Abstract

Event Abstract Back to Event Expression levels of TRα, LAT1, and PKM2 alter the rate of metamorphic change Jinyoung Choi1* and Daniel R. Buchholz1 1 University of Cincinnati, Department of Biological Science, United States Thyroid hormone (TH) plays a key role for most physiological and developmental changes during metamorphosis. TH exerts its function by binding thyroid hormone receptors (TRs) in the nucleus to initiate TH-dependent gene expression. Intracellular TH levels are regulated by thyroid hormone transporters (THTs) and cytosolic thyroid hormone binding proteins (CTHBPs). Intracellular TH levels and TR expression levels likely regulate the timing of transformation of different tissues during metamorphosis. We hypothesized that altered TR, LAT1 (a THT), and PKM2 (a CTHBP) expression affects the rate of metamorphosis when overexpressed. In this study, we overexpressed TR α, LAT1, and PKM2 in tail muscle cells by intramuscular plasmid DNA injection and quantified the disappearance of tail muscle cells during T3-induced metamorphosis. In cells overexpressing TR, the rate of cell death was significantly faster compared to controls.. Moreover, cell death was accelerated or delayed in muscle cells overexpressing LAT1 or PKM2, respectively, compared to controls. These results show that the expression levels of TR and proteins affecting intracellular TH levels can affect the rate of metamorphic changes. References Shi, Y., Wong, J., Puzianowska-Kuznicka, M., and Stolow, M.A. (1996). Tadpole competence and tissue-specific temporal regulation of amphibian metamorphosis: roles of thyroid hormone and its receptors. BioEssay 18(5), 391-399. Buchholz, D.R., Moskalik, C.L., Kulkarni, S.S., Hollar, A.R.,and Ng, Allison (2011).Hormone regulation and the evolution of frog metamorphic diversity. Mechanisms of Life History Evolution. Oxford publishers (in press). Hollar, A.R., Choi, J., Grimm, A.T., and Buchholz, D.R. (2011). Higher thyroid hormone receptor expression correlates with short 4 larval periods in spadefoot toads and increases metamorphic rate. Submitted to Gen. Comp. Endocrinol Friesema, E.C., Ganguly S., Abdalla, A., Fox, J.E.M., Halestrap, A.P.H. and Visser, T.J. (2003). Identification of monocarboxlyate transporter 8 as a specific thyroid hormone transporter. J. Bio. Chem. 278 (41), 40128-40315. Luze, A.D., Sachs, B., and Demeneix, B.A. (1993). Thyroid hormone-dependent transcriptional regulation of exogenous genes transfected into Xenopus tadpole muscle in vivo. Pro. Natl. Acad. USA 90 (August) 7322-7326. Kinne, A., Kleinau, G., Hoefig, G.S., Gruters, A., Kohrle, J., Krause, G., and Schweizer, U. (2010). Essential molecular determinants for thyroid hormone transport and first structural implications for monocarboxlyate transporter 8. J. Bio. Chem. 285 (36) 28054-28063 Connors, K.A., Korte, J.J., Anderson, G.W., and Degitz, S.J. (2010). Characterization of thyroid hormone transporter expression during tissue-specific metamorphic events in Xenopus tropicalis. Gen. Comp. Endocrinol. 168, 149-159. Keywords: cytosolic thyroid hormone binding protein, LAT1, metamorphosis, PKM2, Thyroid hormone, Thyroid hormone transporter, tissue asynchrony, TRα 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: Poster Topic: Thyroid Citation: Choi J and Buchholz DR (2011). Expression levels of TRα, LAT1, and PKM2 alter the rate of metamorphic change. Front. Endocrinol. Conference Abstract: NASCE 2011: The inaugural meeting of the North American Society for Comparative Endocrinology. doi: 10.3389/conf.fendo.2011.04.00116 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: 29 Jul 2011; Published Online: 09 Aug 2011. * Correspondence: Miss. Jinyoung Choi, University of Cincinnati, Department of Biological Science, Cincinnati, Ohio, 45221, United States, jinyoung.angela@gmail.com 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 Jinyoung Choi Daniel R Buchholz Google Jinyoung Choi Daniel R Buchholz Google Scholar Jinyoung Choi Daniel R Buchholz PubMed Jinyoung Choi Daniel R Buchholz 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.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call