title: Myofibril-inducing RNA (MIR) is essential for tropomyosin expression and myofibrillogenesis in axolotl hearts.
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.
authors.affiliation: Department of Biomedical Science, Florida Atlantic University, Boca Raton, FL 33431, USA. czhan1@med.miami.edu
authors.forename: Chi
authors.initials: C
authors.lastname: Zhang
authors.forename: Pingping
authors.initials: P
authors.lastname: Jia
authors.forename: Xupei
authors.initials: X
authors.lastname: Huang
authors.forename: Gian Franco
authors.initials: GF
authors.lastname: Sferrazza
authors.forename: Gagani
authors.initials: G
authors.lastname: Athauda
authors.forename: Mohan P
authors.initials: MP
authors.lastname: Achary
authors.forename: Jikui
authors.initials: J
authors.lastname: Wang
authors.forename: Sharon L
authors.initials: SL
authors.lastname: Lemanski
authors.forename: Dipak K
authors.initials: DK
authors.lastname: Dube
authors.forename: Larry F
authors.initials: LF
authors.lastname: Lemanski
mesh_terms: D000558:Ambystoma mexicanum / Q000196:embryology / Q000235:genetics*; D000818:Animals; D001483:Base Sequence; D018076:DNA, Complementary / Q000235:genetics; D004707:Endoderm / Q000502:physiology; D005091:Exons / Q000235:genetics; D018507:Gene Expression Regulation, Developmental; D055785:Gene Knockdown Techniques; D005808:Genes, Recessive; D006321:Heart / Q000196:embryology*; D008957:Models, Genetic; D008969:Molecular Sequence Data; D009124:Muscle Proteins / Q000096:biosynthesis / Q000235:genetics; D009200:Myocardial Contraction / Q000502:physiology; D009210:Myofibrils / Q000378:metabolism* / Q000648:ultrastructure; D020033:Protein Isoforms / Q000096:biosynthesis / Q000235:genetics; D016372:RNA, Antisense / Q000494:pharmacology; D012330:RNA, Double-Stranded / Q000494:pharmacology; D022661:RNA, Untranslated / Q000235:genetics / Q000494:pharmacology / Q000502:physiology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014335:Tropomyosin / Q000096:biosynthesis* / Q000235:genetics
chemical_list: D018076:DNA, Complementary; D009124:Muscle Proteins; D020033:Protein Isoforms; D016372:RNA, Antisense; D012330:RNA, Double-Stranded; D022661:RNA, Untranslated; D014335:Tropomyosin