Cellular bicarbonate accumulation and vesicular proton transport promote calcification in the sea urchin larva.

ABSTRACT: The sea urchin embryo develops a calcitic endoskeleton through intracellular formation of amorphous calcium carbonate (ACC). Intracellular precipitation of ACC, requires [Formula: see text] concentrating as well as proton export mechanisms to promote calcification. These processes are of fundamental importance in biological mineralization, but remain largely unexplored. Here, we demonstrate that the calcifying primary mesenchyme cells (PMCs) use Na⁺/H⁺-exchange (NHE) mechanisms to control cellular pH homeostasis during maintenance of the skeleton. During skeleton re-calcification, pH_i of PMCs is increased accompanied by substantial elevation in intracellular [Formula: see text] mediated by the [Formula: see text] cotransporter Sp_Slc4a10. However, PM

SUBMITTER: Hu MY 

PROVIDER: S-EPMC7542784 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature