Research

Spinal muscular atrophy (SMA) primarily affects motor neurons, but it is not clear why. Patients with SMA typically lack the SMN1 gene coding for SMN protein. SMN's most characterized function is assembling parts of the spliceosome, but this function does not sufficiently explain why motor neurons are most sensitive to lower levels of SMN. We are investigating a potential interaction between SMN and the signal recognition particle (SRP) to perhaps help explain the disease phenotype. With Dr. Sharon Amacher, we are characterizing a mutant SRP54 zebrafish and comparing neural development to the SMA model zebrafish. We have also developed an assay to monitor SRP function to see if SMN knockdown has a functional consequence.

Awards

2019 - Dean’s Distinguished Enrichment Fellowship, The Ohio State University Graduate School