## Abstract The homozygous recessive __spastic__ mutant found in the Mexican axolotl shows violent coiling and thrashing behavior when subjected to strong tactile or electrical stimulation. In order to establish the time of onset of the first behavioral manifestation of the __spastic__ gene, an eth
Heart induction in wild-type and cardiac mutant axolotls (Ambystoma mexicanum)
✍ Scribed by Smith, Steven C. ;Armstrong, John B.
- Publisher
- John Wiley and Sons
- Year
- 1990
- Tongue
- English
- Weight
- 639 KB
- Volume
- 254
- Category
- Article
- ISSN
- 0022-104X
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
We have re‐examined some of the factors affecting the induction of heart‐forming mesodern in the axolotl. The formation of functional, rhythmically contracting myocardial tissue was used as an assay. We have found that heart‐forming mesoderm is fully induced and capable of completing its developmental repertoire by the end of neurulation. As has been previously reported, pharyngeal endoderm appears to be the major inductor of heart mesoderm. Unlike previous workers, we have found that the inducing activity appears to be highly localized in the mid‐ventral pharyngeal endoderm. The endoderm retains its inductive properties, and the mesoderm retains at least some capacity to respond, long after the heart‐forming mesoderm is apparently fully induced.
We have also found that RNA extracts from pharyngeal endoderm, which are capable of causing cardiac‐lethal (c/c) mutant axolotl hearts to begin beating, are not capable of inducing early wild‐type heart‐forming mesoderm. Based on these results, we speculate that induction of heart‐forming mesoderm is a two‐step process. The first signal, occurring during neurulation, directs the mesoderm to begin differentiating into cardiomyocytes, and the second, beginning in mid‐ to late neurulation and continuing until just prior to the onset of heartbeat, causes myofibrillogenesis and the initiation of rhythmic contractions. The latter signal, which is lacking in c/c mutant embryos, appears to be necessary to override an inhibition present in the embryonic milieu.
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Recessive mutant gene c for "cardiac nonfunction" in axolotls results in an absence of normal heart contractions in affected embryos due to a failure of myofibril formation. In the present study, the intermediate filament protein, desmin, is compared in developing normal and mutant hearts by means o
Recessive mutant gene c in axolotls results in a failure of the heart to function because of abnormal embryonic induction processes. The myocardium in this mutant lacks organized sarcomeric myofibrils. The present study was undertaken to determine if developmental abnormalities were evident in other
## 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
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