Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.541492
Title: The role of tropomyosin during heart development (Part I) and neuroanatomical and cardiorespiratory changes associated with metamorphosis (Part II) in the axolotl, Ambystoma mexicanum
Author: Narshi, Aruna
Awarding Body: University of Birmingham
Current Institution: University of Birmingham
Date of Award: 2011
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Abstract:
I: Ambystoma mexicanum is a useful model for the study of heart development as it has a naturally occurring mutant, the cardiac (c/c) lethal, in which the embryos lack organised myofibrils and have low levels of tropomyosin. Antisense oligonucleotides specific to axolotl tropomyosin disrupted myofibril formation in normal heart, whereas sense oligonucleotides encouraged myofibrillogenesis in the mutant hearts, demonstrating the importance of tropomyosin in cardiac muscle development and the effectiveness of cationic liposome transfection system. A novel isoform of the human tropomyosin, TPM1κ, was discovered and found to be cardiac specific in humans. Ectopic expression of GFP.TPM1κ fusion protein promoted myofibrillogenesis in the cardiac mutant axolotl heart. Tropomyosin N- and C-termini modification did not affect its function. II: The neotenous form had vagal preganglionic neurons (VPN) in the dorsal vagal nucleus (DVN) only. In the metamorphosed, VPN were found in the DVN but 18% were relocated in a ventro-lateral position. Neotenous ventilation rate followed heart rate. In the metamorphosed, ventilation caused heart rate variability. This may have been induced by the ventral-lateral VPN, which may be equivalent to a primitive nucleus ambiguus, an area that generates rhythmic sinus arrhythmia in mammals. Thus, ventrolateral VPN may be involved in cardiorespiratory control.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.541492  DOI: Not available
Keywords: QH301 Biology ; RC Internal medicine
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