37th Annual Graduate Student Symposium

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37th Annual
Graduate Student Symposium
February 11, 2013
Stanley G. Stephens Room
3503 Thomas Hall
The Genetics Graduate Students Association
welcomes you to their
37th Annual Graduate Student Symposium
9:45 a.m.
Opening Remarks
Dr. Stephanie E. Curtis
Director of Graduate Program
Session I
10:00 a.m.
10:15 a.m.
10:30 a.m.
10:45 a.m.
Moderator: Lauren Dembeck
Jessica Nye
Bill Barrington
Emily Moore
Steven Vensko
11:00 a.m.
Coffee Break
Session II
11:15 a.m.
11:30 a.m.
11:45 a.m.
Moderator: Becky Edman
Tiffany Garbutt
Bhupinder Sehra
Megan Garlapow
12:00 p.m.
Lunch
Continued on Next Page
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Session III
1:00 p.m.
1:15 p.m.
1:30 p.m.
1:45 p.m.
2:00 p.m.
Moderator: April Wynn
John Shorter
Richard Gell
Lauren Dembeck
Chad Hunter
Hayley Crockett
2:15 p.m.
Break
Session IV
2:30 p.m.
2:45 p.m.
3:00 p.m.
3:15 p.m.
3:30 p.m.
Moderator: Randi Wheatley
Matt Robinson
Kate Coyle
Shante Bryant
Katherine Knudsen
Sarah Cash
4:30 p.m.
Presentation of Department of Genetics Awards
East Village, Hillsborough Street
Outstanding Teaching Apprentice Awards
Dr. Stephanie Curtis
Dr. Ted Emigh
Presentation of the Department of Genetics
Outstanding Presentation Speaker Awards
Dr. David Threadgill
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Genetic Variation of Heart Rate in Drosophila
Jessica Nye
Advisor: Trudy Mackay
Cardiovascular disease is the leading cause of death in the world and claims a life every thirtynine seconds in the United States. The heritability of cardiovascular disease in humans is currently estimated between 38% and 66%. While this disease has a high genetic component, other
factors are known to impact its prevalence such as environment, diet, exercise, and personality
characteristics. All these confounding factors make determining the genetic basis of variation in
susceptibility to cardiovascular disease difficult in humans. Drosophila is the only invertebrate
model organism with a pumping heart developmentally homologous to that of a vertebrate. By
combining the advantages of the invertebrate model system with evolutionary conservation of
basic biological processes between Drosophila and humans, Drosophila can be used to identify
genes homologous to those affecting vertebrate heart rate. The Drosophila Genetic Reference
Panel (DGRP) is a newly created collection of inbred lines derived from a wild population,
and poses a promising model for identifying genes affecting natural variation in heart rate. I
have screened DGRP lines for heart rate variation. Larval heart rate has significant genetic and
phenotypic variation. I have identified 78 candidate genes from a genome-wide association
study to identify the molecular variants associated with heart rate and their human orthologs.
Societal Influences on Disease Susceptibility as Reflected by Diet
Bill Barrington
Advisor: David Threadgill
Colorectal cancer is the second leading cause of cancer-related deaths in the United States. Mouse
models provide a valuable research tool for investigating cancer susceptibility, and have been
used to show that diet plays an important role in the development of colorectal cancer. However,
little is know about how diets interact with genetic background to alter cancer susceptibility. In
my research, I use mouse models on different genetic backgrounds to compare the impact of six
different diets, mimicking popular diets consumed by many individuals today, on susceptibility to developing colorectal cancer. I am using gene expression analysis from mice on different
diets to investigate the relationship between diet, gene expression, and genetic background on
development of colorectal cancer. Additionally, I am examining the impact these diets have on
the mouse gut microbiome, which is emerging as an important mediator of health and disease.
Lastly, I am comparing the effect of diets on a variety of phenotypes such as activity level,
inflammation, and health biomarkers. Ultimately, this research will determine relationships between diet and cancer susceptibility, identify genes involved in cancer susceptibility, and investigate interactions between diet, gut microbiome, and genetic background on cancer susceptibility.
