Abstract

In nature, Caenorhabditis elegans eats bacteria from rotting fruits and vegetation. The natural microbiome of C. elegans influences growth, lifespan and stress (Dirksen et al., 2016. Zhang et al, 2017. Samuel et al., 2017). We are interested in understanding how the relationship between C. elegans and its intestinal bacteria influences behavior and phenotype. We showed that specific metabolites from laboratory bacteria affect the rate at which mechanosensory neurons (MN) degenerate in a genetic model of neuronal necrosis (Urrutia et al., under review). The bacterial enzyme involved in MN neuroprotection is the glutamate decarboxylase enzyme (GAD) and the protective metabolite, its product g-aminobutyric acid (GABA). In this work, we studied the impact of a natural microbiome in neurodegeneration of the MN. The natural microbiome we studied was isolated from wild C. elegans obtained from the Universidad Mayor Campus in Huechuraba, Chile. This microbiome was composed of three different culturable bacteria identified by means of ribosomal RNA 16S marker sequencing. Isolate 1 has 100% identify with Brucellaceae bacterium bfzh12, Pseudochrobactrum sp. AR333 and Pseudochrobactrum kiredjianiae. Isolate 2 has a 100% identity with Stenotrophomonas humi and Stenotrophomonas sp. Isolate 3 has a 100% identity with Bacillus pumilus and Bacillus altitudinis. GAD enzymatic activity provided information about the bacteria neuroprotective potential because all isolates displayed higher levels than E. coli OP50 (10%, 15%, and 40% respectively). Functional morphological categories of the MN were significantly higher in animals feeding natural isolates than on E. coli OP50, suggesting a correlation with GABA production. Ongoing and future work includes dissecting the contribution in the abundance of each bacterium to the final intestinal microbiome as well as the metabolite production of individual bacteria and in conjunction.