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Quantitative evaluation of characterized α-L-rhamnosidase effects in sea urchin gastrulation
Gastrulation is a fundamental process that mediates formation of ectoderm, mesoderm and endoderm in most animals. Revealing the mechanism of gastrulation will provide a better understanding of embryonic development. Due to its transparency, simplicity of the structure and similarities to complex organisms, the NIH-designated sea urchin embryo model was used in this study. By treating sea urchin embryos with characterized α-L-rhamnosidase and observation of archenteron development, I investigated the role of L-rhamnose terminal in the mechanism of sea urchin gastrulation. I showed that the α-L-rhamnosidase treatments used did not contain any detectable contamination and using quantitative protein assay I demonstrated that this enzyme inhibited archenteron development during gastrulation. Denatured and sugar-inhibited α-L-rhamnosidase lost most of its inhibitory activity. The results combined with a previous study using L-rhamnose, provide convincing evidence, I believe for the first time, for a role of L-rhamnose in the gastrulation process.