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Background  Porcine congenital splayleg (PCS) is the most important congenital condition of piglets, associated with lameness and immobility, of unknown aetiology and pathogenesis, hence the need to better understand the condition by defining, in the first instance, its histopathology and molecular pathology.    Results   Semitendinosus, longissimus dorsi , and  gastrocnemius  muscles were removed from 4 sets of 2-day-old splayleg piglets, each with a corresponding normal litter mate. Based on immunohistochemistry and histological image analysis, PCS piglets showed significantly smaller fibre size without any accompanying sign of inflammation. Although there was no dramatic change in fibre type composition in affected muscles, several structural myosin heavy chain genes were significantly down-regulated.  MAFbx , a major atrophy marker, was highly up-regulated in nearly all PCS muscles, in comparison with controls from normal litter mates. In contrast,  P311 , a novel 8 kDa protein, was relatively down-regulated in all the PCS muscles. To investigate a functional role of  P311  in skeletal muscle, its full-length cDNA was over-expressed in murine C2C12 muscle cells, which resulted in enhanced cell proliferation with reduced myotube formation. Hence, reduced  P311  expression in PCS piglets might contribute to atrophy through reduced muscle cell proliferation.  P311 , predictably, was down-regulated by the over-expression of calcineurin, a key signalling factor of muscle differentiation.    Conclusion  We demonstrated that PCS is a condition characterised by extensive fibre atrophy and raised fibre density, and propose that the combined differential expression of  MAFbx  and  P311  is of potential in the diagnosis of subclinical PCS.

Porcine congenital splayleg is characterised by muscle fibre atrophy associated with relative rise in MAFbx and fall in P311expression