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Drosophila melanogaster  mount an effective innate immune response against invading microorganisms, but can eventually succumb to persistent pathogenic infections. Understanding of this pathogenesis is limited, but it appears that host factors, induced by microbes, can have a direct cost to the host organism. Mutations in  wntD  cause susceptibility to  Listeria monocytogenes  infection, apparently through the derepression of Toll-Dorsal target genes, some of which are deleterious to survival. Here, we use gene expression profiling to identify genes that may mediate the observed susceptibility of  wntD  mutants to lethal infection. These genes include the TNF family member  eiger  and the novel immunity gene  edin  ( elevated during infection ; synonym  CG32185 ), both of which are more strongly induced by infection of  wntD  mutants compared to controls.  edin  is also expressed more highly during infection of wild-type flies with wild-type  Salmonella typhimurium  than with a less pathogenic mutant strain, and its expression is regulated in part by the Imd pathway. Furthermore, overexpression of  edin  can induce age-dependent lethality, while loss of function in  edin  renders flies more susceptible to  Listeria  infection. These results are consistent with a model in which the regulation of host factors, including  edin , must be tightly controlled to avoid the detrimental consequences of having too much or too little activity.

Pathogenesis of Listeria-Infected Drosophila wntD Mutants Is Associated with Elevated Levels of the Novel Immunity Gene edin