Microbiomes can have a big impact on the general health and wellbeing of their hosts. Both metagenomic-sequencing and experimental studies have shown that the microbiome can alter host immune function, cognitive function, and the pathogenesis of neurodegenerative diseases. The mitochondria, cousins of the free-living bacteria which populate the microbiome, may be crucial for mediating these effects by interacting with bacterial products. Investigating such microbe-mitochondria interactions is a relatively new area of study, but already researchers have shown that mitochondrial components are capable of binding bacterial siderophores to facilitate iron uptake, perceiving bacterial quorum-sensing signals, and interacting with many other bacterial products. Furthermore, C. elegans electron transport chain mutants display constitutive activation of
p38-mediated innate immunity, highlighting the role of mitochondrial dynamics in immune signalling. Our lab has established a model system to study host-microbe interactions using C. elegans in conjunction with an experimental microbiome consisting of 11 bacterial strains derived from the microbiota of wild C. elegans isolates. Members of the microbiome differ in their propensity to colonise the C. elegans gut, resulting in the formation of a gut microbiome which diverges in composition from that of the bacterial lawn. Using the open-source program GapSeq, we have generated genome-scale metabolic models using genomic assemblies of all our bacterial strains. By examining these models and subsequently performing flux-balance analysis, we have demonstrated that our experimental microbiome is metabolically diverse and potentially able to provide its host with many beneficial compounds, including thiamine, butyrate, nicotinamide, and GABA. We have also demonstrated that worms grown on our experimental microbiome display a disordered, globular mitochondrial network. Moreover, worms grown on our experimental microbiome show reductions in mtDNA copy number as early as L3-L4, while whole-body ATP levels are elevated in early adulthood. Together, these results illustrate the metabolic capacity of our experimental microbiome, and demonstrate that it can induce significant changes in host mitochondrial dynamics.