PDF(Pubmed)
Abstract：
Biomineralization had apparently evolved independently in different phyla, using distinct minerals, organic scaffolds, and gene regulatory networks (GRNs). However, diverse eukaryotes from unicellular organisms, through echinoderms to vertebrates, use the actomyosin network during biomineralization. Specifically, the actomyosin remodeling protein, Rho-associated coiled-coil kinase (ROCK) regulates cell differentiation and gene expression in vertebrates\' biomineralizing cells, yet, little is known on ROCK\'s role in invertebrates\' biomineralization. Here, we reveal that ROCK controls the formation, growth, and morphology of the calcite spicules in the sea urchin larva. ROCK expression is elevated in the sea urchin skeletogenic cells downstream of the Vascular Endothelial Growth Factor (VEGF) signaling. ROCK inhibition leads to skeletal loss and disrupts skeletogenic gene expression. ROCK inhibition after spicule formation reduces the spicule elongation rate and induces ectopic spicule branching. Similar skeletogenic phenotypes are observed when ROCK is inhibited in a skeletogenic cell culture, indicating that these phenotypes are due to ROCK activity specifically in the skeletogenic cells. Reduced skeletal growth and enhanced branching are also observed under direct perturbations of the actomyosin network. We propose that ROCK and the actomyosin machinery were employed independently, downstream of distinct GRNs, to regulate biomineral growth and morphology in Eukaryotes.
摘要：
生物矿化显然在不同的门中独立进化，使用不同的矿物质，有机支架,和基因调控网络(GRN)。然而,来自单细胞生物的多种真核生物，通过棘皮动物到脊椎动物，在生物矿化过程中使用肌动球蛋白网络。具体来说,肌动球蛋白重塑蛋白，Rho相关卷曲螺旋激酶(ROCK)调节脊椎动物生物矿化细胞的细胞分化和基因表达,然而，人们对岩石在无脊椎动物生物矿化中的作用知之甚少。这里,我们发现岩石控制着地层，增长,海胆幼虫方解石针状体的形态。ROCK表达在血管内皮生长因子（VEGF）信号传导下游的海胆骨骼细胞中升高。ROCK抑制导致骨骼丢失并破坏骨骼生成基因表达。针状形成后的ROCK抑制降低了针状伸长率并诱导异位针状分支。当在骨骼生成细胞培养物中抑制ROCK时，观察到类似的骨骼生成表型。表明这些表型是由于在骨骼形成细胞中特异性的ROCK活性。在肌动球蛋白网络的直接扰动下，还观察到骨骼生长减少和分支增强。我们建议ROCK和肌动球蛋白机械是独立使用的，不同GRN的下游，调节真核生物的生物矿物生长和形态。
