Actomyosin remodeling regulates biomineral formation, growth and morphology during eukaryote skeletogenesis

Biomineralization, the ability of organisms to use minerals to harden their tissues, has attracted scientists from various disciplines to decipher the molecular mechanisms that control it. Many of these studies focus on the gene regulatory networks (GRNs) that control biomineralization and are apparently, phylum specific. Yet, downstream to the GRNs lays the cellular machinery that drives morphogenetic processes that are commonly used in biomineralization, such as, vesicular motion and secretion. The actomyosin network is a key regulator of these processes and participates in biomineralization across Eukaryotes, from unicellular organisms to vertebrates, yet, little is known about its regulation of biomineral growth. Here we reveal that the actomyosin remodeling protein, Rho-associated coiled-coil kinase (ROCK), controls the formation, growth and morphology of the calcite spicules in the sea urchin larva. We show that ROCK expression is elevated in the sea urchin skeletogenic cells and its inhibition impairs the organization of F-actin around the spicules and leads to skeletal loss. We discovered that ROCK inhibition after spicule formation, slows down mineral deposition, induces ectopic spicule branching and disrupts skeletogenic gene expression. We propose that ROCK and the actomyosin network are an essential part of the common biomineralization tool-kit in Eukaryotes.