Fig 6. A model for the effect of reduced PABPN1 levels on muscle atrophy.

Reduced PABPN1 levels induced a alternative polyadenylation site (APA) utilization in the 3’-UTR of a subset of transcripts whose gene product regulates muscle waste, including Atrogin-1/Fbxo32 and proteasomal genes. In these muscles, Atrogin-1 is overexpressed, whilst proteasome activity is reduced. This leads to pathological hallmarks of muscle atrophy including reduction in myofiber cross-sectional area, increase in extracellular matrix (ECM) and a switch in myosin heavy chain (MyHC) expression pattern in myofibers.