The 7th
Annual
NC
Undergraduate
Summer Research Symposium
Howard Hughes Research Scholars (HHRS) abstracts
Abstracts are listed in
alphabetical order by the last name of the corresponding author.
|
Crowther,
Andrew J. |
|
|
Home Institution: |
NCSU |
|
Program: |
Howard Hughes Research Scholars (HHRS) |
|
College: |
CALS |
|
Department(s): |
Biological Sciences |
|
Research |
Heather B.
Patisaul/Zoology |
|
Title of Presentation: |
Differences
in the Adult Brains of Male Rats Exposed Neonatally to Endocrine Active
Compounds or Estrogen Receptor Agonists |
Estrogen can affect male behavior
including anxiety and aggression. There are two subtypes of estrogen receptors
(ERs), ERα and ERβ, which differ in structure and function. The functional roles of each ER can be
examined by using agonists specific for each one. ERs
also bind to endocrine active compounds (EACs).
EACs have been shown to disrupt sex-specific development and behavior.
To determine if neonatal administration of EACs changes anxiety and aggression
levels in adulthood, and to examine through which form of ER these compounds
might be acting, male rat neonates were injected with either 0.05 ml sesame oil
(control), 50 μg estradiol benzoate, 1 mg/kg
1,3,5-tris(4-Hydroxyphenyl)-4-propyl-1H-pyrazole (PPT; ERα agonist), 1
mg/kg Diarylpropionitrile (DPN; ERβ agonist), 50 μg/kg bisphenol-A (a synthetic EAC),
or 10 mg/kg equol (an organic EAC) daily for 4 days beginning on the day of
birth. The DPN and equol treated males displayed higher anxiety and aggression
levels compared to the oil treated controls. Anabolic steroids have been shown
to increase aggression and anxiety by altering vasopressin (AVP) and serotonin
(5-HT) content in the anterior hypothalamus (AH). To see if this same trend was
present in the EAC treated neonates, immunocytochemistry and confocal
microscopy were used to quantify AVP and 5-HT fibers in the AH. No significant
treatment effect was observed. To broadly explore where in the brain EACs might
have produced an effect, brain sections containing the amygdala were
immunostained for Fos, a common marker of neuronal
activity. The DPN and PPT treated males had a lower density of Fos staining in the amygdala compared to the controls.
Future studies will investigate ERα and ERβ receptor density in the
hypothalamus.
|
Hahn,
Lauren E. |
|
|
Home Institution: |
NCSU |
|
Program: |
Howard Hughes Research Scholars (HHRS) |
|
College: |
CALS |
|
Department(s): |
Zoology Genetics |
|
Research |
Susan T. Harbison/Genetics
Trudy F. C.
Mackay/Genetics |
|
Title of Presentation: |
Effects of Interactions
between Genetic Backgrounds and Calreticulin
on Sleep in Drosophila melanogaster |
Although well studied, the biological importance of
sleep remains a mystery. One possibility is that large numbers of genes with
a wide range of functions affect sleep behavior. Large numbers of genes
increase the possibility of genetic interactions. The results of recent
studies imply that genetic interactions mitigate the effects of mutations on
sleep. However, no attempt has been made to quantify background effects
or identify candidate genes contributing to these effects. Here we used
mutations in a gene previously shown to limit sleep duration to quantify
background effects. Calreticulin
has proposed roles in neural development, protein folding, and calcium
signaling and homeostasis. We measured sleep phenotypes in lines of flies
bearing a mutation in Calreticulin
but having different genetic backgrounds. Each mutant Calreticulin line has a corresponding
control line with a wild-type Calreticulin
allele in the same genetic background. Analysis of the first 12 lines
screened shows that Calreticulin
impacts sleep duration, but not necessarily in the expected direction.
Five of the lines showed significant increases in sleep duration, while three
lines had significantly reduced sleep. We also observed differences in
sleep consolidation (bout number)and waking
activity. Our preliminary results indicate that genetic interactions
between the background and Calreticulin
are present and that they are sex-specific. Further work will determine
the number and identity of candidate genes that enhance or suppress the effects
of Calreticulin on sleep.
|
Muhirwa, Nyira Lucy |
|
|
Home Institution: |
NCSU |
|
Program: |
Howard Hughes Research Scholars (HHRS) |
|
College: |
CALS |
|
Department(s): |
Genetics |
|
Research |
Patricia
Estes/Genetics |
|
Title of Presentation: |
The
Effect of the Notch Signaling Pathway on Gene Expression in Glia and Neurons
within the Drosophila CNS Midline |
To understand how cells of the nervous system are generated during development,
we are studying midline cells of the Drosophila central nervous system (CNS). For
these studies, we focus on the transcriptional control of wrapper, a gene
expressed in midline glia. The regulatory sequences responsible for the
expression of wrapper in midline glia are known, providing a tool for the study
of transcription factors that regulate midline gene expression. Through
examining the transcription factor, Suppressor of Hairless (SuH), within
specific reporter genes, its capability to alter neuron and glia expression was
observed. Previous studies in many organisms, have demonstrated the importance
of the Notch signaling pathway in CNS development. To determine if and how the
Notch signaling pathway impacts gene expression in the Drosophila embryonic
CNS, we are testing the effect of ectopic expression of two components of the Notch
signaling pathway: 1) activated Notch and 2) the transcription factor,
Suppressor of Hairless (SuH), on both the endogenous wrapper gene and wrapper
reporter genes. The results indicate that both components can cause the
expression of wrapper reporter genes, but not of the endogenous gene, to be
inappropriately activated in midline neurons. These results suggest that the
Notch pathway functions to repress midline glial genes in midline neurons, but
that other factors must be present to function together with the Notch pathway
to restrict genes to the midline glia.
