Regulates Cell Signaling to Combat Infection.

DT104 infection causes the death of , which can be prevented by certain isolates. However, the molecular mechanisms of both the host response to the infection and the protection by are largely unclear. The present study has investigated the life-span and gene expression of both wild-type (WT) and mutants in some key components of cell signaling in response to infection and protection from . The results indicated that the gene expression of in the DAF/ insulin-like growth factor (DAF/IGF) pathway, and in the programmed cell death (PCD) pathway, , and for antimicrobial peptide production, and involved in the production of other defense molecules was all significantly upregulated when the wild-type (WT) was subjected to DT104 infection. On the contrary, the gene expression of , and in the p38 mitogen-activated protein kinase (MAPK) pathway and , and for the production of other defense molecules was significantly suppressed by DT104. Pretreatment of the worms with LB1 significantly upregulated the expression of almost all the tested genes except for , and compared with the nematode infected with DT104 only. Mutants defective in the cell signaling or other defense molecules of were either more susceptible (defective in , or ) or more resistant (defective in or ) to DT104 infection than the WT except for the mutant defective in . Mutants defective in antimicrobial peptides ( or ) were also more susceptible than the WT. In contrast, the mutant defective in became more resistant. When all the mutants were pretreated with LB1, five mutants that are defective in , or showed no response to the protection from LB1. These results suggest that LB1 can regulate cell signaling including the p38 MAPK pathway and downstream production of antimicrobial peptides and defense molecules to combat infection.