Click here to close Hello! We notice that you are using Internet Explorer, which is not supported by Echinobase and may cause the site to display incorrectly. We suggest using a current version of Chrome, FireFox, or Safari.
Dev Growth Differ 1999 Dec 01;416:769-75. doi: 10.1046/j.1440-169x.1999.00479.x.
Show Gene links Show Anatomy links

Phosphorylation-dependent regulation of skeletogenesis in sea urchin micromere-derived cells and embryos.

Cervello M , Sanfilippo R , Isola G , Virruso L , Scalia G , Cammarata G , Gambino R .

Sea urchin embryo micromeres when isolated and cultured in vitro differentiate to produce spicules. Although several authors have used this model, almost nothing is known about the signaling pathways responsible for initiating skeletogenesis. In order to investigate the potential involvement of phosphorylation events in spiculogenesis, the effect of inhibitors of protein kinases and phosphatases on skeleton formation was studied. Results obtained using both cultured micromeres and embryos revealed that protein tyrosine kinase and phosphatase inhibitors blocked skeleton formation, but not serine/threonine phosphatase inhibitors. The inhibitors showed a dose-dependent effect and when removed from micromere or embryo culture, spicule formation resumed. Inhibition of tyrosine phosphatases resulted in an increase in the tyrosine phosphorylation level of two major proteins and a modest decrease in the expression of the mRNA coding for type I fibrillar collagen. These findings strongly suggest that tyrosine phosphorylation and dephosphorylation is required for micromere differentiation and for normal skeletogenesis during sea urchin embryo development.

PubMed ID: 10646807
Article link: Dev Growth Differ

Genes referenced: LOC100887844 LOC100892350