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Impact of a Novel Sex Determination Locus on Regulatory Gene Networks
and Reproductive Fitness in African Cichlid Fish
Emily Moore
Advisor: Reade Roberts
African cichlid fish are an excellent evolutionary model for studying diversity within many phenotypically divergent but closely related species in a natural context. Adaptive radiations within
the African Great Lakes led not only to a variety of morphological and habitat specializations,
but also instances of novel sex determination loci (SDL) which (when present) interact with
ancestral sex determiners to create a polygenic sex determination system. Laboratory families
of Metriaclima pyrsonotus with female (W) and male (Y) SDL will be used to examine gene expression and fitness differences between individuals of four genotypic sexes (XX/ZZ, XX/WZ,
and XY/WZ females; XY/ZZ males). RNA-seq from key time-points in developing gonads will
allow investigation into the gene modules that regulate sex differentiation, and may lead to identification of novel sex determination mechanisms and insight into control of the core vertebrate
sex determination network. Studies of animals with recently evolved, polygenic SDL suggest
higher reproductive fitness in individuals with the newest locus, so relative reproductive fitness
between genotypic classes of M. pyrsonotus will be assessed through gonad histology, egg production, and conspecific, intrasex aggression levels. Preliminary data suggest that females with
the W sex determiner have differential gene expression and produce more eggs; ongoing research
in the Roberts lab is currently addressing behavioral dominance between W and non-W females.
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Understanding the Spread of the Selfish Genetic Element Medea in
Populations of Red Flour Beetles
Sarah Cash
Advisors: Fred Gould and Marcé Lorenzen
Selfish genetic elements spread by causing their own inheritance in more than the fifty percent of a heterozygous individual’s offspring expected under Mendelian inheritance. One such
element, called Medea, is found in some populations of the red flour beetle (Tribolium castaneum), and it increases in frequency by killing off any offspring of a Medea-carrying mother
that do not inherit Medea. While models make predictions about how the element should spread
in natural populations, no prior empirical studies had been performed to test these models in
the lab or field. We have addressed an assumption of these models by demonstrating that a
single copy of a Medea allele inherited by heterozygous offspring is sufficient to compensate
for any potential increase in egg toxicity produced by a homozygous Medea mother. Further,
we have examined how Medea allele frequency changes over time within a single lab population. To assess the field-level dynamics of Medea, red flour beetles were collected from populations across the United States, and Medea-1 genotyping is revealing the current distribution
of this element. Future research will focus on examining what factors are responsible for the
contemporary Medea distributions by testing whether Medea distribution and Tribolium castaneum population structure are reflective of one another, and whether the genetic backgrounds
of wild Tribolium populations influence the spread of Medea elements. Uncovering how selfish genetic elements like Medea spread and maintain themselves within populations—and ultimately, species—is critical for expanding our overall understanding of evolutionary biology.
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Identification and Characterization of Seminal Fluid Proteins in
Monogamous and Promiscuous Vole Species
Katherine Knudsen
Advisor: Lisa McGraw
A long-standing question in evolutionary biology lies in how mating systems evolve. Prairie
voles (Microtus ochrogaster) are unique among mammals in that they are socially monogamous and sexual partners often form long-term pair bonds. To the contrary, the closely related
meadow vole (Microtus pennsylvanicus) is promiscuous. Studies in a variety of taxa suggest
that seminal fluid proteins (SFPs) may play an important role in the evolution of mating systems. For example, in Drosophila, SFPs have been shown to have numerous effects on female
mating behavior including increasing ovulation rate and egg-laying and decreasing female receptivity to mating with other males. Some SFPs have been shown to have toxic effects in the
female, including decreasing her lifespan. While several studies have identified SFPs in mouse
(Mus musculus) and rat (Rattus norvegicus), the contribution of SFPs to mating system evolution and how they might influence the female’s behavior has been largely unexplored. I plan to
utilize the vole models to identify and characterize SFPs in a monogamous and promiscuous
species to begin to understand the contribution of these proteins to mammalian mating system
evolution. By identifying and characterizing the SFP profiles in the prairie vole and meadow
vole, I will be able to exploit these model organisms for study of reproductive behavior physiology and begin to understand how the evolution of reproductive traits relates to mating system
evolution. Given that most SFP studies have been performed in insects, this research will provide a deeper understanding of the effects of SFPs on female mating behavior in mammals.
