Model
Digital Document
Publisher
Florida Atlantic University
Description
The Mexican axolotl (Ambystoma mexicanum) carries a cardiac lethal mutation
resulting in mutant embryos with no heartbeat. This homozygous recessive gene results
in tropomyosin deficiency and absence of organized myofibrils. Co-culturing mutant
hearts with bioactive RNA, termed myofibril-inducing RNA (MIR), from normal axolotl
embryonic anterior endoderm causes the mutant hearts to beat. It is hypothesized that the
secondary structure of the MIR binds a specific protein(s) and this is required to
synthesize tropomyosin and form organized myofibrils. In this study mutant hearts are
co-cultured with human fetal and adult heart total RNA to assess rescue of the mutant
hearts. Results show that both human fetal and adult heart total RNA rescue the mutant
condition in a manner similar to the MIR. Thus, the MIR human functional homologs
induce events leading to normal heart differentiation and function. This finding may help
people with heart muscle damage regain normal heart function again.
resulting in mutant embryos with no heartbeat. This homozygous recessive gene results
in tropomyosin deficiency and absence of organized myofibrils. Co-culturing mutant
hearts with bioactive RNA, termed myofibril-inducing RNA (MIR), from normal axolotl
embryonic anterior endoderm causes the mutant hearts to beat. It is hypothesized that the
secondary structure of the MIR binds a specific protein(s) and this is required to
synthesize tropomyosin and form organized myofibrils. In this study mutant hearts are
co-cultured with human fetal and adult heart total RNA to assess rescue of the mutant
hearts. Results show that both human fetal and adult heart total RNA rescue the mutant
condition in a manner similar to the MIR. Thus, the MIR human functional homologs
induce events leading to normal heart differentiation and function. This finding may help
people with heart muscle damage regain normal heart function again.
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