Fusion of monomyoblasts to form multinucleated myotubes is a prerequisite for skeletal myogenesis, and muscle fibroblast-myoblast interaction plays an important role in the process; however, relative studies are limited. In the current study, SLD (sex-linked dwarf) chicken, a myogenic deficient model caused by OH (growth hormone)-IGF-I axis deficiency due to dw gene mutation, was introduced to study effects of fibroblasts on myodifferentiation. Using a membrane insert co-culture system, we identified that, compared with SLD fibroblasts, normal fibroblasts promoted myogenesis of primary SLD myoblasts by improving their differentiation potential in a paracrine fashion, and this effect was involved in both primary and secondary fusions. This process was also coupled with up-regulation of beta 1 integrin, and reduced myogenesis, resulting from siRNA interference demonstrated that beta 1 integrin was required for the response. Further, in terms of genetic discrepancy between normal and SLD fibroblasts, GH-IGF-I signalling might play a role in this paracrine control.