Expression of tropomyosin protein, an essential component of the thin filament, has been found to be drastically reduced in cardiac mutant hearts of the Mexican axolotl (Ambystoma mexicanum) with no formation of sarcomeric myofibrils. Therefore, this naturally occurring cardiac mutation is an approp
Differential expression of tropomyosin during segmental heart development in Mexican axolotl
✍ Scribed by Robert W. Zajdel; Matthew D. McLean; Christopher R. Denz; Syamalima Dube; Harold L. Thurston; Bernard J. Poiesz; Dipak K. Dube
- Publisher
- John Wiley and Sons
- Year
- 2006
- Tongue
- English
- Weight
- 638 KB
- Volume
- 99
- Category
- Article
- ISSN
- 0730-2312
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✦ Synopsis
Abstract
The Mexican axolotl, Ambystoma mexicanum, serves as an intriguing model to investigate myofibril organization and heart development in vertebrates. The axolotl has a homozygous recessive cardiac lethal gene “c” which causes a failure of ventricular myofibril formation and contraction. However, the conus of the heart beats, and has organized myofibrils. Tropomyosin (TM), an essential component of the thin filament, has three known striated muscle isoforms (TPM1α, TPM1κ, and TPM4α) in axolotl hearts. However, it is not known whether there are differential expression patterns of these tropomyosin isoforms in various segments of the heart. Also, it is not understood whether these isoforms contribute to myofibril formation in a segment‐specific manner. In this study, we have utilized anti‐sense oligonucleotides to separately knockdown post‐transcriptional expression of TPM1α and TPM4α. We then evaluated the organization of myofibrils in the conus and ventricle of normal and cardiac mutant hearts using immunohistochemical techniques. We determined that the TPM1α isoform, a product of the TPM1 gene, was essential for myofibrillogenesis in the conus, whereas TPM4α, the striated muscle isoform of the TPM4 gene, was essential for myofibrillogenesis in the ventricle. Our results support the segmental theory of vertebrate heart development. J. Cell. Biochem. 99: 952–965, 2006. © 2006 Wiley‐Liss, Inc.
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## Abstract TPM1κ is an alternatively spliced isoform of the __TPM1__ gene whose specific role in cardiac development and disease is yet to be elucidated. Although mRNA studies have shown TPM1κ expression in axolotl heart and skeletal muscle, it has not been quantified. Also the presence of TPM1κ p
## Abstract A striated muscle isoform of a Tropomyosin (TM‐4) gene was characterized and found to be necessary for contractile function in embryonic heart. The full‐length clone of this isoform was isolated from the Mexican axolotl (__Ambystoma mexicanum__) and named Axolotl Tropomyosin Cardiac‐3 (
## Abstract The article to which this erratum refers was published in J. Cell. Biochem. 100:1–15. (2007), 2008 Wiley‐Liss, Inc.
## 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 my