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Poster Full Abstracts - Neurophysiology and Behavior
Poster board number is above title. The first author is the presenter
297
mutation. We found that
dati
1
is expressed in the nervous system, and began investigating specifically where in the nervous system the gene is required. To
this end, we knocked down its expression in the entire CNS and in specific neuronal populations using RNA interference. We also analyzed the loss of
dati
1
function in somatic clones in discrete brain regions using a novel technique we developed that allows the generation and analysis of fourth chromosome
mutations. Here we show the status of the ongoing mapping of brain regions and present data that suggests that a subset of neurons is most affected by the
loss of
dati
1
.
620B
The role of Juvenile Hormone in
Drosophila melanogaster
male courtship behavior.
Thilini P Wijesekera, Brigitte Dauwalder. Biology and
Biochemistry, University of Houston, Houston, Texas.
Juvenile hormone binding proteins (JHBPs) of many insects have a similarity to
takeout
, a male preferentially expressed protein, shown to influence male
courtship behavior. This raises the possibility for a role for Juvenile Hormone in male courtship behavior. To test this hypothesis, we reduced the amount of
Juvenile Hormone Acid Methyl Transferase (JHAMT), a key enzyme involved in the synthesis of Juvenile hormone, specifically in the
corpora allata
and
examined its effect on the behavior.
To test whether Juvenile Hormone has a role in male courtship behavior in
Drosophila
, we reduced the amount of JHAMT by RNA interference. We
created transgenic
JHAMT-GAL4
lines that express Gal4 in the
corpora allata
. Expression of JHAMT-RNAi by
hsp-GAL4
and
JHAMT-GAL4
reduced male
courtship. Juvenile hormone is a vital hormone strongly influencing the development of insects. Therefore, the possibility of the above mutant phenotype
being a developmental defect arises. Therefore, JHAMT levels were reduced conditionally in the adult flies using the GAL80ts system. When the resulting
flies were studied for courtship defects, they also indicated a reduced courtship index. These results demonstrate that the reduction of Juvenile hormone
levels in adult males leads to a mutant courtship phenotype. This strongly suggests that normal Juvenile hormone levels are vital for courtship behavior in
Drosophila melanogaster.
This work was funded by NSF grant No. IOS-0919697.
621C
Drosophila
sNPF regulates feeding through the dFOXO post-translational modification.
Kyu-Sun Lee
1,2
, Seung-Hyun Hong
1
, Su-Jin Kwak
1
, Ae-
Kyeong Kim
1
, Hua Bai
3
, Marc Tatar
3
, Kweon Yu
1
. 1) Aging Res Ctr, KRIBB, Daejeon; 2) Functional Genomics Program, University of Science and
Technology, Daejeon; 3) Department of Ecology and Evolutionary Biology, Brown University, Providence, RI.
Feeding behavior is one of the most essential activities in animals, which is tightly regulated by neuroendocrine factors.
Drosophila
short neuropeptide F
(sNPF) is an orexigenic neural hormone. Understanding the regulative mechanism of sNPF signaling is critical for elucidating feeding regulation. Here, we
found that
minibrain
(
mnb
), which is a target gene of sNPF signaling, regulated feeding in
Drosophila
and fasting-feeding cycles are controlled by the post-
translational modification of the dFOXO transcription factor. During fasting, increased Mnb kinase phosphorylated and activated NAD+ deacetylase Sir2,
which in turn deacetylated and activated the dFOXO transcription factor. This activated dFOXO turned on the
sNPF
expression and increased feeding.
Conversely, during feeding, insulin signaling activated the Akt kinase, which phosphorylated and inhibited dFOXO. This inactivated dFOXO suppressed the
sNPF
expression and decreased feeding. These findings demonstrate that the post-translational modification of dFOXO play a critical role in the regulation
of sNPF-mediated feeding in
Drosophila
.
622A
The Role of Odorant Binding Proteins in Aversive Taste Perception in
Drosophila melanogaster
.
Sruthipriya Sridhar
1,2
, Michael Nokes
1,2,4
, Shilpa
Swarup
2,3
, Tatiana V. Morova
1,2
, Robert R.H. Anholt
1,2,3
. 1) Department of Biology; 2) W. M. Keck Center for Behavioral Biology; 3) Department of
Genetics, NCSU, Raleigh NC; 4) University of Notre Dame, Notre Dame IN.
Chemosensation in
Drosophila
is mediated by large multigene families of chemoreceptors, including olfactory receptors, gustatory receptors, and odorant
binding proteins (OBPs). Although the contribution of OBPs to olfaction is well documented, their role in mediating taste remains largely unknown. We
used the “CAFE” (capillary feeder) assay to quantify intake of “bitter” (i.e. aversive) compounds. We used a tubulin-GAL4 driver to express UAS-RNAi
constructs targeting 17
Obp
genes and their co-isogenic control to systematically dissect the functions of OBPs in mediating aversive taste perception. Single
sex groups of eight flies were food deprived for 24h and placed in a vial with three capillaries filled with either 50mM sucrose solution alone or a sucrose
solution supplemented with denatonium benzoate, berberine chloride, N-phenylthiourea, papaverine hydrochloride, quinine hydrochloride, escin,
theophyline, coumarin, or caffeine. After allowing flies to feed 24h, the amount of each solution consumed compared to the control was calculated, while
accounting for evaporation. Targeted knockdown of several OBPs resulted in either reduced or increased consumption of aversive tastants, presumably due
either to reduced removal of tastants or reduced transport of tastants to the chemoreceptors, respectively. To distinguish post-ingestive effects from
gustation, we also measured proboscis extension responses in tubulin-GAL4/UAS-RNAi-Obp hybrids that showed altered intake of tastants in the CAFE
assay. Our results implicate a function for OBPs in aversive taste avoidance. Supported by NIH grant GM059469.
623B
Identification of regulatory elements impacting AKH signaling.
Jason T Braco, Greg E Alberto, Emily L Gillespie, Erik C Johnson. Biology, Wake
Forest University, Winston-Salem, NC.
The mechanisms of how organisms maintain metabolic homeostasis in light of significant environmental variation in food availability are not completely
understood. We are particularly interested in the starvation stress response and the mechanisms that form homeostatic responses to starvation. The
Adipokinetic Hormone (AKH) has been identified as a principal component in maintaining metabolic homeostasis. AKH is responsible for increasing lipid
mobilization, energy availability, and starvation induced hyperactivity. We have previously identified that the energy sensor, AMP-activated kinase (AMPK)
is a critical element that regulates AKH signaling. Reduced AMPK function partially phenocopies AKH null alleles, suggesting additional, and AMPK -
independent mechanisms which also regulate AKH secretion. To identify these additional AKH regulatory mechanisms, we initiated a candidate gene screen
employing RNAi elements targeting hormone receptors. We hypothesized that the loss of excitatory transmitters would lead to a reduction in secreted AKH