Arnar Palsson, M.Sc. Ph.D.

apalsson (AT) uchicago.edu

Education and work experiences

2003-2006 Post doctoral fellow, Department of Ecology and Evolution, University of Chicago.

1998-2003 Ph.D. Department of Genetics, North Carolina State University.

1995-1998 M.Sc. Department of Biology, University of Iceland.

1991-1995 B.Sc. Department of Biology, University of Iceland.

Biological questions and projects

The fundamental questions that I have sought to answer up to this point have been on the nature and the mechanistic forces shaping natural variation. Initially I was most curious about the homeostatic properties of ontogenetic systems, which naturally led me to study quantitative genetics. Lately I have developed an interest in the biological determinants of naturally occurring genetic variation, across the multiple dimensions of phenotype, genotype, and ultimately Darwinian fitness.

My thesis work was on the quantitative genetics and evolution of wing shape in flies. The work was initiated by Greg Gibson my advisor at NC State and now the torch is being carried by Ian Dworkin. Through a series of experiments we managed to map a QTL for wing shape down to a nucleotide change in the promoter of the Epidermal growth factor receptor locus in Drosophila melanogaster. The variant disrupts a previously undescribed element in the promoter that shows sequence and architectural similarity to GAGA factor binding sites. Quite impressively, Ian has found this association also in wild caught flies.

The current research, with Martin Kreitman and Misha Ludwig at the University of Chicago, focuses on variation in embryonic features in flies and consists of three main projects. 1) Misha has refined a transgenic system to test whether even-skipped (eve) stripe 2 enhancers from different species can complement an artificially generated deficiency in this regulatory element in D. melanogaster. We designed methods for quantifying the abundance of EVE protein in the embryo which allowed us to demonstrate that strains carrying these genetic constructs showed significant differences in EVE concentration possibly due to dose and species of origin. Most bafflingly, the D. erecta stripe 2 enhancer failed to complement while the more distantly related enhancer from D. pseudoobscura did. (Full description of the quantification methods and Mathematica Scripts are available). 2) Building on this project, I am currently working with Susan Lott, a graduate student in the same lab, to quantify variation in the magnitude, spacing and timing of expression of early developmental genes in D. melanogaster. The aim is to quantify variation in mRNA levels for eve and other early development transcription factors across inbred lines and species in the Drosophila species group. 3) The third project is a characterization of a putative major allele that lacks an otherwise conserved hunchback transcript factor binding site in the eve regulatory region. The deletion removes 72 bp at the 3’ end of an enhancer known to participate in the regulation of stripes 3 and 7 during early embryo development. We are investigating the phenotypic effects of this mutation as well as documenting the pattern of sequence variation in the adjacent DNA.

Future projects include studying the forces shaping the evolution of novel functions using transcriptional activation as a case study. Along with Marty and Casey Bergman I am conducting a comparative study of the population genetics of the orthologous enhancer sequences in multiple closely related Drosophila species. Analyses of such data are bound to reveal the signature of negative selection on both deeply conserved and evolutionarily more recent regulatory sequences. Finally, from this summer on I will start work on the genetics of complex disease in collaboration with researchers at the University of Oxford and deCode genetics.

Publications

1. Tests for the replication of an association between Egfr and natural variation in Drosophila melanogaster wing morphology. 2005 Palsson, A. Dodgson, J. Dworkin, I. and G. Gibson BMC Genetics 2005, 6:44. [Abstract, PDF, Extras]

2. Functional evolution of a cis-regulatory module. 2005 Ludwig, M.Z. Palsson, A. Alekseeva, E. Nathan, J. and M. Kreitman. Plos Biology, 3(4): e93 [Abstract, PDF, Extras]

3. Replication of an Egfr-wing shape association in a wild-caught cohort of Drosophila melanogaster. 2005 Dworkin, I. Palsson, A. and G. Gibson Genetics, 169, 2115-2125, [Abstract, PDF]

4. Association between nucleotide variation in Egfr and wing shape in Drosophila melanogaster 2004 Palsson, A. and G. Gibson. Genetics 167: 1187-1198. [Abstract, PDF, Extras]

5. Nucleotide variation in the Egfr locus of Drosophila melanogaster 2004 Palsson, A., Rouse, A. Riley-Berger, R. Dworkin, I. and G. Gibson. Genetics 167: 1199-1212. [Abstract, PDF, Extras]

6. Evidence that Egfr contributes to cryptic genetic variation for photoreceptor determination in natural populations of Drosophila melanogaster 2003 Dworkin, I., A. Palsson, K. Birdsall, and G. Gibson. Current Biology, 13: 1888-1893. [Abstract, PDF, Extras]

7. A complement for evolutionary genetics. 2001 Gibson G. and A. Palsson. Current Biology 11 (2): R74-6. [Abstract, PDF]

8. Quantitative developmental genetic analysis reveals that the ancestral dipteran wing vein prepattern is conserved in Drosophila melanogaster. 2000 Palsson A. and G. Gibson. Dev Genes Evol. 210 (12): 617-22. [Abstract, PDF]

9. Quantitative trait loci affecting components of wing shape in Drosophila melanogaster. 2000 Zimmerman E., Palsson A. and G. Gibson. Genetics. 155 (2): 671-83. [Abstract, PDF]