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Biology subjects

Prinz, C. K.

Publications and source records attributed to Prinz, C. K..

2 recordsLinked to original sources

Intracellular pH dynamics promotes zebrafish larval tail regeneration

Intracellular pH (pHi) dynamics regulates numerous cell behaviors, including migration and proliferation. While these functions are well-established in cell lines, the role of pHi changes in vivo is less well understood. We generated a transgenic zebrafish line expressing a fluorescent ratiometric pHi biosensor and identified functional changes in pHi during zebrafish larval tail regeneration. We found that tail amputation led to a transient decrease in pHi, followed by a prolonged increase in pHi above pre-amputation values. Moreover, we showed that pharmacologically inhibiting Na+/H+ exchanger (NHE) activity or decreasing extracellular pH attenuated the post-amputation increase in pHi, reduced subsequent cell proliferation, and impaired tail regeneration. We further found that inhibiting NHE activity post-amputation led to elevated inflammation, disrupted myeloid cell behavior, decreased reactive oxygen species, and increased glycogen synthase kinase-3 (GSK3) activity. Finally, we showed that the regeneration defects in larvae with disrupted pHi were partially rescued by the GSK3 inhibitor BIO. Our data reveal a previously unrecognized role for pHi dynamics in coordinating tissue behaviors in vivo and enabling zebrafish larval tail regeneration.

developmental biology↗

Post-injury hydraulic fracturing drives fissure formation in the zebrafish basal epidermal cell layer

The skin epithelium acts as the barrier between an organisms internal and external environments. In zebrafish and other freshwater organisms, this barrier function requires withstanding a large osmotic pressure differential. Wounds breach this epithelium, causing a large disruption to the tissue microenvironment due to the mixing of isotonic interstitial fluid with the external hypotonic fresh water. Here we show that, following acute injury, the larval zebrafish epidermis undergoes a dramatic fissuring process that resembles hydraulic fracturing, driven by the influx of external fluid. The fissuring starts in the basal epidermal layer nearest to the wound, and then propagates at a constant rate through the tissue spanning over one hundred micrometers; during this process the outermost superficial epidermal layer remains intact. Fissuring is completely inhibited when larvae are wounded in an isotonic external media, suggesting that osmotic pressure gradients drive fissure. Additionally, fissuring partially depends on myosin II activity, as its inhibition reduces fissure propagation away from the wound. During and after fissuring, the basal layer forms large macropinosomes (with cross-sectional areas ranging from 1-10 {micro}m2), presumably to clear the excess fluid. We conclude that excess external fluid entry through the wound and subsequent closure of the wound through actomyosin purse string contraction in the superficial cell layer causes fluid pressure buildup in the extracellular space of the zebrafish epidermis. This excess fluid pressure causes tissue to fissure, and eventually the fluid is cleared through macropinocytosis.

cell biology↗