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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. |
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