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Molecular and immunohistochemical analyses of cardiac troponin T during cardiac development in the Mexican axolotl, Ambystoma mexicanum

✍ Scribed by C. Zhang; K.M. Pietras; G.F. Sferrazza; P. Jia; G. Athauda; E. Rueda-de-Leon; J.A. Maier; D.K. Dube; S.L. Lemanski; L.F. Lemanski


Publisher
John Wiley and Sons
Year
2007
Tongue
English
Weight
573 KB
Volume
100
Category
Article
ISSN
0730-2312

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✦ Synopsis


Abstract

The Mexican axolotl, Ambystoma mexicanum, is an excellent animal model for studying heart development because it carries a naturally occurring recessive genetic mutation, designated gene c, for cardiac nonfunction. The double recessive mutants (c/c) fail to form organized myofibrils in the cardiac myoblasts resulting in hearts that fail to beat. Tropomyosin expression patterns have been studied in detail and show dramatically decreased expression in the hearts of homozygous mutant embryos. Because of the direct interaction between tropomyosin and troponin T (TnT), and the crucial functions of TnT in the regulation of striated muscle contraction, we have expanded our studies on this animal model to characterize the expression of the TnT gene in cardiac muscle throughout normal axolotl development as well as in mutant axolotls. In addition, we have succeeded in cloning the full‐length cardiac troponin T (cTnT) cDNA from axolotl hearts. Confocal microscopy has shown a substantial, but reduced, expression of TnT protein in the mutant hearts when compared to normal during embryonic development. J. Cell. Biochem. 100: 1–15, 2007. © 2006 Wiley‐Liss, Inc.


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