Open AccessModulation of C aenorhabditis elegans infection sensitivity by the LIN ‐7 cell junction protein
Author(s) -
Sem XiaoHui,
Kreisberg Jason F.,
Kawli Trupti,
Tan ManWah,
Rhen Mikael,
Tan Patrick
Publication year - 2012
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/j.1462-5822.2012.01824.x
Subject(s) - biology , caenorhabditis elegans , pdz domain , microbiology and biotechnology , mutant , gene silencing , phenotype , function (biology) , rna interference , gene , genetics , rna
Summary In C aenorhabditis elegans , the LIN ‐2/7/10 protein complex regulates the activity of signalling proteins. We found that inhibiting lin ‐7 function, and also lin ‐2 and lin ‐10 , resulted in enhanced C . elegans survival after infection by B urkholderia spp., implicating a novel role for these genes in modulating infection outcomes. Genetic experiments suggested that this infection phenotype is likely caused by modulation of the DAF ‐2 insulin/ IGF ‐1 signalling pathway. Supporting these observations, yeast two‐hybrid assays confirmed that the LIN ‐2 PDZ domain can physically bind to the DAF ‐2 C ‐terminus. Loss of lin ‐7 activity also altered DAF ‐16 nuclear localization kinetics, indicating an additional contribution by hsf ‐1 . Unexpectedly, silencing lin ‐7 in the hypodermis, but not the intestine, was protective against infection, implicating the hypodermis as a key tissue in this phenomenon. Finally, consistent with lin ‐7 acting as a general host infection factor, lin ‐7 mutants also exhibited enhanced survival upon infectionby two other Gram‐negative pathogens, P seudomonas and S almonella spp.