title: Intrinsic JNK-MAPK pathway involvement requires daf-16-mediated immune response during Shigella flexneri infection in C. elegans.
abstract: The c-Jun N-terminal kinase-mitogen-activated protein kinase (JNK-MAPK) pathway assists in modulating signals for growth, survival, and metabolism, thereby coordinating many cellular events during normal and stress conditions. To understand the role of the JNK-MAPK pathway during bacterial infection, an in vivo model organism Caenorhabditis elegans was used. In order to check the involvement of the JNK-MAPK pathway, the survival rate of C. elegans wild type (WT), and JNK-MAPK pathway mutant worms' upon exposure to selective Gram-positive and Gram-negative pathogenic bacteria, was studied. Among the pathogens, Shigella flexneri M9OT was found to efficiently colonize inside the WT and JNK-MAPK pathway mutant worms. qPCR studies had suggested that the above pathway-specific genes kgb-2 and jnk-1 were prominently responsible for the immune response elicited by the host during the M9OT infection. In addition, daf-16, which is a major transcription factor of the insulin/insulin growth factor-1 signaling (IIS) pathway, was also found to be involved during the host response. Crosstalk between IIS and JNK-MAPK pathways has probably been involved in the activation of the host immune system, which consequently leads to lifespan extension. Furthermore, it is also observed that daf-16 activation by JNK-MAPK pathway leads to antimicrobial response, by activating lys-7 expression. These findings suggest that JNK-MAPK is not the sole pathway that enhances the immunity of the host. Nonetheless, the IIS pathway bridges the JNK-MAPK pathway that influences in protecting the host in counter to the M9OT infection.
authors.affiliation: Department of Biotechnology, Science Campus, Alagappa University, Karaikudi, Tamil Nadu, 630 003, India.
authors.forename: Shanmugam
authors.initials: S
authors.lastname: Marudhupandiyan
authors.affiliation: Department of Biotechnology, Science Campus, Alagappa University, Karaikudi, Tamil Nadu, 630 003, India. bsuryar@yahoo.com.
authors.forename: Krishnaswamy
authors.initials: K
authors.lastname: Balamurugan
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D017173:Caenorhabditis elegans / Q000276:immunology* / Q000382:microbiology; D029742:Caenorhabditis elegans Proteins / Q000235:genetics / Q000378:metabolism*; D002478:Cells, Cultured; D004195:Disease Models, Animal; D004405:Dysentery, Bacillary / Q000276:immunology*; D051858:Forkhead Transcription Factors / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D007113:Immunity, Innate; D007328:Insulin / Q000378:metabolism; D048031:JNK Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism*; D020928:Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism*; D020239:Receptor Cross-Talk; D012763:Shigella flexneri / Q000502:physiology*; D015398:Signal Transduction
chemical_list: D029742:Caenorhabditis elegans Proteins; D051858:Forkhead Transcription Factors; D007328:Insulin; C108831:daf-16 protein, C elegans; D048031:JNK Mitogen-Activated Protein Kinases; C437322:JNK-1 protein, C elegans; D020928:Mitogen-Activated Protein Kinases
keywords: C-Jun N-terminal kinase MAPK; Colonization; Innate immunity; Insulin/IGF signaling; Shigella flexneri; daf-16/FOXO transcription factor