Mouse myoblasts can fuse and form a normal sarcomere in the absence of β1 integrin expression

Open Access
Publisher Website
Google Scholar
Abstract
Antibody perturbation experiments suggested that migration, terminal differentiation and fusion of myoblasts are dependent on β1 integrin expression. In addition, several studies have postulated that β1 integrins have a role in the formation of sarcomeres. In the present report we have analysed skeletal myogenesis in wild-type/β1-null chimeric mice and β1-null embryoid bodies. Trunk and limbs of β1-null chimeric mice contained muscle tissue composed of normal and β1-null myoblasts indicating that all myotomic sublineages can form, migrate to their peripheral targets and fuse in the absence of β1 integrin expression. Pure populations of β1-null myoblasts and satellite cells isolated from β1-null chimeric embryos and chimeric newborn mice, respectively, were able to differentiate in vitro and to fuse into multinucleated myotubes. Quantitative and qualitative comparisons between normal and β1-null myoblasts revealed no apparent difference in their capacity to terminally differentiate and fuse. Furthermore, β1-null myotubes developed sarcomeres which were indistinguishable from wild-type controls. When normal and β1-null ES cells were differentiated into embryoid bodies, they contained fully differentiated myotubes with normal sarcomeres and normal deposition of costameric components. However, formation of β1-null myotubes was delayed and was less efficient in β1-null embryoid bodies than in wild-type controls. High expression of αv integrin subunit at the tips of normal as well as β1-null myotubes indicated that the lack of β1 integrins did not result in a significant redistribution of αv-containing receptors.