Drosophila melanogaster Thor and response to Candida albicans infection.
We used Drosophila melanogaster macrophage-like Schneider 2 (S2) cells as a model to study cell-mediated innate immunity against infection by the opportunistic fungal pathogen Candida albicans. Transcriptional profiling of S2 cells coincubated with C. albicans cells revealed up-regulation of several genes. One of the most highly up-regulated genes during this interaction is the D. melanogaster translational regulator 4E-BP encoded by the Thor gene. Analysis of Drosophila 4E-BP(null) mutant survival upon infection with C. albicans showed that 4E-BP plays an important role in host defense, suggesting a role for translational control in the D. melanogaster response to C. albicans infection.
Levitin
A
A
Genetics Group, Biotechnology Research Institute, National Research Council, Montreal, Quebec H4P 2R2, Canada. anastasia.levitin@cnrc-nrc.gc.ca
Marcil
A
A
Tettweiler
G
G
Laforest
M J
MJ
Oberholzer
U
U
Alarco
A M
AM
Thomas
D Y
DY
Lasko
P
P
Whiteway
M
M
D000818:Animals; D002176:Candida albicans / Q000502:physiology*; D002177:Candidiasis; D029721:Drosophila Proteins / Q000235:genetics / Q000378:metabolism*; D004331:Drosophila melanogaster / Q000166:cytology / Q000382:microbiology*; D023381:Endpoint Determination; D005786:Gene Expression Regulation; D017344:Genes, Insect; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism*; D009154:Mutation / Q000235:genetics; D010448:Peptide Initiation Factors / Q000235:genetics / Q000378:metabolism*; D010587:Phagocytosis; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D016019:Survival Analysis; D014158:Transcription, Genetic
D029721:Drosophila Proteins; D047908:Intracellular Signaling Peptides and Proteins; D010448:Peptide Initiation Factors; D012333:RNA, Messenger; C410006:Thor protein, Drosophila