Neural and molecular mechanisms underlying food preference have been poorly understood. We previously showed that Bifidobacterium infantis, one of the well-known probiotic bacteria, extend the lifespan of Caenorhabditis elegans (Ikeda et al., Appl. Environ. Microbiol., 2007). In this study, we found that C. elegans exhibited low preference to B. infantis when compared with a standard food E. coli. Genetic screens identified
tol-1 (a sole homolog of mammalian Toll-like receptors) and
daf-16/FoxO as positive regulators of low preference to B. infantis. Worms with mutations in canonical TLR signaling molecules (
pmk-3,
mom-4 and
ikb-1) that are employed in avoidance behavior to a pathogenic bacterium Serratia marcescens (Brand et al.,Curr. Biol., 2015) showed a normal behavior to B. infantis, suggesting alternative mechanisms. Genetic analyses revealed that the function of
daf-16 isoform b in AIY neurons is responsible for the behavior to B. infantis. Because
daf-16b regulates the AIY neurons morphology during development (Christensen et al., Development, 2011),
daf-16b may play roles in AIY development to organize low preference to B. infantis.