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Poster Full Abstracts - Evolution and Quantitative Genetics
Poster board number is above title. The first author is the presenter
266
some are statistical (e.g. appropriate models for allele specific expression). Without proper consideration of all three sets of challenges bioinformatic,
technical and statistical, inferences may be misleading. This presentation focuses on steps for dealing with these challenges that reduce or eliminate some of
these concerns.
501C
Male-specific effects of mitochondrial-nuclear genetic interactions.
Katelyn Mika, Sonya Joseph, Kristi Montooth. Biology, Indiana University,
Bloomington, IN.
Over time, the majority of the original mitochondrial genome has migrated to the nuclear genome, but mtDNA still harbor genes specific to their metabolic
function. Because of this, efficient oxidative metabolism in the mitochondria relies on interactions between protein products from both the nuclear and
mitochondrial genomes. If mitochondrial and nuclear genomes co-evolve, then mitochondrial-nuclear incompatibilities are predicted to result when
divergent genomes are brought together. Montooth et al. (2010) have shown that a particular incompatibility between a nuclear genetic variant in
Drosophila
melanogaster
and a mitochondrial variant in
D. simulans
affects female fitness and line productivity. We have since shown that this mitochondrial-nuclear
incompatibility lengthens development time by approximately three days and decreases female fecundity by 50%. To test for effects of genetic interactions
(or intergenomic epistasis) between the mitochondrial and nuclear genomes on male fertility in Drosophila, we mated males of each of 12 mitochondrial-
nuclear genotypes with virgin females of a common genotype and counted the offspring produced. We did not find strong epistatic effects on male fertility.
Rather we found strong main effects of mitochondrial genotype on male fertility. While mitochondrial-nuclear genotypes have defects in developmental
timing, female fecundity and male fertility, remarkably we find no adverse effects on adult metabolic rate. We hypothesize that there may be strong
homeostasis driving a set maintenance metabolic rate. For flies with compromised mitochondrial function, running this maintenance metabolic rate may
result in resource allocation tradeoffs that compromise reproductive fitness. In our set of mitochondrial-nuclear genotypes there is evidence for both shared
and distinct outcomes of this tradeoff across the sexes.
Montooth KL, Meiklejohn CD, Abt DN, and Rand. 2010. Evolution 64: 3364-3379.
502A
The how of the Y: Direct versus indirect effects of heterospecific Y chromosomes on gene expression in Drosophila.
Timothy Sackton, Daniel Hartl.
Organismic & Evol Bio, Harvard Univ, Cambridge, MA.
The Drosophila Y chromosome is a degenerated, heterochromatic chromosome with few functional genes. Nevertheless, we have recently shown that
disruption of conspecific Y/autosome and Y/X interactions via interspecifc Y chromosome introgressions in Drosophila leads to significant effects on gene
expression and male reproductive fitness. In particular,
D. simulans
lines carrying a
D. sechellia
Y chromosome have reduced expression of testis-specific
genes, reduced lifetime fecundity, and reduced sperm competitive ability. These results imply a significant role for Y/X and Y/autosome interactions in
maintaining proper expression of male-specific genes, but do not distinguish between direct effects on gene expression or indirect effects mediated by
heterospecific Y chromosomes on male reproductive tissue development or function. To identify direct Y interactions and test the role of indirect effects on
the gene expression, we used RNA-seq to estimate allele-specific expression in
D. simulans
/
D. sechellia
hybrids carrying either a
D. simulans
or a
D.
sechellia
Y chromosome. Allele-specific expression in F1s allows us to estimate the relative proportion of
trans
and
cis
effects of Y regulatory divergence
and infer the relative proportions of direct interactions, allele-specific chromatin modifications, and downstream effects.
503B
Mitochondrial-nuclear incompatibilities are worse when temperature accelerates the rate of life.
Mohammad Siddiq, Luke Hoekstra, Kristi Montooth.
Biology, Indiana University, Bloomington, IN.
An efficient and coordinated metabolism is essential for an organism's ability to develop and respond to environmental conditions. We are using
Drosophila
strains that pair divergent mitochondrial and nuclear genomes to explore how unique mitochondrial-nuclear genotypes affect metabolism and
life-history. Previously, we identified an incompatibility between
D. melanogaster
nuclear genomes and
D. simulans
mitochondrial genomes that
significantly impacts fitness. Mapping the genetic basis in collaboration with Colin Meiklejohn (Univ of Rochester) and David Rand (Brown Univ) reveals
that this incompatibility likely arises through compromised mitochondrial protein translation. Here we demonstrate that the phenotypic effects of this
mitochondrial-nuclear incompatibility are conditional on environmental temperature. Using flow-through respirometry to measure larval metabolic rate, we
find that mitochondrial-nuclear genotype significantly affects the ability of larval metabolic rate to acclimate to the thermal environment. Development time
and pupation height, both of which are traits potentially associated with energetics, are also significantly affected by interactions between mitochondrial-
nuclear genotype and developmental temperature. We find that the deleterious effect of mitochondrial-nuclear incompatibility increases with temperature,
but there is also evidence that developmental plasticity provides homeostasis for metabolic rate. Together these results demonstrate thermodynamic
constraint on performance
via
energy limitation, such that inefficiencies in metabolic processes are revealed when temperature accelerates the rate of life.
504C
Zinc finger proteins and the distribution of meiotic recombination events.
Caiti Smukowski, Mohamed Noor. Duke University, Durham , NC.
The discovery of a 13-mer degenerate motif that recruits recombination events in the majority of human hotspots significantly advanced the study of
meiotic recombination initiation. This motif binds to the Cys
2
His
2
zinc finger (ZNF) protein PRDM9 in humans, and allelic variation in the protein affects
hotspot activity in humans and mice. While transcription factors have long been recognized for their required role in yeast hotspots, the discovery of
Prdm9
is the first implication of ZNF proteins and sequence motifs as major determinants of hotspot location and usage in an animal. Recent findings on the ZNF
protein
Trade Embargo
in
Drosophila melanogaster
recombination initiation further suggest a general role for ZNF proteins in the process of recombination.
Using BLAST, several ZNF protein motif prediction programs, and other bioinformatic analyses, we identified all ZNF-protein-binding sequence motifs in
D. melanogaster
and
D. pseudoobscura
and tested for significant associations with regions of high and low recombination. We failed to find any ZNF motifs
predictive of recombination rate. Hence, based on these results, we see no evidence that zinc finger proteins affect crossover rate variation within Drosophila
genomes. We consider several limitations with our bioinformatic approach, but it is likely that other factors besides ZNF protein binding play a dominant
role in the determination of regional recombination rates. These results could even suggest that Drosophila possess a unique recombination initiation system