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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-β 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., Competing Interests: Declaration of Competing Interest The authors declare no conflict of interest., (Copyright © 2022. Published by Elsevier Ltd.)

Salmonella infection is known to cause a 50% reduction in the lifespan of Caenorhabditis elegans. But the mechanism behind this reduction is not reported. The current study deals with the Salmonella infection mediated egg retention in the worm leading to various developmental and morphological defects and disruption of temporal regulation of developmental timing in C. elegans. Worm's delayed egg-laying response to Salmonella infection causes several defects in eggs, including over-folding of developing embryo, increased egg size, and losing the osmotic stress resistance. Also, the infected eggs show delayed and reduced hatching. With significantly downregulated lin-28a, col-72 and col-87, we observed a disrupted L2, but L3, L4, and adult developmental stages reach faster during infection. The precocious development of L3, L4, and the adult stage is further indicated by upregulation of stage-specific genes viz. rnh-1.3, col-158 and col-176 (L3), col-17, col-38 and col-49 (L4), and col-19, col-7 (adult). The significant upregulation of the flp-1 gene indicates reduced egglaying, and the flp-1(ok2811) null mutant further supported the Salmonella infectionmediated phenotype. Similar phenotypes are primarily evident in multiple generations up to F5 and F6. Salmonella infection causes a range of developmental anomalies and shortening of worm life span through various regulatory pathways., Competing Interests: Declaration of competing interest The authors declare no conflict of interest., (Copyright © 2021 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.)