Based on the data of phenotypic suppression described above, we further analyzed three constructs that were closely related and spanned the conservation threshold: xSmn, dSmn, and cSmn. Specifically, we investigated the capacity of these SMN homologs to correct neuromuscular junction (NMJ) structure and integrity, which represent a clinically-relevant SMA phenotype. Here, SMN1 is linked to proximal spinal muscular atrophy.