In vivo cell tracking of mouse embryonic myoblasts and fast fibers during development

Abstract

Fast and slow TnI are co-expressed in E11.5 embryos, and fast TnI is present from the very beginning of myogenesis. A novel green fluorescent protein (GFP) reporter mouse lines (FastTnI/GFP lines) that carry the primary and secondary enhancer elements of the mouse fast troponin I (fast TnI), in which reporter expression correlates precisely with distribution of the endogenous fTnI protein was generated. Using the FastTnI/GFP mouse model, we characterized the early myogenic events in mice, analyzing the migration of GFP+ myoblasts, and the formation of primary and secondary myotubes in transgenic embryos. Interestingly, we found that the two contractile fast and slow isoforms of TnI are expressed during the migration of myoblasts from the somites to the limbs and body wall, suggesting that both participate in these events. Since no sarcomeres are present in myoblasts, we speculate that the function of fast TnI in early myogenesis is, like Myosin and Tropomyosin, to participate in cell movement during the initial myogenic stages. genesis

Troponin Variants as Markers of Skeletal Muscle Health and Diseases

“…Evidence indicates that primary myoblasts express primarily slow-type myofilament proteins and secondary myoblasts express primarily fast-type myofilament proteins, though isoform switching among a number of myofilament proteins in developing fibers makes this assessment more complex ( Condon et al, 1990 ; Hallauer and Hastings, 2002a ). Still, such isoform switching demonstrates that primary and secondary myoblasts are not confined to a specific fate as slow or fast fibers ( Guerrero et al, 2014 ).…”

“…Fast and slow TnI are co-expressed in embryonic muscles, and fast TnI is present from the very beginning of myogenesis. The expression of fast TnI is parallel with fast-twitch MHC IIx in adult mouse muscles ( Guerrero et al, 2014 ). There is a slow-to-cardiac TnI isoform switch during postnatal development of vertebrate hearts where the timing is species dependent based on not birth but functional demands placed on the heart ( Hunkeler et al, 1991 ; Jin, 1996 ; Krüger et al, 2006 ).…”