Basic HTML Version
Poster Full Abstracts - Evolution and Quantitative Genetics
Poster board number is above title. The first author is the presenter
262
pericentric heterochromatin using cytological methods. The molecular relationship between
Rsp
repeat number and segregation distortion is not understood.
Recently, RNAi has been implicated in Drosophila meiotic drive systems, including
SD
. Small RNAs corresponding to
Rsp
repeats are found in both female
and male flies, consistent with the involvement of RNAi in
SD
. We present a bioinformatics study with two objectives: 1) To study the evolution of the
Rsp
satellite; and 2) to determine whether the small RNAs corresponding to
Rsp
are consistent with their involvement in
SD
. To study the evolution of the
Rsp
satellite, we surveyed the
D. melanogaster
genome assembly and BAC sequences, and other Drosophila species genome assemblies for
Rsp
repeats. We
found several
Rsp
-like repeat families on all major chromosome arms in
D. melanogaster
. Although components of the
SD
system are assumed to be specific
to
D. melanogaster
, we find
Rsp
-like repeats in other Drosophila species, however their relative ages are unclear. To determine whether small
Rsp
RNAs
correspond to the
Rsp
repeats on chromosome
2
targeted by
SD
, we mapped small RNAs to their respective genomic locations.
486C
Experimental study of evolutionary conflict between the mitochondrial and nuclear genomes.
Aimee J. Littleton
1
, Maulik R. Patel
1
, Ganeshkumar
Miriyala
1
, Ala Soofian
1
, Harmit S. Malik
1,2
. 1) Basic Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA; 2) Howard Hughes Medical
Institute, Seattle, WA.
The eukaryotic cell is a product of symbiosis between an ancient protobacteria and the mitochondria. Despite being one of the most successful
relationships in evolution, it is also rife with conflict. The nuclear DNA is transmitted through both parents, whereas the mitochondria possess their own
genome (mtDNA) that is maternally transmitted. Since males are an evolutionary dead-end, mtDNA is predicted to skew the sex ratio of a population in
favor of having more females. While this appears to be true in plants, it is unknown whether animal mitochondrial genomes can similarly act selfishly. We
are currently conducting experimental evolution in Drosophila melanogaster to test whether the mitochondrial genome can be artificially selected to increase
fitness of females at the expense of male fitness. We are doing this by crossing daughters from every generation to naïve males over the span of fifty
generations. Mating the females to naïve males every generation allows the mitochondrial genome to evolve independent of the nuclear genome. As a
control we are coevolving females with males. Every ten generations we are conducting a series of fitness assays to detect any phenotypic changes. This
includes counting female to male ratios of the progeny and eggs laid by the evolved females. We are also measuring male and female fecundity. Here I will
present the current status of this experimental evolution including preliminary results suggesting skewed male-female fitness in at least one of the replicate
lines.
487A
Sex-specific embryonic expression at different stages of sex chromosome evolution.
Susan E. Lott
1
, Jacqueline E. Villalta
2
, Doris Bachtrog
3
, Michael B.
Eisen
1,2,3
. 1) Molecular and Cell Biology, Univ California, Berkeley, CA; 2) Howard Hughes Medical Institute, Univ California, Berkeley, CA; 3)
Department of Integrative Biology, Univ California, Berkeley, CA.
Sex chromosome dosage differences between males and females are a major form of natural genetic variation in many species. In
Drosophila
, females
have two X chromosomes, while males have one X and one Y. Several fusions of sex chromosomes with autosomes have occurred along the branches
leading to
D. pseudoobscura
and
D. miranda
. The resulting neo-X chromosomes are gradually acquiring the properties of classical sex chromosomes, and
becoming targets for the complex molecular mechanisms that have evolved to compensate for the differences in X chromosome dose between sexes. We
have recently shown that
D. melanogaster
possess at least two mechanisms for dosage compensation: the well-characterized MSL-mediated dosage
compensation active in most somatic tissues, and a second mechanism during early embryogenesis. To better understand the evolutionary constraints on sex
chromosome expression and evolution, we have used single embryo mRNA-seq to characterize gene expression in female and male embryos of
D.
pseudoobscura
and
D. miranda
, from ~0.5-8 hours of development. Examining expression from these X chromosomes throughout embryonic development,
we observe a relationship between the age of the X chromosome and the number of genes that are compensated. We also characterize what kinds of genes
and processes are more likely to be compensated or have their expression level more constrained, at various stages in embryonic development, which we can
then use to test whether expression constraint is predictive of fitness consequences.
488B
Is the Drosophila X chromosome demasculinized?
Colin D. Meiklejohn, Daven C. Presgraves. Dept Biol, Univ Rochester, Rochester, NY.
Male biased genes— those expressed at higher levels in males than in females— are underrepresented on the X chromosome of Drosophila melanogaster.
Several evolutionary models have been posited to explain this so-called demasculinization of the X. Here we show that the apparent paucity of male-biased
genes on the X chromosome occurs for a simple developmental reason and thus requires no special evolutionary explanation. As most sex-biased genes in
Drosophila involve those expressed in the germline, we studied the chromosomal distribution of genes whose expression was measured using RNA-seq and
microarrays from adult testes, ovaries, and somatic tissues. We find, first, that the underrepresentation of testes-biased genes on the X disappears once the
lack of dosage compensation in the Drosophila male germline is accounted for. Second, we find that computationally demasculinizing the autosomes is not
sufficient to produce an expression profile similar to that of the X chromosome in the testes, whereas correcting for the lack of dosage compensation in testes
does. These findings show that the lack of sex chromosome dosage compensation in the testes can explain the apparent demasculinization of the X, whereas
any evolutionary demasculinization of the X cannot explain its reduced expression in the testes.
489C
Adaptive Evolution and the Birth of CTCF binding events in the Drosophila genomes.
Xiaochun Ni
1,2
, Yong Zhang
1
, Nicolas Negre
2,3
, Sidi Chen
1
,
Manyuan Long
1
, Kevin White
1,2,3
. 1) Department of Ecology & Evolution, University of Chicago, Chicago, IL; 2) Institute for Genomics and Systems
Biology, University of Chicago , Chicago, IL; 3) Department of Human Genetics, University of Chicago, Chicago, IL.
Changes in the physical interaction between cis-regulatory DNA sequences and proteins drive the evolution of gene expression. However, it has proven
difficult to accurately quantify evolutionary rates of such binding change, or to estimate the relative effects of selection and drift in shaping the binding
evolution. Here we examine the genome-wide binding of CTCF in four species of Drosophila separated by between ~2.5 and 25 million years. CTCF is a
highly conserved protein known to be associated with insulator sequences in the genomes of human and Drosophila. Although the binding preference for
CTCF is highly conserved, we find that CTCF binding itself is highly dynamic and has adaptively evolved. Between species binding divergence increased