Salmonella Typhimurium fepB negatively regulates C. elegans behavioral plasticity

AWC mediated behavioral plasticity inC. elegansagainstSalmonellaTyphimurium infection

“…However, worms had reduced olfactory preference for Δ fepB strain at an early course of the bacterial encounter. This information made us curious to understand the involvement of chemosensory neurons in sensing this particular bacterial strain which was not as pathogenic as WT-STM [8]. Thereafter, we were interested in looking at the participation of olfactory neurons, i.e., AWA, AWB, and AWC, in worms’ olfaction toward the WT-STM and mutant strain along with non-pathogenic E. coli OP50 strain as worms can sense volatile odor either attractant or repellent secreted by bacterial strains [4, 5].…”

“…Often sensing stressful environmental stimuli, i.e., high temperature, pheromone, food limitation, and overcrowding, lead to generating an alternative third larval stage called dauer which can withstand such harsh conditions. Pathogens also act as a stress factor and can modulate worms’ behavioral plasticity [2, 8, 12, 24]. However, the molecular mechanism behind the dauer phenomenon is well studied but how chemosensory neurons participate in raising dauer larvae under pathogen infection needs more study.…”

“…[15, 17, 25]. In our previous study, we found deletion of Salmonella Typhimurium fepB gene alters worms’ physiology and develop dauer larva in their second generation [8]. From this initial outcome, we wanted to understand how this Δ fepB strain affects worms’ chemosensory system and modulating worms’ behavioral plasticity during infection.…”

“…The survival assay was performed as described earlier [8]. In brief 60 L4 worms (N2 and AWC ablated) were transferred to NGM plates seeded with E. coli OP50, WT-STM, Δ fepB , and Δ fepB c and kept for 12 hours for infection at 22 °C.…”

“…Salmonella Typhimurium 14028s strain (WT-STM), a Gram-negative, facultative anaerobic bacteria is well known to cause persistent infection in C. elegans and leading to their death [6, 7]. Our previous study demonstrated that deletion of fepB genes from bacterial genome enable worms to enter into a dauer stage deciphering food providing some signals, which modulate worms normal physiology [8]. In our current study, we are interested to explore the mechanisms of worms’ chemosensory response toward this Δ fepB strain and how such chemosensation mediate worms’ developmental decision under Δ fepB strain infection condition.…”