An Investigation into the Role of Alternative Polyadenylation in Striated Muscle

This thesis examines alternative mRNA 3' end processing in mammalian striated muscles. In skeletal muscle cells, it identifies minor alternative processing during differentiation, contrasting with previous mouse model findings. In cardiac muscle cells, it reveals substantial gene alternative processing in non-diseased hearts and between non-diseased and dilated cardiomyopathy-affected hearts. When functionally investigated, longer mRNA 3’ ends of cardiac genes correlate with lower mRNA levels and reduced protein expression. This work is crucial for developing future gene therapies that could fix problems caused by these different ways of processing mRNA.