Mechanistic impacts of bacterial diet on dopaminergic neurodegeneration in a Caenorhabditis elegans a-synuclein model of Parkinson's disease

Using distinct mutant strains deficient in key aspects of gene silencing machinery, we provide evidence that neuroprotection appears to stem from dsRNAs that originate from the bacteria themselves, and Systemic RNA Interference Defective (SID) mutants deficient in dsRNA-mediated gene silencing do not allow for neuroprotection from the bacteria. Transcriptomic analysis between worms reared on OP50 and HB101 E. coli for multiple generations in an a-syn background revealed that the primary cellular processes involved in neuroprotection of this nature included but were not limited to endopeptidase activity, transcriptional regulation, calcium ion binding activity, and water channel activity. Overall design: Comparative gene expression profiling analysis of RNA-seq data for C. elegans in an a-synuclein background reared on OP50 or HB101 E. coli, 3 biological replicates.