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Poster Full Abstracts - Immunity and Pathogenesis
Poster board number is above title. The first author is the presenter
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of transcriptional modulation to both types of infection for both protein-encoding and miRNA genes were significantly different in the space-raised flies
compared to ground controls. Overall, the spaceflight data correlate with a differential effect based on the infecting microbe and the Imd and Toll pathways.
600C
Trade-offs and immune defense: the effect of mating and reproduction on immunity in female
D. melanogaster
.
Sarah M. Short, Mariana F. Wolfner,
Brian P. Lazzaro. Field of Genetics & Development, Cornell University, Ithaca, NY.
Immune defense is costly and is involved in multiple trade-offs with life history traits. A major barrier to understanding how immune defense functions at
a whole-organism level is our lack of knowledge of the physiological bases of these trade-offs. In this work, we demonstrate that female
Drosophila
melanogaster
suffer reduced immune defense after mating, an observation that is consistent with a trade-off between reproduction and immunity. We have
determined that, while females are highly genetically variable for the degree of immunosuppression they experience after mating, males are not significantly
variable in the level of immunosuppression they elicit in their mates. We also failed to detect a genetic interaction between males and females. These data
are not consistent with an inter-sexual interaction such as sexual conflict, and instead suggest that the evolution of this trait is likely to involve an
evolutionary trade-off between female reproductive traits and the humoral immune response. Were this to be the case, we would predict that lower immune
defense after mating should give some benefit in terms of reproductive fitness. We are therefore currently testing for a negative genetic correlation between
post-mating immune defense and short-term egg production. We are also investigating the mechanistic basis of post-mating immunosuppression. Using a
series of reproductive mutants, we have shown that transfer of both sperm and sex peptide (a seminal fluid protein) are crucial to elicit post-mating
immunosuppression in females. We have also found that females that fail to produce eggs demonstrate no effect of mating on immune defense, and that
mated females have significantly lower levels of expression in multiple antimicrobial peptide genes after infection compared to virgin females. We are
assaying changes in gene expression on a genome-wide basis in mated and unmated, infected and uninfected individuals to gain additional insight into the
physiological and genetic intersections between reproduction and immune defense.
601A
Investigating the alleles responsible for immune natural variation of Drosophila melanogaster.
Alejandra Guzman, David Schneider. Microbiology and
Immunology, Stanford University, Stanford, CA.
Immune natural variation increases the fitness of a population because, as a whole, the population can better respond to a wider range of pathogens and
environmental conditions. This study aims to discover alleles responsible for natural variation in Drosophila melanogaster immunity. Until recently,
immunity has largely been studied with non-natural mutations of essential immune genes (e.g. Toll and Imd) and little focus has been given to the genes and
alleles that cause the natural variation of immunity. In 2004, Lazzaro et. al. (Science) showed that in D. melanogaster there are polymorphisms in the regions
surrounding previously described immunity genes. Our work uses an unbiased approach to discover alleles responsible for the natural variation in D.
menlaogaster immunity. In this study, we use a panel of 162 fully sequenced inbred Drosophila lines derived from a single population in North Carolina
called the Drosophila Genetic Reference Panel. We infect these homozygous lines with Listeria monocytogenes and measure changes in fly survival and
bacterial growth. Using this data we perform quantitative trait loci (QTL) analysis to find natural genetic polymorphisms responsible for variation in
immunocompetance.
602B
Regulation of Hematopoietic Stem-Like Cell Multipotency in
Drosophila
.
Hongjuan Gao, Xiaorong Wu, Nancy Fossett. Center for Vascular and
Inflammatory Diseases, University of Maryland School of Medicine, Baltimore, MD.
Studies using
Drosophila
have contributed significantly to our understanding how stem cells are regulated
in vivo
. Work from our laboratory has shown
that the Friend of GATA protein, U-shaped, regulates stem-like cell potency and differentiation. U-shaped expression is expressed in stem-like cells and
downregulated in a sub-population of terminally differentiated blood cells. Our studies indicate that U-shaped maintains the stem cell population by blocking
differentiation and that
u-shaped
expression is controlled by a complex regulatory network that includes the JAK/STAT and TGF-β signal transduction
pathways. Collectively, these findings suggest that U-shaped is an important component of the stem cell regulatory machinery and may act as a key
regulatory node that integrates multiple signals from the surrounding microenvironment to control stem-like cell potency and differentiation. To extend these
studies, we are investigating the downstream effectors of the GATA:FOG complex that control stem-like cell multipotency. Given the functional
conservation of Friend of GATA proteins and the role of the GATA:FOG complex in the control of cell-fate choice, our studies may identify novel
interactions between conserved factors that control vertebrate stem cell fate choice.
603C
Steroid modulation of immune function in
Drosophila
.
Jeanette E. Natzle, Patrick Finnegan, Damian Kuo, Phi Nguyen, Deborah Kimbrell. Dept Molec &
Cellular Biol, Univ California, Davis, Davis, CA.
Several lines of evidence support a link between steroid hormones and immune cell regulation in
Drosophila
. A number of early studies implicated 20-
hydroxyecdysone (20E) in regulation of blood cell development and function, however little is known about how the steroid response is integrated with other
signaling pathways and what steps in control of blood cell growth and differentiation are controlled by steroids. Our preliminary studies are consistent with a
requirement for a functional cell-autonomous 20E-response pathway within
Drosophila
immune cells. We have inhibited the activity of the Ecdysone
Receptor (EcR) within immune cells by using several primarily immune-cell specific GAL4 drivers (Dorothy-Gal4, Hemese-Gal4, Hemolectin(HML)-Gal4)
to express a UAS-regulated EcR-RNAi construct (UAS-CA104; C. Antoniewski) in hemocytes and/or lymph glands. Dorothy-Gal4 and Hemese-Gal4 in
combination with UAS-CA104 lead to almost complete pupal lethality. A high proportion of adult escapers and arrested pupae show melanotic nodules, a
hallmark of aberrant hemocyte proliferation, differentiation and function associated with a state similar to chronic inflammation. Immunostaining of Gal4-
expressing hemocytes from pupae verified that EcR in the nucleus is absent or substantially depleted in the HemeseGal4; UAS-CA104 circulating
hemocytes.In contrast, immunostaining of pupal UAS-CA104; HML-Gal4 hemocytes revealed a substantial level of nuclear EcR expression, presumably
due to a lower level of RNAi expression produced by the Gal4 driver in this line. Consistent with the significant residual EcR function, the UAS-CA104;
HML-Gal4 flies appear normal. Taken together, these results correlate loss of ecdysone signaling in the immune cells to aberrant function. In the absence of