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Reassessment of the Contributions by Dosage Compensation to the
Demasculinization of the Drosophila melanogaster X Chromosome
Steven Vensko
Advisor: Eric Stone
The forces believed to shape the Drosophila melanogaster X chromosome, including dosage compensation, meiotic sex chromosome inactivation and sexual antagonism, are not well
understood and remain a controversial subject. Improved models of these forces allow for a
better understanding of Drosophila sex chromosome evolution. Recent research suggests the
mechanism which equalizes X-linked gene expression between the heterogametic Drosophila
males and homogametic Drosophila females through two-fold upregulation of expression in
males, X-linked dosage compensation, creates a disadvantageous environment for male-biased
expressed genes. It has been proposed that this unfavorable environment has contributed to
an enrichment of X chromosome -> Autosome retrotransposition events, a deficit of X-linked
male-biased expressed genes near dosage compensated regions of the X chromosome, and a
significant positive correlation between the degree of male-bias and distance from dosage compensated regions on the X chromosome. Other research provides conflicting yet indirect evidence of dosage compensation having neutral or beneficial effects on X-linked male-biased
expressed genes. We utilized publicly available datasets to reconsider the effects of dosage
compensation on X-linked male-biased expressed genes. Our results do not corroborate previous claims of detrimental effects by dosage compensation on male-biased expressed genes
and instead provide examples directly contradicting current theory. We find no evidence that
dosage compensation has detrimental effects on male-biased expressed genes, suggesting
it has neither played a role in the enrichment of X chromosome -> Autosome retrotransposition events nor shaped the distribution of male-biased expressed genes on the X chromosome.
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Identifying the Genetic Cause of the NOD and WSB iPSC Phenotype
Tiffany Garbutt
Advisor: David Threadgill
Mouse embryonic stem cells (mESCs) are a useful molecular research tool due to their undifferentiated, proliferative state. Induced pluripotent stem cells (iPSCs) are artificially derived stem cells generated through somatic reprogramming and are an attractive alternative to mESCs. However, non-permissive mouse strains cannot form mESCs or iPSCs under
standard conditions for unknown genetic reasons. We have generated fibroblast-derived iPSCs from six of the eight parental strains of the Collaborative Cross Mouse Genetic Reference Population. The two remaining strains, NOD and WSB fail to produce stable iPSCs and
form developmentally primed epiblast stem cell (EpiSC)-like colonies in response to somatic
fibroblast reprogramming. We are investigating the genetic mechanism and inheritance pattern
governing the EpiSC-like iPSC phenotype and will identify candidate gene(s) through genetic
mapping. Candidate gene(s) will be functionally tested using a targeting vector with a docking site for overexpression and knockdown experiments. This research will provide insights
into the genetic networks controlling pluripotency identity and successful iPSC generation.
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Genetic Analysis of a Post-infectious Model of Irritable Bowel Syndrome
Shante Bryant
Advisor: David Threadgill
Irritable bowel syndrome (IBS) is one of the most predominant functional bowel disorders
affecting approximately 20% of the population in the developed world and 7-10% of people
worldwide. Quality of life for patients suffering from IBS can be greatly reduced by symptoms such as changes in bowel habits, abdominal pain and bloating, cramping, flatulence, and
passage of mucus. The etiology of IBS is likely to be multi-factorial; environmental factors,
genetics, variation in gut flora, nervous system alterations, dysfunction of the brain-gut axis,
and psychosocial stressors have all been examined and are thought to contribute to the development of the disorder. Treatment options vary tremendously and are generally aimed at treating symptoms individually and not at addressing IBS as a physiopathological entity. A major
limitation to understanding the development of IBS and creating more effective treatment options is the absence of a valid animal model. Existing animal models can be categorized as
either post-inflammatory or post-infectious. We plan to develop an appropriate mouse model
in which symptoms of human IBS can be replicated and examined collectively by comparing three post-infectious models for their ability to induce two major problematic symptoms
that IBS patients experience, intestinal motility dysfunction and visceral hypersensitivity.
The infectious agents to be examined include Trichnella spiralis (pathogenic worm), Cryptosporidium parvum (infectious protozoan species), and Citrobacter rodentium (gram-negative
bacterium). Once a model is selected, we will identify casual genetic links that contribute
to the development of IBS symptoms using the Collaborative Cross genetic reference panel.
