smn-1 plays an important role in spinal muscle atrophy and it is a common cause of death of infants. Recently has been shown that smn-1 is also an important factor in secretion of insulin from pancreas β cells since the loss of smn-1 leads to hypoglycemia and reduces the number of β cells. The main secretion effect of smn-1 in C. elegans model organism has been analyzed in order to further understand the molecular mechanism and its role in secretion. To understand this effect, three transgenic GFP stairs have been used: DAF-28::GFP (insulin tagged with GFP), ANF::GFP (dense core vesicle cargo tagged with GFP) and secreted GFP, along with DAF-16/FOXO::GFP (transcription factor). Those strains were analyzed using a fluorescence microscope, western blot and quantitative polymerase chain reaction (qPCR) techniques to understand how the smn-1 mutation affects secretion mechanism. General secretion defects were observed, together with a defect in insulin secretion (DAF-28::GFP and ANF::GFP), while DAF-16::GFP indicated rescue effect on the sterility phenotype of smn-1 mutant. Western blot analysis has shown normal DAF-28::GFP expression, however the localization of DAF-28::GFP in non-neuronal neuronal cells was significant. By using qPCR, upregulation of daf-28 and daf-16 genes were detected in a strain that over expresses smn-1 gene (cMYC::SMN-1), indicating that the manipulation of the smn-1 level, leads to changes in gene expression. This study shown that using smn-1 mutant (ok355) and SMN-1 tagged with cMYC (cMYC::SMN-1) to study human disease spinal muscle atrophy in C. elegans, provides useful information about the secretion pathway.