Abstract
Oculopharyngeal muscular dystrophy (OPMD) is a late-onset, usually autosomal dominantly inherited human muscle disorder characterised clinically by slowly progressive ptosis, dysphagia and proximal limb girdle weakness. Hallmarks are a trinucleotide expansion in the PABPN1 gene and unique intranuclear inclusions (INI). We investigated a Drosophila model of OPMD (generated by M. Simonelig and A. Chartier in Montpellier France) and compared the histological alterations of this model with the alterations in human OPMD muscles.
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