title: Participation of the p38 pathway in Drosophila host defense against pathogenic bacteria and fungi.
abstract: The signaling network of innate immunity in Drosophila is constructed by multiple evolutionarily conserved pathways, including the Toll- or Imd-regulated NF-κB and JNK pathways. The p38 MAPK pathway is evolutionarily conserved in stress responses, but its role in Drosophila host defense is not fully understood. Here we show that the p38 pathway also participates in Drosophila host defense. In comparison with wild-type flies, the sensitivity to microbial infection was slightly higher in the p38a mutant, significantly higher in the p38b mutant, but unchanged in the p38c mutant. The p38b;p38a double-mutant flies were hypersensitive to septic injury. The immunodeficiency of p38b;p38a mutant flies was also demonstrated by hindgut melanization and larvae stage lethality that were induced by microbes naturally presented in fly food. A canonical MAP3K-MKK cascade was found to mediate p38 activation in response to infection in flies. However, neither Toll nor Imd was required for microbe-induced p38 activation. We found that p38-activated heat-shock factor and suppressed JNK collectively contributed to host defense against infection. Together, our data demonstrate that the p38 pathway-mediated stress response contribute to Drosophila host defense against microbial infection.
authors.affiliation: Key Laboratory of the Ministry of Education for Cell Biology and Tumor Cell Engineering, School of Life Sciences, Xiamen University, Xiamen, Fujian 361005, China.
authors.forename: Jianming
authors.initials: J
authors.lastname: Chen
authors.forename: Changchuan
authors.initials: C
authors.lastname: Xie
authors.forename: Lili
authors.initials: L
authors.lastname: Tian
authors.forename: Lixin
authors.initials: L
authors.lastname: Hong
authors.forename: Xiurong
authors.initials: X
authors.lastname: Wu
authors.forename: Jiahuai
authors.initials: J
authors.lastname: Han
mesh_terms: D000818:Animals; D001419:Bacteria / Q000276:immunology*; D001424:Bacterial Infections / Q000276:immunology / Q000517:prevention & control; D003470:Culture Media; D029721:Drosophila Proteins / Q000235:genetics / Q000378:metabolism; D004331:Drosophila melanogaster / Q000201:enzymology* / Q000235:genetics / Q000276:immunology* / Q000382:microbiology; D004789:Enzyme Activation; D005502:Food; D005658:Fungi / Q000276:immunology*; D041981:Gastrointestinal Tract / Q000378:metabolism / Q000382:microbiology; D005786:Gene Expression Regulation; D017344:Genes, Insect / Q000235:genetics; D006360:Heat-Shock Proteins / Q000378:metabolism; D007109:Immunity / Q000235:genetics / Q000276:immunology*; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D020935:MAP Kinase Signaling System; D008543:Melanins / Q000378:metabolism; D009154:Mutation / Q000235:genetics; D018805:Sepsis / Q000201:enzymology / Q000517:prevention & control; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism*
chemical_list: D003470:Culture Media; D029721:Drosophila Proteins; D006360:Heat-Shock Proteins; D008543:Melanins; D048031:JNK Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases