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> Home  /  Biomedical & Life Sciences  /  Series  /  Innate Immunity  /  Talk Details
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Innate immunity in C. elegans
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    SPEAKER(S)

Dr. Jonathan Ewbank - INSERM, France

Jonathan Ewbank is a Research Director at INSERM, the French medical research council. He received a MA in biochemistry from the University of Oxford. Research for his PhD in biophysics, from the University of Cambridge, was split between the MRC LMB and the EMBL in Heidelberg. After postdoctoral work at the Sloan-Kettering in New York, and McGill University, Montreal, he moved to the Centre d'Immunologie de Marseille Luminy (CIML) in 1997. In 1999, he started his own group at the CIML and has subsequently focused on host-pathogen interactions using the nematode C. elegans as a model.

Talk Online Publication: Jul 2009

TOPICS COVERED IN INNATE IMMUNITY IN C. ELEGANS

Anatomy of C. elegans - C. elegans as an experimental animal - Infection models - Screening for virulence factors - TLR 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

How to cite this talk:
Ewbank, J. (2009), "Innate immunity in C. elegans", in Gordon, S. (ed.), Innate Immunity: Host recognition and response in health and disease, The Biomedical & Life Sciences Collection, Henry Stewart Talks Ltd, London (online at http://hstalks.com/bio)

Direct talk access link:
http://hstalks.com/lib.php?t=HST61.2054_1_2&c=252

    DETAILED SLIDE INDEX

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. C. elegans eats bacteria
11. The grinder of C. elegans
12. S. marcescens destroys the grinder
13. Replication within intestinal lumen of C. elegans
14. Symptoms of the infection
15. S. marcescens kills C. elegans
16. Known pathogens of C. elegans
17. Screening for virulence factors
18. Identity of P. aeruginosa mutants
19. Universal virulence factors
20. Identifying antimicrobials using an infection model
21. Compounds that reduce virulance of E. faecalis
22. Host response
23. A conserved innate defence pathway
24. Deletion alleles for the Toll homologue
25. tol-1(nr2013) developmental phenotype
26. Pharyneal invasion in tol-1 mutants
27. C. elegans is attracted by bacteria
28. C. elegans prefers S. marcescens
29. Worms are repelled by S. marcescens
30. tol-1 mutants are not repelled by S. marcescens
31. tol-1 is expressed in neurons
32. Worms are not repelled by SM267
33. SM267 contains an insertion in swrA gene
34. swrA is necessary for synthesis of serrawettin W2
35. swrA- mutant is not able to swarm
36. Specific detection of serrawettin W2
37. Implications
38. Transcriptional response to P. luminescens
39. Host response to infection is specific
40. Host response includes a common signature
41. Response genes induced are by S. marcescens
42. EASE with the common response genes
43. P.l. infection induces asp-4::GFP in the intestine
44. Regulation of necrosis
45. Effect of necrosis suppression on resistance
46. D. coniospora spores adhere to C. elegans cuticle
47. Infection of C. elegans by D. coniospora
48. D. coniospora kills C. elegans
49. Phylogenetic analysis of nlp and cnc genes (1)
50. Phylogenetic analysis of nlp and cnc genes (2)
51. nlp clusters in three Caenorhabditis species
52. nlp cluster in C. elegans
53. nlp cluster over-expression increases resistance
54. Induction of nlp-29 after Drechmeria infection
55. Quantification of pnlp-29::GFP induction
56. Stimuli which do not induce nlp-29
57. Stimuli which induce nlp-29
58. Physical injury induces pnlp-29::GFP
59. Induction of pnlp-29::GFP by high salt
60. Use of reporter gene to identify signaling pathways
61. Blocking induction of pnlp-29::gfp
62. p38 MAPK pathway involved in defence
63. No induction of peptide after Drechmeria infection
64. nipi-1 corresponds to PKC-delta
65. PKC mutants resist PMA treatment
66. Not all PKC alleles block the response
67. Protein kinase C activation
68. PMA induces pnlp-29::GFP
69. PKC activation pathway
70. High activated GPA-12 expression induces nlp-29
71. Summary of nlp-29 induction
72. Separate pathways for infection/wound and salt
73. Will pmk-1 mutant block response to PMA?
74. p38 MAPK pmk-1
75. Effects of pmk-1 and PKC mutants are similar
76. p38 pathway
77. nipi-3 responds to injury
78. nipi-3 encodes a kinase
79. Separate pathways for infections and wounding
80. Conclusions
81. Thanks to our collaborators
82. Equipe FRM
83. END