Page 293 - 53rd Annual Drosophila Research Conference

Poster Full Abstracts - Immunity and Pathogenesis
Poster board number is above title. The first author is the presenter
291
Drosophila melanogaster is able to control the extracellular growth of L. monocytogenes through two innate immune effectors, antimicrobial peptides and
melanization. Flies mutated for the enzymes that convert monoacylglycerol to diacylglycerol (CG4729, CG4753) and diacylglycerol to triglyceride
(midway) died faster than control flies. However expression level of antimicrobial peptides in midway mutant fly was not significantly different compared to
controls. We monitored levels of triglyceride and glucose and found that they were significantly lower in mutant flies. Listeria infected flies lose fat stores.
Our hypothesis is that infected midway mutants lost triglyceride and died more rapidly than wild type flies as the mutants reached the end of their energy
stores more rapidly.
596B
Spiroplasma in Drosophila melanogaster populations: prevalence, male-killing, molecular identification and no association with Wolbachia. Iuri M.
Ventura1, Ayana B. Martins1,2 , Mariana L. Lyra1,3 , Carlos C.A. Andrade4, Klélia A. Carvalho1 , Louis B. Klaczko1. 1) Dept. Genética e Evolução,
Universidade Estadual de Campinas, SP, Brazil; 2) Dept. de Ecologia, USP, SP; 3) Dept. de Zoologia, UNESP, SP; 4) Dept. de Biologia Marinha, UFF, RJ.
Spiroplasma endosymbionts are maternally transmitted bacteria that may kill infected sons resulting in the production of female-biased broods. The
prevalence of male killers varies considerably both between and within species. Here, we evaluate the spatial and temporal status of male-killing and non-
male-killing Spiroplasma infection in three Brazilian populations of D. melanogaster, nearly a decade after our lab reported the first world-wide occurrence
for this species. The incidence of the male-killing Spiroplasma ranged from close to 0 to 17.7% (so far the highest estimate for a Drosophila species) with a
suggestion of temporal decline in one of the studied populations. We also found non-male-killing Spiroplasma in lower prevalence (3% to 5%) in one
population; and we did not detect it in the other two. This may be taken as a suggestion of a spreading advantage conferred by the male-killing strategy.
Sequencing two loci, we identified the phylogenetic position of eleven Spiroplasma strains from the three localities, showing that all strains group closely in
the S. poulsonii clade. We were able to test the association between Spiroplasma infections and another widespread endosymbiont, Wolbachia, whose
prevalence ranged from 81.8% to 100%. The prevalence of Wolbachia did not differ between Spiroplasma infected and uninfected strains in our largest
sample, nor were the two endosymbionts’ prevalences associated across localities. We also assayed the male-killing effect of seven Spiroplasma strains in a
standard Canton-S D. melanogaster strain. All strains induced a complete male-killing phenotype. In this scenario, a combination of other host and
environmental conditions, as well as population historic factors, may be responsible for establishing the prevalence heterogeneity observed in the field.
597C
The Drosophila protein Mustard regulates targets of Relish. Paula Ivonne Watnick, Zhipeng Wang, Cristin Berkey. Division of Infectious Diseases,
Children's Hospital Boston, Boston, MA. 02115.
As part of a genetic screen, we isolated a P-element insertion mutant with resistance to oral Vibrio cholerae infection. Here we identify the protein Mustard
(Mtd) that is responsible for the resistance phenotype of the insertion mutant. Mtd contains a LysM domain, thought to be important for carbohydrate
recognition, and a TLDc domain, whose function is unknown. We show that a short, nuclearly localized Mtd isoform comprised almost entirely of the TLDc
domain inhibits multiple targets of the Drosophila NF-κB homolog Relish and provide genetic evidence for an interaction between these two proteins.
598A
Priming with S. pneumoniae infection causes changes in gene expression in Drosophila melanogaster. Junaid Ziauddin, David Schneider. Microbiology
& Immunology, Stanford Univ SOM, Stanford, CA.
We found Drosophila melanogaster can raise a stronger specific immune response to Streptococcus pneumoniae, Beauveria bassiana or Serratia
marcescens when the flies have been previously exposed to sublethal doses of each microbe. We call this phenomenon priming. Since flies lack B and T
cells, to some it seems theoretically impossible that flies could have an adapting immune response. Data trumps theory. Still, we need to find a mechanistic
explanation for this phenomenon, which has now been seen in a variety of insects. We injected Drosophila with a sublethal dose of dead S. pneumoniae,
waited for 3 days, re- injected the flies, and measured fly survival, bacterial growth rates and gene expression. We performed a microarray analysis to
identify genes modulated by priming during a S. pneumoniae infection. There are many changes in primed flies and we found multiple classes of genes that
are modulated following priming: some whose expression rise in only early infection, some whose expression increase at later time points, and some whose
expression are reduced post-infection. We followed 34 transcripts at a high level of resolution using QRT-PCR of tight timelines of infected primed and
naïve flies. We conclude that environment changes the immune response of the fly and this includes past exposure to microbes. We hypothesize that these
changes are evolved to be adaptive, where the fly’s immunity changes in a fashion that allows it to respond more effectively to that infection in subsequent
exposures. Most of these genes have not been implicated in immunity previously and we are exploring how the altered expression of these genes could lead
to altered immunity.
599B
Modeling the effects of altered gravity on the immune response using Drosophila. D Kimbrell1 , C Fuller1 , L von Kalm2, K Beckingham3 , M George1 , J
Parker4, M Thomson 5, D Hoshizaki6 , A Gibbs6, J Alley7 , K Taylor1, P Fuller1, K Kleinhesselink 1, A Hammonds8, R Morgan2, T Smallwood 2, A Kloehn 1. 1)
Univ California, Davis; 2) Univ Central Florida, Orlando; 3) Rice Univ, Houston, TX; 4) Expression Analysis, Inc; 5) Vanderbilt Univ, TN; 6) Univ Nevada,
Las Vegas; 7) Laverlam Inter Corp, MT; 8) Lawrence Berkeley Nat Lab, CA.
Astronauts have immune dysfunction during and after spaceflight that is a serious health concern for expanding the human exploration of space. A
fundamental understanding of the relationship between altered gravitational fields (g) and the immune system is required in order to enable this exploration.
Toward this understanding, we initiated study of the well-established Drosophila immunity model. First we analyzed hypergravity, and these results were
fast-tracked to microgravity flight studies on the space shuttle Discovery STS-121. At hyper g vs. normal 1g, wild type and immune defective flies infected
with B. bassiana fungus survived at significantly higher levels. Gravitaxis mutants were tested to begin discerning this as host and/or pathogen related.
Infected gravitaxis yuri mutants were different, surviving the same at hyper and 1g. UAS-yuri rescue reverted survival back to higher at hyper g. These
results indicate that hyper g has a positive effect on host post-infection survival. In microgravity-related experiments, flies that developed during flight on the
space shuttle were returned to earth and infected with B. bassiana or E. coli. Gene expression was assessed by microarray analyses. Development in space
altered many gene networks. For infection, antimicrobial protein gene induction was more normal in response to bacteria than fungus. However, the profiles