Bioelectricity
Cells hold a voltage across their membranes and share it with their neighbors. After my regeneration analysis flagged the gap junction gene Gja1 (connexin 43), I simulated how a wound might change those voltages. Scroll, then touch the tissue.
simulation projectVmem: the resting voltage
Every cell keeps a resting membrane voltage, Vmem, set by ion channels and pumps. Color shows Vmem across this sheet of cells: dark is polarized, orange is depolarized. Tap any cell to depolarize it.
Neighbors share voltage
Gap junctions, built from connexins such as Cx43 (the Gja1 gene), are tiny pores joining neighboring cells. A voltage change spreads through them. Tap a cell, which holds it depolarized for a moment, then drag the coupling slider: stronger coupling carries the voltage farther.
Break the sheet
A wound removes cells and disturbs the ones at its edge, so the voltage landscape changes there. The question my simulation asks: does that change reshape Vmem enough to cue regeneration?
Block the potassium channels
Potassium channels help hold the resting voltage. Block them and cells depolarize. This was one of my simulated conditions, alongside a baseline run. Try the toggle.
An honest null result
I ran three experiments in BETSE, a bioelectric tissue simulation engine. Under default parameters, none produced a significant shift in Vmem after wounding. I report that as a methodological finding rather than a positive result.
What this page is and is not
The tissue on this page is a simplified teaching model I wrote for the web, not the BETSE output. My actual simulation runs are in the repository.