Manipulation of Myofibrillogenesis in Whole Hearts

Zajdel, Robert W.; McLean, Matthew D.; Denz, Christopher R.; Dube, Syamalima; Lemanski, Larry F.; Dube, Dipak K.

doi:10.1007/978-1-4612-0199-1_6

Cited by 1 publication

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“…Recall, TPM1κ is unique as a sarcomeric TM in that it contains exon 2a instead of exon 2b which is found in TPM1α. The affinity purified anti-TPM1κ antibody upon transfection could disarray the organized myofibrils in axolotl hearts [ 37 ]. The results strongly suggest that TPM1κ plays a critical role in myofibril formation in axolotl hearts.…”

Section: Introductionmentioning

confidence: 99%

Expression of tropomyosin in relation to myofibrillogenesis in axolotl hearts

et al. 2013

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The anatomy, function and embryonic development of the heart have been of interest to clinicians and researchers alike for centuries. A beating heart is one of the key criteria in defining life or death in humans. An understanding of the multitude of genetic and functional elements that interplay to form such a complex organ is slowly evolving with new genetic, molecular and experimental techniques. Despite the need for ever more complex molecular techniques some of our biggest leaps in knowledge come from nature itself through observations of mutations that create natural defects in function. Such a natural mutation is found in the Mexican axolotl, Ambystoma mexicanum. It is a facultative neotenous salamander well studied for its ability to regenerate severed limbs and tail. Interestingly it also well suited to studying segmental heart development and differential sarcomere protein expression due to a naturally occurring mendelian recessive mutation in cardiac mutant gene “c”. The resultant mutants are identified by their failure to beat and can be studied for extended periods before they finally die due to lack of circulation. Studies have shown a differential expression of tropomyosin between the conus and the ventricle indicating two different cardiac segments. Tropomyosin protein, but not its transcript have been found to be deficient in mutant ventricles and sarcomere formation can be rescued by the addition of TM protein or cDNA. Although once thought to be due to endoderm induction our findings indicate a translational regulatory mechanism that may ultimately control the level of tropomyosin protein in axolotl hearts.

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Section: Introductionmentioning

confidence: 99%