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Research

Myofibril-Inducing RNA (MIR) is essential for tropomyosin expression and myofibrillogenesis in axolotl hearts

Chi Zhang¹ , Pingping Jia¹ , Xupei Huang¹ , Gian Franco Sferrazza¹ , Gagani Athauda¹ , Mohan P Achary² , Jikui Wang³ , Sharon L Lemanski³ , Dipak K Dube⁴ and Larry F Lemanski^3,5

¹  Department of Biomedical Science, Florida Atlantic University, Boca Raton, FL 33431, USA

²  Department of Radiation Oncology, Temple University School of Medicine, Philadelphia, PA 19140, USA

³  Department of Anatomy and Cell Biology and The Cardiovascular Research Center, Temple University, Philadelphia, PA 19140, USA

⁴  Department of Medicine, Upstate Medical University, Syracuse, NY 13210, USA

⁵  Department of Biological and Environmental Sciences, Texas A&M University-Commerce, Commerce, TX 75429-3011, USA

author email corresponding author email

Journal of Biomedical Science 2009, 16:81doi:10.1186/1423-0127-16-81

Published:	3 September 2009

Abstract

The Mexican axolotl, Ambystoma mexicanum, carries the naturally-occurring recessive mutant gene 'c' that results in a failure of homozygous (c/c) embryos to form hearts that beat because of an absence of organized myofibrils. Our previous studies have shown that a noncoding RNA, Myofibril-Inducing RNA (MIR), is capable of promoting myofibrillogenesis and heart beating in the mutant (c/c) axolotls. The present study demonstrates that the MIR gene is essential for tropomyosin (TM) expression in axolotl hearts during development. Gene expression studies show that mRNA expression of various tropomyosin isoforms in untreated mutant hearts and in normal hearts knocked down with double-stranded MIR (dsMIR) are similar to untreated normal. However, at the protein level, selected tropomyosin isoforms are significantly reduced in mutant and dsMIR treated normal hearts. These results suggest that MIR is involved in controlling the translation or post-translation of various TM isoforms and subsequently of regulating cardiac contractility.