Abstract

The role of essential amino acids (AA) in the cellular signaling and physiology of organisms has been studied in recent years, and have been demonstrated that AAs are involved in eukaryotes life span1, and small amino acids unbalance are related to the development of neurodegenerative2. previously observed in the mec-4d neurodegeneration model in C. elegans, that the rate of degeneration depends on the type of bacterial diet varying from 72 hours after hatching, in E. coli OP50, to xx time in E. coli HT115. To decipher which are the specific neuroprotective metabolites of E. coli HT115, we performed three strategies. 1) genomic and transcriptomic differences between bacterial strains, focus in differential expressed genes, 2) molecular assays in single-gene knockouts for metabolic regulation analysis in neurotransmitters pathways (glutamate and GABA), and 3) biochemical activity and neuroprotection confirmation for metabolic supplementation and functional bacterial mutants3. Preliminary transcriptomic analysis pipeline pointed out uniquely expressed transcripts in HT115 for glutamate decarboxylase (gadA, gadB), glyceraldehyde 3-phosphate dehydrogenase (gap1, gap2, gapA1), compared to E. coli OP50. A supplemented diet with HT115 methanolic extract and relevant metabolites had demonstrated partial effects in maintenance in AVM morphology integrity. The validation of these relevant individual neuroprotective components will lead us to the understanding of the role of specific components of diet in cellular degenerative processes. 1. Edwards, C. (2015). BMC Genetics. 16:8 2. Fuentes, A. et al. (2015). 20th International Meeting C. elegans. Poster N° 650A. 3. Rice, E.W. et al. (1993). App Environ Microbiol. 59 (12) 4347-4349.