Friday, October 28, 2011
Hall 1-2 (San Jose Convention Center)
Most cases of proximal SMA result from the deletion of the survival motor neuron gene, SMN1. SMN1 is necessary for the binding and assembly of Sm proteins onto U snRNA to form mature U snRNPs, which play a part in pre-mRNA splicing. It was found that the Sm protein ring structure protects RNA from being degraded by nucleases in vitro. We hypothesized that SMN1 may play other roles within cells and are currently exploring the existence of Sm protein interactions with other RNAs such as miRNAs and mRNAs through the use of immunoprecipitation. Where interactions are found, the involvement of SMN in the Sm-RNA binding interaction is being explored. We are also looking into the extent of Sm protein involvement in protecting RNAs from cleavage by overexpressing Sm proteins in HeLa cells, induced pluripotent stem cells, and fibroblasts. Results have yet to show the same preserving effect of Sm proteins in vivo.