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Evolution of Sex-determining Loci and Associated Traits in
African Cichlid Fishes
Kate Coyle
Advisor: Reade Roberts
Several species of East African cichlid fishes display sexually dimorphic “blotched” pigmentation patterns that confer an adaptive advantage to females by making them less conspicuous
to predators, but males with a similar pattern suffer in their ability to attract a mate. Selection
has caused linkage of the pigmentation allele to a sex-determining locus, ensuring that only
females inherit this trait. Previous research has mapped Lake Malawi blotched morphs to the
paired-box transcription factor gene Pax7, located on chromosome 5 at a W female-determining
locus. Another nearby lake, Lake Victoria, contains cichlids displaying similar female-specific
blotched morphs that appear to have evolved in parallel. An association study has indicated
two candidate genes for similar blotched morphs on chromosome 14 in Lake Victoria cichlids; Pax3, from the same family as Pax7, and Epha4, an ephrin receptor gene that may play a
part in migration of dark-colored melanophores during development. We will use a q-RTPCR
expression assay to determine if there is a significant change in transcribed levels of Pax3 or
Epha4 between fin tissue from blotched and plain individuals. Additionally, we will use nextgeneration sequencing of several species carrying these blotch/sex loci to look for hallmarks
of sex chromosome evolution such as lack of recombination and proliferation of tandem repeats. The assembled sequences will also serve as powerful tools for elucidating the evolutionary
history of sex chromosomes by showing signatures of selective sweeps, inversions, and other
genetic rearrangements that have caused Pax7 to remain tightly connected to this sex locus.
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Identifying cis-regulatory Elements Involved in Ovule Formation in
Arabidopsis thaliana
Bhupinder Sehra
Advisor: Bob Franks
In Arabidopsis thaliana the gynoecium (seed pod) contains the Carpel Margin Meristem (CMM),
which gives rise to the ovules and is essential for plant reproduction. Mutations in the transcriptional regulators SEUSS (SEU) and AINTEGUMENTA (ANT) display a synergistic phenotypic
enhancement within the gynoecium. The seu ant double mutants show loss of ovules and disruption of other CMM derived structures, while single mutants display only mild phenotypes.
Transcriptomics and qRT-PCR revealed candidate genes thought to be downstream targets of
SEU and ANT. In-situ hybridization showed several transcripts to be preferentially expressed in
the developing CMM, including members of the REPRODUCTIVE MERISTEMS (REM) family,
PERIANTHA, PHABULOSA, LEAFY and GROWTH REGULATING FACTOR 5, which are transcription regulators. In addition, TRYPTOPHAN AMINOTRANSFERASE OF ARABIDOPSIS 1
(TAA1) and SHATTERPROOF2 (SHP2) have been also been identified as genes that are likely
important for ovule development. Promoter analysis of these genes using computational and
experimental approaches identified cis-regulatory elements that contribute to gene expression in
the CMM. A REM15:GUS reporter construct revealed a region of putative elements spanning
1.1kb upstream of the transcription start site, thought to be required for expression during late
ovule development. Conserved sequences and putative motifs were discovered in this region, by
aligning orthologs in several Brassicacaeae species and via de novo motif finding. Computational
approaches in analyzing the promoter, intronic and downstream regions of PAN, TAA1, SHP2 and
REM15 have identified several areas of putative regulatory elements that may be responsible for
gene expression and these regions will be tested in-planta. Identifying cis-regulatory elements important for gene expression during ovule development will allow us to understand the regulatory
mechanisms of CMM development and the transcriptional hierarchy controlled by SEU and ANT.
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Comparative Genetics of Food Consumption
Megan Garlapow
Advisors: Trudy Mackay and David Threadgill
Consumption of excessive calories associates with an increased incidence of type 2 diabetes,
obesity, cardiovascular disease, and other disorders and diseases. To examine genetic variation and evolutionary conservation of food consumption, we will use a comparative approach
consisting of the 192 sequenced lines of the Drosophila Genetic Reference Panel (DGRP) and
available data on Mus musculus. Food consumption ad lib in 164 lines of the DGRP has shown
significant differences among the lines, between the sexes, and in line-by-sex interactions. Preliminary analyses of predicted significant genes from correlating phenotype with single nucleotide polymorphisms analyzed via DavID indicate an Epidermal Growth Factor (EGF) signaling pathway enrichment of 43%. The role of EGF signaling in control of invertebrate food
consumption remains largely unexplored. Correlatively, perturbed M. musculus EGF signaling associates with differences in volume of food consumed, supporting the evolutionary hypothesis that the primary controls of volume of food consumed are conserved across divergent
species. Our two model organisms are likely to reveal ways in which food consumption is
controlled by EGF signaling and genetics that would not be known using just one of the systems and will reveal ways in which overall food consumption is conserved between divergent
species. Conserved genetic elements in both D. melanogaster and M. musculus are more likely
to be conserved in humans. Validation experiments in both organisms will improve understanding of the components of the EGF signaling cascade that function to affect food consumption.
