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1. Introduction
2. C. elegans - structure
3. C. elegans - inner structure
4. Why C. elegans? physical properties
5. Life cycle of C. elegans
6. Why C. elegans? genetic aspects
7. Micro-injection of C. elegans
8. Transgenic C. elegans
9. Why C. elegans? advantages as genetic model
10. Growing method of C. elegans in the lab
11. C. elegans in the natural environment
12. The dauer stage
13. A dauer pheromone
14. Pheromones
15. Attraction of males by hermaphrodites
16. C. elegans is attracted by bacteria
17. C. elegans prefers S. marcescens
18. Worms are repelled by S. marcescens
19. Worms are not repelled by SM267
20. SM267 does not make serrawettin W2
21. Implications of the detection mechanism
22. C. elegans eats bacteria
23. The grinder
24. E. coli is broken down in the pharynx
25. S. marcescens destrys the grinder
26. Infection by S. marcescens
27. Response to P. luminescens & Db11
28. Host response to infection is specific
29. Response specificity - live vs. dead bacteria
30. Response specificity - virulence
31. Response specificity - virulence and viability (1)
32. Response specificity - virulence and viability (2)
33. Response specificity - bacteria strain
34. Response to infection - a common signature
35. EASE with the common response genes
36. Infection by P. luminescens - necrotic reporter
37. Regulation of necrosis
38. Suppression of necrosis
39. D. coniospora spores
40. Infection of C. elegans by D. coniospora
41. nlp and cnc genes are highly up-regulated
42. Phylogenetic analysis of nlp and cnc genes
43. nlp clusters in three Caenorhabditis species
44. nlp cluster in C. elegans
45. Over-expression of nlp and resistance
46. Epidermal expression of AMP genes
47. Induction of nlp-29 after Drechmeria infection
48. Induction of pnlp-29::GFP
49. Induction of nlp-29
50. No induction of nlp-29
51. D. coniospora penetrates the cuticle
52. Physical injury of C. elegans
53. Physical injury triggers wound repair
54. Physical injury induces pnlp-29::GFP
55. Abnormal epithelial cell development
56. Osmotic shock induces pnlp-29::GFP
57. AMP gene expression in Drosophila
58. Rel homology domain proteins
59. TIR domain proteins
60. A TIR domain adaptor protein in C. elegans
61. p38 MAPK pathway involved in defence
62. dapk-1 mutants have a wounded epidermis
63. AMP genes are upregulated in dapk-1 mutants
64. DAPK is a negative regulator of AMP expression
65. A suppressor of the epidermal defects
66. Two roles for DAPK
67. Open questions
68. The nipi mutants (1)
69. An example of a nipi mutant
70. The nipi mutants (2)
71. nipi-1 = PKCdelta
72. PKC-delta activation
73. Induction by PMA
74. G-protein/PKC upstream of the p38 pathway
75. nipi-3 affects transcriptional response to infection
76. Two signals in response to infection
77. Sodium-neurotransmitter symporter family (1)
78. Sodium-neurotransmitter symporter family (2)
79. Sodium-neurotransmitter symporter family (3)
80. Interaction with a STAT like transcription factor
81. Physical interaction - SNF-12 and STA-2
82. sta-2 is required for nlp-29 induction
83. AMP gene regulation in C. elegans
84. Conclusions
85. Thanks to our collaborators
86. The lab members

Topics Covered

• Anatomy of C. elegans
• C. elegans as an experimental animal
• Pheromone signalling and pathogen detection
• Specific and general transcriptional responses to bacterial infection
• Necrosis
• Fungal infection and injury induce antimicrobial peptide genes
• Signal transduction pathways that control antimicrobial peptide gene expression

Links

Series:

• Innate Immunity

Categories:

• Immunology

Therapeutic Areas:

• Immunology & Inflammation

Talk Citation

Publication History

• Published on July 9, 2009
• Updated on November 3, 2011
• Archived on February 28, 2018

Financial Disclosures

• Dr. Jonathan Ewbank has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.