02 March 2011
Vol 3, Issue 72

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ONLINE COVER When Antisense Makes Sense. Shown are neuromuscular junctions from the intercostal muscles of a mouse with spinal muscular atrophy (SMA) treated with the antisense oligonucleotide ASO-10-27. This neuromuscular wasting disease is caused by mutations in the SMN1 gene. Passini et al. treated mice with a severe form of SMA with antisense oligonucleotides that alter messenger RNA splicing to boost SMN protein production and rescue neuromuscular junction defects. Motor neuron axons at the presynaptic termini (green) and acetylcholine receptors at the postsynaptic termini (red), when superimposed (yellow), show innervation of muscle and nerve at the neuromuscular junction motor end plate. [CREDIT: M. A. PASSINI]