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Maintaining Flexibility: Recombination Rate in a
Fluctuating Environment
Matthew Robinson
Advisor: Nadia Singh
Meiotic recombination is a critical factor in the generation and maintenance of genetic variation.
Genetic variation is the substrate of the evolutionary process, and it has been suggested that the
more genetic variation that exists in a natural population, the greater the potential for adaptation.
It has therefore been hypothesized that fluctuating environments should favor increased recombination rate, as the increased adaptive potential provided by increased recombination rate has a
greater fitness benefit in the context of a dynamic adaptive landscape. Here we test this hypothesis directly using D. melanogaster as an experimental model system. For this experiment, we
exploited laboratory populations of D. melanogaster that had been maintained for three years in
one of three thermal environments: 16 oC, 25 oC, or fluctuating temperature (alternating 16 and
25oC every generation). We used a two-step crossing scheme using the visible markers ebony and
rough to measure the recombination rate of chromosome 3 as a proxy for genomic recombination
rate. We measured recombination rate at 16o, 25o and at 20.5o, the midpoint between the two
extremes of the laboratory selection process. The results obtained from this experiment will help
shed light on the evolution of recombination rate in general, and in particular will allow us to test
whether increased recombination rate is favored within fluctuating environments. Given that we
are measuring recombination rate at a variety of temperatures, our results will also illuminate the
degree to which recombination rates are plastic as a function of temperature. Particularly exciting
is our ability to glean insight into the evolution of phenotypic plasticity in recombination rate, as
one might predict that fluctuating environments should also favor increased phenotypic plasticity.
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Do Males Matter?
Exploring Male-mediated Effects on Female Meiotic Recombination
Chad Hunter
Advisor: Nadia Singh
Meiotic recombination is a critical genetic process as well as a driving evolutionary force.
Rates of crossing-over are highly variable within and between species due to both genetic and
environmental factors. Early studies in Drosophila implicated female genetic background as a
major determinant of recombination rate and recent work has highlighted male genetic background as a possible mediator as well. This latter result is puzzling since Drosophila males do
not undergo meiotic recombination. We used classical genetics to address the question of how
maternal and paternal genetic background affect crossover rate. We devised a two-step crossing
scheme exploiting visible markers to measure rates of crossing over in a 33 cM region of the
D. melanogaster X chromosome. In total, we measured crossover rates daily in females from
ten inbred lines crossed to males from each of the same ten inbred lines over a period of 10
days. Our experimental design facilitates measuring the contributions of maternal age, female
genetic background, male genetic background, and male by female interaction effects on rates
of crossing-over in females. Our results indicate both maternal and paternal genotypes, their
interaction as well as maternal age significantly affect female meiotic crossover rates in Drosophila. This study confirms a previous effect of male genetic background and also is the first
implicating the interaction of male and female genotypes to mediate recombination rate. Our
results have implications for deciphering the molecular and genetic basis of recombination rate
variation in Drosophila.
Creation of a Model to Genetically Engineer Peromyscus maniculatus
Hayley Crockett
Advisor: David Threadgill
Peromyscus maniculatus (Deer mouse) is the most common species of native mice in North
America and a known carrier of Hantavirus and Lyme disease. The aim of the study is to create a method to genetically engineer P. maniculatus to generate resistance to the species acting as a disease vector. To achieve this goal, we require stem cells that can be used for genetic engineering and subsequent re-introduction into the germline. To achieve this we have
derived P. maniculatus induced pluripotent stem (iPS) cells from mouse embryo-derived
fibroblasts via lentiviral induction of four genes coding for transcription factors; Sox2, Oct4,
Myc, and Klf4. The quality of the cells is being examined by karyotype analysis and analysis
of endogenous transcription factor expression. Future research with the iPS cells will involve
the induction of a GFP reporter gene and injection of the engineered cells into blastcysts to
create a chimeric mouse. Once the ability to engineer P. maniculatus is established, mice will
be engineered to be resistant to carrying the disease vectors for Hantavirus and Lyme disease.
