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Carbonic anhydrase activity in developing sea urchin embryos with special reference to calcification of spicules
Institution:1. Department of Biology, School of Education, Waseda University, 1-6-1, Nishiwaseda, Shinjuku-ku, Tokyo, 160, Japan;2. Zoological Institute, Faculty of Science, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo, 113, Japan;3. Department of Pharmacology, Teikyo University School of Medicine, 2-11-1, Kaga, Itabashi-ku, Tokyo, 173, Japan;4. 2-1-58-401, Takanawa, Minato-ku, Tokyo, 105, Japan;1. Departamento de Genética e Evolução, Universidade Federal de São Carlos, São Carlos 13565-905, Brazil;2. Brazilian Biosciences National Laboratory (LNBio), Brazilian Center for Research in Energy and Materials (CNPEM), Campinas, SP, Brazil;1. Department of Cell and Developmental Biology, University College London, London, UK;2. Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA, USA;3. Department of Physiology and Biophysics, University of Washington, Seattle, WA, USA;4. Institute for Neuro- and Behavioral Biology, University of Münster, 48149 Münster, Germany
Abstract:Eggs and embryos of the sea urchins Anthocidaris crassispina and Hemicentrotus pulcherrimus did not exhibit significant changes in carbonic anhydrase activity during early development. Acetazolamide inhibited enzyme activity in homogenates of embryos and inhibited the formation of calcified spicules in a culture of micromeres at concentrations between 40 and 100 μM. Acetazolamide allowed intact embryos to develop to quasi-normal plutei but inhibited calcium deposition in the spicules. It is suggested that carbonic anhydrase contributes to CaCO3 deposition in the spicule.
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