|
Pareja,
Rebecca L. Hill,
Mindy M. |
|
|
Home Institution: |
NCSU |
|
Program: |
Howard Hughes Research Scholars (HHRS) |
|
College: |
CALS |
|
Department(s): |
Biological Sciences |
|
Research |
Heather B.
Patisaul/Zoology |
|
Title of Presentation: |
What Is the Effect of
Neonatal Endocrine Disrupting Compound Exposure on Male Behavior? |
Hormones influence male behavior,
including anxiety and aggression. Although testosterone is widely accepted to
be the major hormone involved with male-typical behavior, estrogen is critical
for masculinizing the brain during development.
There are two different estrogen receptors, ERα and ERβ;
ERα is thought to be the most important for masculinizing the brain. Endocrine disrupting compounds (EDCs) can
disrupt estrogen action in the brain, and therefore have the potential to alter
male behavior. To test this hypothesis,
male neonatal rats were injected daily for 4 days beginning on the day of birth
with sesame oil (0.05 mL), the ERa agonist propyl-pyrazole-triol (PPT, 1 mg/kg bw), or bisphenol-A (BPA, 50 mg/kg bw or 50 mg/kg bw). BPA
is a chemical used in the manufacturing of plastics and is found in certain
food product consumed by humans. The
animals were first tested for anxiety using the elevated plus maze test and the
light/dark box test. Results yielded no
significant change in anxiety in any of the treatment groups. The animals were then tested for aggression
using the resident/intruder paradigm.
Results of this test revealed a dosage-dependent increase in the BPA
treatment group for aggressive behavior. We next sought to determine if
elevated aggression was associated with increased neural activity in the
hypothalamus by immunolabeling the protein FOS.
No significant differences among the groups in the amygdala, lateral
septum, and bed nucleus of the stria terminalis were observed. In summary, there was an increase in
aggression in the group treated with the higher dose of BPA. Future research will investigate the
mechanistic processes and neural interactions through which BPA increased
aggression.
|
Williams,
Stephanie N. |
|
|
Home Institution: |
NCSU |
|
Program: |
Howard Hughes Research Scholars (HHRS) |
|
College: |
CALS |
|
Department(s): |
Genetics |
|
Research |
Laura K. Reed/Genetics Greg Gibson/Genetics |
|
Title of Presentation: |
Drosophila as a Model for Metabolic
Syndrome: Natural Variation for Genotype by Environment Interaction Underlying
Hemolymph Sugar Concentrations |
Although the general public
may not immediately recognize the term “Metabolic Syndrome” (MetS), they are
very familiar with the host of symptoms that it incorporates, such as insulin
resistance, high blood pressure, and central obesity. It is also highly
predictive of developing Type-II Diabetes and Cardiovascular Disease. Because
MetS incorporates a variety of symptoms, each with intricate pathways that are
influenced by a high calorie diet and low activity level, it is a highly
complex phenotype that has become particularly prevalent in westernized
societies. The purpose of this project is to elucidate the natural
variation observed in the genotype by environment (GxE) interaction that
underlies the development of MetS. This variation has been hidden by
environmental conditions during human evolution and therefore not selected
against. However, humans serve as a poor system in which to study MetS
because diet and genotype cannot be controlled for. Therefore, Drosophila
melanogaster was chosen as the system in which to study MetS. Like
Humans, Drosophila regulate sugar levels in their
hemolymph via insulin signaling. Furthermore, any cryptic genetic variation
underlying MetS-like symptoms is likely to be present in Drosophila and will be
exposed with diet perturbation. I used 150 inbred isofemale lines of homozygous
individuals of Drosophila melanogaster, raised them on four different caloric
diets (“Normal”, “Control”, “High Sugar” and “High Fat”), and to measure the
GxE effect on sugar concentration in their hemolymph. I exposed the cryptic
genetic variation in glucose levels present in this population of
Drosophila. From my data, I found significant Genotype (p=0.001),
Environmental (p=0.0125), and GxE (p=0.0001) interactions. Furthermore,
the genetic variation I observed supports the theory that MetS is due to
cryptic genetic variation exposed by an environmental shift.
[ Undergraduate Summer
Research Symposium Main Page ]
[ Agenda | Frequently Asked Questions
| Format Requirements
]
[ Summer Programs | Sponsors ]
[ Participant Listing
| Abstracts ]
Last modified June 2008 by Sharon E. Hunt