Salmonella Typhimurium fepB negatively regulates C. elegans behavioral plasticity

Objectives: Dauer is an alternative developmental stage of Caenorhabditis elegans (C. elegans) that gives survival benefits under unfavorable environmental conditions. Our study aims to decipher C. elegans dauer larvae development upon Salmonella Typhimurium infection and how the bacterial gene regulating the worm's behavioural plasticity for better survival. Methods: Age-synchronized L4 C. elegans worms were infected with Salmonella Typhimurium 14028s (WT-STM) strain and mutant strains to check the dauer larvae development using 1% SDS. Besides, bacterial load in animals' gut, pharyngeal pumping rate and viability were checked. Worm's immune genes (e.g., ilys-3, lys-7, pmk-1, abf-2, clec-60) and dauer regulatory genes (e.g., daf-7, daf-11, daf-12, daf-16, daf-3) were checked by performing qRT-PCR under infection conditions. Results: We found that deletion of the fepB gene in S. Typhimurium strain became less pathogenic with reduced flagellar motility and biofilm-forming ability. Besides, there was decreased bacterial burden in the worm's gut with no damage to their pharynx. The fepB mutant strain was also able to enhance the immune responses for better survival of worms. Infection with mutant strain could activate dauer signaling via the TGF-beta pathway leading to a significant increase in dauer formation than WT-STM infection. Conclusion: Our study indicated that the bacteria act as a food source for the growth of C. elegans and development and can act as a signal that might be playing an essential role in regulating the host physiology for their survival. Such a study can help us in understanding the complex host-pathogen interaction benefiting pathogen in host dissemination. (C) 2021 Published by Elsevier Ltd on behalf of The British Infection Association.

Automated summary

This study aims to explore the development of C. elegans dauer larvae upon Salmonella Typhimurium infection and investigate the role of bacterial genes in regulating the worm's behavioral plasticity. The results revealed that the deletion of the fepB gene in the Salmonella strain reduced pathogenicity and bacterial burden in the worm's gut without damaging the pharynx. The fepB mutant strain enhanced the worm's immune responses and activated dauer signaling via the TGF-beta pathway, leading to increased dauer formation.