmental organ size, ensuring functional organ recovery.

developmental biology↗

Injury-induced electrochemical coupling triggers regenerative cell proliferation

Organ injury triggers non-neuronal electric currents essential for regeneration. Yet, the mechanisms by which electrical signals are generated, sensed and transmitted upon damage to promote organ growth remain unclear. Here, we uncover that organ regeneration relies on dynamic electrochemical coupling between tissue-wide depolarization and intracellular proliferative signalling. By sub-second live imaging of injured zebrafish larval fins, we identify events across timescales: a millisecond tissue depolarization gradient, followed by seconds-persistent intracellular Calcium responses. Subsequently within one hour, Voltage Sensing Phosphatase activity translates depolarisation into proliferation. Connecting these timescales with an electro-diffusive model showed that ionic fluxes and electric potential become coupled in the fins interstitial space, enabling organ-wide signal spreading. Our work reveals the coupling between fast electrical signals and slower intracellular signalling, ensuring organ regeneration.

biophysics↗