- THIS ARTICLE
- Full Text
- Full Text (PDF)
- Data Supplement
-
All Versions of this Article:
genetics.107.083782v1
178/3/1807 most recent - Alert me when this article is cited
- Alert me if a correction is posted
- SERVICES
- Email this article to a friend
- Similar articles in this journal
- Similar articles in PubMed
- Alert me to new issues of the journal
- Download to citation manager
- Reprints & Permissions
- CITING ARTICLES
- Citing Articles via HighWire
- Citing Articles via Google Scholar
- GOOGLE SCHOLAR
- Articles by Ayres, J. S.
- Articles by Schneider, D. S.
- Search for Related Content
- PUBMED
- PubMed Citation
- Articles by Ayres, J. S.
- Articles by Schneider, D. S.
Originally published as Genetics Published Articles Ahead of Print on February 1, 2008.
Genetics, Vol. 178, 1807-1815, March 2008, Copyright © 2008
doi:10.1534/genetics.107.083782
Identification of Drosophila Mutants Altering Defense of and Endurance to Listeria monocytogenes Infection
Janelle S. Ayres*,
Nancy Freitag
and
David S. Schneider*,1
* Department of Microbiology and Immunology, Stanford University, Stanford, California 94305 and Department of Microbiology and Immunology, University of Illinois, Chicago, Illinois 60612
1 Corresponding author: Department of Microbiology and Immunology, Stanford University, D333 Fairchild Bldg., 299 Campus Dr., Stanford, CA 94305.
E-mail: dschneider{at}stanford.edu
We extended the use of Drosophila beyond being a model for signaling pathways required for pattern recognition immune signaling and show that the fly can be used to identify genes required for pathogenesis and host–pathogen interactions. We performed a forward genetic screen to identify Drosophila mutations altering sensitivity to the intracellular pathogen Listeria monocytogenes. We recovered 18 mutants with increased susceptibility to infection, none of which were previously shown to function in a Drosophila immune response. Using secondary screens, we divided these mutants into two groups: In the first group, mutants have reduced endurance to infections but show no change in bacterial growth. This is a new fly immunity phenotype that is not commonly studied. In the second group, mutants have a typical defense defect in which bacterial growth is increased and survival is decreased. By further challenging mutant flies with L. monocytogenes mutants, we identified subgroups of fly mutants that affect specific stages of the L. monocytogenes life cycle, exit from the vacuole, or actin-based movement. There is no overlap between our genes and the hundreds of genes identified in Drosophila S2 cells fighting L. monocytogenes infection, using genomewide RNAi screens in vitro. By using a whole-animal model and screening for host survival, we revealed genes involved in physiologies different from those that were found in previous screens, which all had defects in defensive immune signaling.
This article has been cited by other articles:
 |
|
 |
|
  R. Medzhitov Damage control in host-pathogen interactions PNAS, September 15, 2009; 106(37): 15525 - 15526. [Full Text] [PDF]
|
|
|
|
 |
|
 L. Raberg, A. L Graham, and A. F Read Decomposing health: tolerance and resistance to parasites in animals Phil Trans R Soc B, January 12, 2009; 364(1513): 37 - 49. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. M. Brandt, G. Jaramillo-Gutierrez, S. Kumar, C. Barillas-Mury, and D. S. Schneider Use of a Drosophila Model to Identify Genes Regulating Plasmodium Growth in the Mosquito Genetics, November 1, 2008; 180(3): 1671 - 1678. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Schwegmann and F. Brombacher Host-Directed Drug Targeting of Factors Hijacked by Pathogens Sci. Signal., July 22, 2008; 1(29): re8 - re8. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. S. Dionne and D. S. Schneider Models of infectious diseases in the fruit fly Drosophila melanogaster Dis. Model. Mech., July 1, 2008; 1(1): 43 - 49. [Abstract] [Full Text] [PDF]
|
|
|