PMID:20668681

Citation	TeKippe, M and Aballay, A (2010) C. elegans germline-deficient mutants respond to pathogen infection using shared and distinct mechanisms. PLoS ONE 5:e11777
Abstract	Reproduction extracts a cost in resources that organisms are then unable to utilize to deal with a multitude of environmental stressors. In the nematode C. elegans, development of the germline shortens the lifespan of the animal and increases its susceptibility to microbial pathogens. Prior studies have demonstrated germline-deficient nematodes to have increased resistance to gram negative bacteria. We show that germline-deficient strains display increased resistance across a broad range of pathogens including gram positive and gram negative bacteria, and the fungal pathogen Cryptococcus neoformans. Furthermore, we show that the FOXO transcription factor DAF-16, which regulates longevity and immunity in C. elegans, appears to be crucial for maintaining longevity in both wild-type and germline-deficient backgrounds. Our studies indicate that germline-deficient mutants glp-1 and glp-4 respond to pathogen infection using common and different mechanisms that involve the activation of DAF-16.
Links	PubMed PMC2909909 Online version:10.1371/journal.pone.0011777
Keywords	Animals; Animals, Genetically Modified; Bacterial Physiological Phenomena; Caenorhabditis elegans/genetics; Caenorhabditis elegans/immunology; Caenorhabditis elegans/metabolism; Caenorhabditis elegans/microbiology; Caenorhabditis elegans Proteins/genetics; Caenorhabditis elegans Proteins/metabolism; Cryptococcus neoformans/physiology; Gram-Negative Bacteria/physiology; Gram-Positive Bacteria/physiology; Immunity/genetics; Immunity/physiology; Longevity/genetics; Longevity/physiology; RNA Interference; Transcription Factors/genetics; Transcription Factors/metabolism
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