The lifespan of wild-type C. elegans is affected by different types of bacterial food sources through a mechanism that is distinct from food level restriction [1]. Because the mechanism that underlies the food type-dependent effects on lifespan remains unknown, we used microarray analyses to identify genes that are involved in this process. Through this approach, we have identified a set of 26 genes whose expression changes are correlated with longevity on different E. coli strains [1]. Strikingly, this set is enriched for "pathogen-response" genes. However, unlike their expression on different E. coli strains, these genes do not exhibit a similar effect in response to pathogenic bacteria [2]. Indeed, in some cases, the same gene could be up-regulated on one pathogen, but strongly down-regulated on another pathogen. Hence, the regulation of these genes does not necessarily reflect food toxicity, but a more complex modulation of gene expression in response to different food types.
To gain a better understanding of how these genes might affect lifespan in a food type-dependent manner, we are characterizing one of these genes, the acyl coA dehydrogenase
acdh-1, which has also been recently identified as a dietary sensor [3]. Thus, we are determining the
acdh-1 mutant phenotypes in correlation with the gene's spatial and temporal expression patterns on different food sources. Since we have also found that sensory neurons and neuropeptide signaling are involved in the food-type effects on lifespan [1], we are assessing whether sensory inputs and neuropeptides affect
acdh-1 function on different food types. Together, these studies could yield insight into the mechanisms underlying the food-type effects on lifespan and physiology.
Refs: [1] Maier et al., 2010. Plos Biol 8,
e1000376; [2] Shapira et al., 2006. PNAS 103, 14086-14091; [3] MacNeil et al., 2013. Cell 153, 240-252.