Caenorhabditis elegans AWC neuron-mediated chemosensation negatively modulates dormancy during Salmonella fepB mutant infection.

Abstract

In our earlier work, we demonstrated that continuous 8-day exposure of Caenorhabditis elegans to a Salmonella enterica serovar Typhimurium fepB mutant strain negatively regulates dauer larva development in the second generation of the population. Our current study aims to understand how specific chemosensory neurons in C. elegans recognize the ∆fepB Salmonella Typhimurium strain and undergo plasticity in response to infection. We observed the olfactory preference of C. elegans toward the pathogenic wild type Salmonella (WT-STM). However, prolonged exposure showed enhanced lawn occupancy of nematodes in the ∆fepB strain with better associative learning response than the WT-STM counterpart. We also observed upregulation of chemosensory genes odr-7, ceh-36, daf-11, tax-2, and tax-4 at 24 hours post ∆fepB infection. However, continuous exposure to defective olfactory neuron mutants of the C. elegans emphasizes AWC neurons' participation in sensing the ΔfepB strain, ultimately mediating plasticity in C. elegans' second generation. Our research shows how the olfactory neurons of C. elegans detect Salmonella Typhimurium upon encounter and adjust their behavior accordingly. Furthermore, it highlights the strong connection between the chemosensory neurons of nematodes and the bacterial signals that regulate host physiology for survival.

Importance: Bacteria act as food signals for the Caenorhabditis elegans. Our work gives insight into how worms' olfactory neurons recognize pathogen Salmonella Typhimurium exposure and modulate behavioral plasticity, giving a better survival strategy against the pathogens. How specific chemosensory neurons in worms recognize the ∆fepB strain and undergo behavioral plasticity in response to infection. Furthermore, it highlights the strong connection between the chemosensory neurons of worms and the bacterial signals that regulate host physiology for survival when exposed to mutant strain infection, which might be under check in wild-type bacteria for their own benefit in an evolutionary adaptation. This mechanism might help the worm to select the pathogenic or non-pathogenic microbes as food and avoid infection-mediated lethality.