Project description:C-type lectin-like domain (CTLD) encoding genes are highly diverse in C. elegans, comprising a clec gene family of 283 members. Since vertebrate CTLD proteins have characterized functions in defense responses against pathogens and since expression of C. elegans clec genes is pathogen-dependent, it is generally assumed that clec genes function in C. elegans immune defenses. In this study we challenged this assumption and focused on the C. elegans clec gene clec-4, whose expression is highly upregulated upon infection with various pathogens. We tested the involvement of clec-4 in the defense response to infection with Pseudomonas aeruginosa PA14, Bacillus thuringiensis BT18247, and the natural pathogen Serratia rubidaea MYb237. Contrary to our expectation clec-4(ok2050) mutant worms were not more susceptible to pathogen infection than wildtype worms. To explore potential redundant function between different C. elegans clec genes, we investigated expression of several clec-4 paralogs, finding that clec-4, clec-41, and clec-42 expression shows similar infection-dependent changes and co-localizes to the intestine. We found that only clec-42 is required for the C. elegans defense response to BT18247 infection and that clec-4 genetically interacts with clec-41 and clec-42. The exact role of clec-4 in pathogen defense responses however remains enigmatic. Our results further indicate that a complex interplay between different clec genes regulates C. elegans defense responses.
Project description:Young adult fer-15;fem-1 Caenorhabditis elegans were infected with Staphylococcus aureus for 8 h to determine the transcriptional host response to Staphylococcus aureus. Analysis of differential gene expression in C. elegans young adults exposed to two different bacteria: E. coli strain OP50 (control), wild-type Staphylococcus aureus RN6390. Samples were analyzed at 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: response to pathogen infection, innate immunity, host-pathogen interactions
Project description:Young adult N2 Caenorhabditis elegans were infected with Enterococcus faecalis or Enterococcus faecium for 8 h to determine the transcriptional host response to each enterococcal species. Analysis of differential gene expression in C. elegans young adults exposed to four different bacteria: heat-killed Escherichia coli strain OP50 (control), wild-type E. faecalis MMH594, wild-type E. faecium E007, or Bacillus subtilis PY79 (sigF::kan). Samples were analyzed at 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Brain-heart infusion agar plates (10 ug/ml kanamycin) were used.
Project description:Sexual dimorphism affects diverse biological functions such as immune responses. However, mechanisms by which different sexes alter immunity remained largely unknown. By using Caenorhabditis elegans as a model, here we show that male animals exhibit enhanced immunity against various pathogenic bacteria via upregulating autophagy. We found that male C. elegans displayed upregulation of helix loop helix 30 (HLH-30)/transcription factor EB (TFEB), a transcription factor crucial for autophagy, which contributed to the enhanced anti-bacterial immunity. We showed that autophagy-related protein 2 (atg-2) that is upregulated by HLH-30/TFEB, mediated increased immunity in male animals. Thus, male C. elegans appear to be equipped with enhanced autophagy for increasing pathogen resistance, likely conferring prolonged mate search with less infection.
Project description:We sequenced the transcriptome of a host (Caenorhabditis elegans) following its interaction with a non-native bacterium (Enterococcus faecalis) that has protective traits against the pathogen, Staphylococcus aureus. We also investigated the impact that the evolutionary history of the protective bacterium has on the transcriptional history of the host. We tested protective bacteria that had either coevolved against the pathogen within C. elegans, or had evolved on its own within C. elegans.