Gene Expression in Thyroxin-Induced Metamorphosing Axolotl Hearts

Dipak K Dube

doi:10.4172/2329-6607.1000e122

Abstract

The Mexican axolotl (Ambystoma mexicanum) is a unique model to study vertebrate heart development for several reasons. In addition to the wild-type animal, there is also an embryonic lethal condition caused by a homozygous recessive mutation in cardiac gene “c” [1,2]. These mutant embryonic hearts do not contract, are deficient in tropomyosin, and lack organized myofibrils [3,4], making them an excellent model to study the process of cardiac myofibrillogenesis [5,6]. In contrast to most other model organisms currently being utilized, axolotl embryos are comparatively large (2mm diameter), hence, they can be studied with relative ease. Being amphibians, axolotl embryos mature externally within jelly coats. Therefore, unlike using mammalian embryos, it is unnecessary to sacrifice the parent. Moreover, an average of a hundred axolotl embryos are produced from a single spawning and these embryos develop relatively slowly which is useful for studying vital developmental stages of interest [7]. In fact the timing of developmental stages of interest may be controlled to some extent, as the rate of development for these poikilothermic animal embryos is temperature dependent [8].

Highlights

The Mexican axolotl (Ambystoma mexicanum) is a unique model to study vertebrate heart development for several reasons
We hypothesize that thyroxin induces HoxA5, which in turn augments the expression of p53 gene and subsequently brings about higher levels of apoptosis in metamorphosing axolotl hearts
The axolotl is an apt animal model to study the ontogeny of heart rate variability and related neural changes, as it predominantly uses its gills when in the larval form, and upon metamorphosis, becomes a committed lung breather

Summary

Introduction

The Mexican axolotl (Ambystoma mexicanum) is a unique model to study vertebrate heart development for several reasons. Coleman & Hessler [15] found: (1) lung volume increased to more than three times that of neotenous form; (2) lung wall thickness reduced by approximately one-third (as the surface area of the lumen increased); (3) there was approximately 12% increase in the length of the lung; and (4) many new small blood vessels vascularised the metamorphosed lung These changes increase the effectiveness of oxygen and carbon dioxide gas exchange concomitant with lung-dependent respiration. The metamorphosed heart shows more organized myofibrils and increased trabeculation in comparison with the neotenous salamander (Figure 2) For these respiratory and cardiovascular changes to occur there must be some associated neurological changes too. This ventrolateral location may be involved in the ontogeny and evolution of lung breathing (and/or its control)

Gene Expression and Apoptosis in Metamorphic Axolotl Hearts

Findings

Concluding Remarks