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The Genetic Architecture of Aggression in Drosophila melanogaster
John Shorter
Advisor: Trudy Mackay
Most animals display aggressive behavior to secure food resources, protect against predators
and facilitate access to mating partners. Among social animals, appropriately balanced aggressive behavior gives rise to a stable social organization by creating and maintaining dominance
hierarchies. Inappropriate or excessive aggression has detrimental consequences for the individual and a society. Aggressive behavior is genetically complex, influenced by many genes as
well as interactions with the environment. However, the genetic pathways affecting variation in
aggressive behavior are evolutionarily conserved, enabling general inferences to be drawn from
genetic analysis using a model system. We investigated the natural genetic variation of aggression using the Drosophila melanogaster Genetic Reference Panel (DGRP), a collection of 192
inbred lines with fully sequenced genomes. We performed a genome wide association study
(GWAS) and identified 244 SNPs associated with variation in aggression. Additionally, we performed an independent experiment to replicate causal candidate SNPs by creating an outbred
population from lines representing the extremes of the DGRP. We measured aggressive behavior of 3,000 individuals across 7 generations from this outbred population and will perform
QTL mapping to identify loci associated with aggression. We will then compare results between
the outbred population and the DGRP to identify overlap between genes and gene networks that
influence aggression. We will confirm candidates by using RNAi knockdown to reduce gene
expression and quantify its effect on aggression. These experiments will provide insight into the
genetic architecture of aggression and identify novel genetic variants responsible for naturally
occurring variation in this complex trait.
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Classical and Next-Generation Mapping of a Novel Mutant in
Arabidopsis thaliana
Richard Gell
Advisors: José Alonso and Anna Stepanova
Using molecular genetic approaches, we are investigating the function of plant hormones ethylene and auxin in the model species Arabidopsis thaliana. One of the mutants we are studying,
rus1, was isolated as a genetic suppressor of an auxin overproducing mutant sur2. rus1 shows
a characteristic pale reticulated leaf phenotype due to a dramatic reduction in the density of
mesophyll cells. RUS1 gene encodes a plastidic protein of unknown function. To shed light on
the molecular function of RUS1, we performed a suppressor mutagenesis in the rus1 mutant
background and identified a second-site mutation, R6-11F, that reverts the cell density of rus1
to wild-type levels and suppresses leaf paleness. In order to to clone the suppressor gene, we
performed a mapping cross between the rus1 R6-11F double mutant in Columbia background
and rus1 single mutant in the Landsberg erecta background, allowed the F1 plants to self, and
in the F2 generation selected plants with the suppressed (i.e. non-pale) phenotype. PCR-based
in/del markers spanning the five Arabidopsis chromosomes were used to map the mutant to
a 700kb region on the bottom of chromosome 3. In order to identify the mutant locus and the
causal mutation within the mapped interval, we pooled the DNA of 50 F2s and are now deepsequencing the library with the Illumina HiSeq. We will then use next-generation mapping to
call all non-Columbia and non-Ler polymorphisms in the region and to test T-DNA mutants in
the candidate polymorphic loci to identify the causal gene.
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Natural Variation in Cuticular Hydrocarbons in the
Drosophila melanogaster Genetic Reference Panel
Lauren Dembeck
Advisor: Trudy Mackay
Drosophila melanogaster mate choice is strongly influenced by the presence of contact
pheromones, which consist of cuticular hydrocarbons (CHCs), on the insect’s cuticle. Hence,
variation in CHCs can potentially alter mate choice leading to assortative mating and incipient
speciation. We studied natural variation in CHCs using the Drosophila melanogaster Genetic
Reference Panel (DGRP). The DGRP is a panel of inbred lines of D. melanogaster derived
from a Raleigh, NC, natural population. Complete genome sequences are available for the
lines, which enable genome-wide association (GWA) analyses to uncover the genetic basis of
natural variation in CHCs. We collected gas chromatography spectra of female DGRP flies and
quantified relative abundance of CHC components. We identified 60 CHCs in 170 DGRP lines,
including 16 dienes and methyl alkanes that were not previously described. A majority of the
CHCs show significant variation, including 7,11-heptacosadiene and 7,11-nonacosadiene, the
predominant female pheromones. All CHCs show significant among-line variance with univariate analysis of variance except for two x-C25 monoenes and 9,13-C29. Heritabilities ranged
from H2 = 0.98 for 5-C25 to H2 = 0.22 for 7-C29. Future analyses will provide associated loci
and correlations with other phenotypes measured in the DGRP. These results may offer insight
into the link between variation in pheromone composition with mating behavior and incipient
speciation.
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