Project description:(Part 1) Gene expression profiles of C. elegans in response to a 120 hour S. enterica infection. Synchronized larval stage 1 (L1) animals were exposed to S. enterica SL1344 for 36, 72, 96, or 120 hours. As an uninfected control, synchronized L1 animals were exposed to E. coli OP50 for 36 hours. (Part 2) Gene expression profiles of C. elegans in response to Tetracycline-mediated recovery from 72 hour and 96 hour S. enterica infections. Synchronized L1 animals were exposed to S. enterica SL1344 for 72 hours and then shifted to E. coli HT115 plus Tetracycline plates for 24 hours to resolve the infection. Synchronized L1 animals were exposed to S. enterica SL1344 for 96 hours and then shifted to E. coli HT115 plus Tetracycline plates for 24 hours to resolve the infection.
Project description:(Part 1) Gene expression profiles of C. elegans in response to a 120 hour S. enterica infection. Synchronized larval stage 1 (L1) animals were exposed to S. enterica SL1344 for 36, 72, 96, or 120 hours. As an uninfected control, synchronized L1 animals were exposed to E. coli OP50 for 36 hours. (Part 2) Gene expression profiles of C. elegans in response to Tetracycline-mediated recovery from 72 hour and 96 hour S. enterica infections. Synchronized L1 animals were exposed to S. enterica SL1344 for 72 hours and then shifted to E. coli HT115 plus Tetracycline plates for 24 hours to resolve the infection. Synchronized L1 animals were exposed to S. enterica SL1344 for 96 hours and then shifted to E. coli HT115 plus Tetracycline plates for 24 hours to resolve the infection. Samples include 36 hours on OP50 (36hOP), 36 hours on SL1344 (36hSL), 72 hours on SL1344 (72hSL), 96 hours on SL1344 (96hSL), 120 hours on SL1344 (120hSL), 72 hours on SL1344 plus 24 hours on HT115-Tet (96hHT), 96 hours on SL1344 plus 24 hours on HT115-Tet (120hHT). Duplicate biological samples were included for each timepoint. 14 total samples. Agilent C. elegans expression microarray (GPL14144).
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: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.