Abstract

Event Abstract Back to Event STANNIOCALCIN: A CALCIUM REGULATOR WITH AN ANCIENT ORIGIN IN UNICELLULAR EUKARYOTES Graeme J. Roch1 and Nancy M. Sherwood1* 1 University of Victoria, Canada Stanniocalcin (STC) is a large glycoprotein hormone that was originally isolated in teleost fishes, where it is secreted by specialized glands known as the corpuscles of Stannius to inhibit calcium uptake at the gills. Orthologs of this hormone, STC1, were later isolated in mammals, where they were found to regulate calcium and phosphate homeostasis and influence a variety of physiological actions including bone formation, growth and neuroprotection. A paralog, STC2, was also identified in vertebrates, with a role in phosphate regulation. We identified and isolated novel forms of stanniocalcin in the protchordate models Ciona intestinalis (tunicate) and Branchiostoma floridae (amphioxus). The protochordate STCs shared structural features with their vertebrate homologs, such as the conserved core cysteine residues and gene organization. One of the amphioxus peptides also shared the C-terminal dimerization motif, although the other two protochordate STCs did not. Quantitative PCR analysis revealed the majority of tunicate STC expression was in the heart. More recently, we discovered a number of homologous STC gene models and ESTs from a variety of protostomes, cnidarians, sponges and unicellular eukaryotes. Although these putative STCs shared little sequence conservation with the vertebrate hormones, they retained critical structural characteristics including the conserved cysteine residues, and most had a signal peptide for secretion. Phylogenetic analysis demonstrated that these STCs have evolved as a distinct group from their chordate counterparts, with the exception of a third STC from amphioxus that was homologous with the non-chordate hormones. Although the receptor and signaling mechanism for stanniocalcin is not yet understood, we propose that this diverse family of hormones with an ancient origin may directly influence cation channels that have similar evolutionary roots, like the voltage-dependent calcium channels. Acknowledgements Supported by NSERC Keywords: Calcium, cation channel, evolution, mineral homeostasis, stanniocalcin, superfamily, unicellular Conference: NASCE 2011: The inaugural meeting of the North American Society for Comparative Endocrinology, Ann Arbor, United States, 13 Jul - 16 Jul, 2011. Presentation Type: Oral Presentation Topic: Molecular evolution Citation: Roch GJ and Sherwood NM (2011). STANNIOCALCIN: A CALCIUM REGULATOR WITH AN ANCIENT ORIGIN IN UNICELLULAR EUKARYOTES. Front. Endocrinol. Conference Abstract: NASCE 2011: The inaugural meeting of the North American Society for Comparative Endocrinology. doi: 10.3389/conf.fendo.2011.04.00076 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 22 Jul 2011; Published Online: 09 Aug 2011. * Correspondence: Dr. Nancy M Sherwood, University of Victoria, Victoria, Canada, nswherwoo@uvic.ca Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Graeme J Roch Nancy M Sherwood Google Graeme J Roch Nancy M Sherwood Google Scholar Graeme J Roch Nancy M Sherwood PubMed Graeme J Roch Nancy M Sherwood Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

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