Transitions between sexual monomorphism (where the sexes look alike) and sexual dimorphism (where males and females look different) have occurred often throughout evolutionary history in a number of taxa. These transitions are interesting because they ultimately represent gains or losses in sex-specific gene regulation. As more genetic variation affecting human disease is discovered to be sex-specific, it is increasingly important to study the origin of sexually dimorphic gene regulation. My research synthesizes both evolutionary and developmental approaches to understand: (1) when sexually dimorphic states are selectively favored, and (2) what genetic and developmental mechanisms produce sexually dimorphic traits.
developmental & genetic basis of SEXually dimorphic alleles
Male- and female-biased gene expression can change rapidly among species, indicating that sexual genetic variance exists but is easily modified. What is this sex-specific variance? What molecular changes produce sexually dimorphic gene expression?
To determine how sexually dimorphic alleles originate, I am studying a female-limited color dimorphism in Drosophila serrata, where females have light or dark abdomens but males only have light abdomens. I mapped this female-specific trait to an autosomal non-coding structural variant within the first intron of the transcription factor, POU domain motif 3 (pdm3) (Yassin & Delaney et al. 2016). Although pdm3 has been identified as an important regulator of neuronal development, its role in pigmentation is unknown. Using molecular methods and genome editing with CRISPR/Cas9, my research aims to determine the developmental effect of this structural variant on pdm3 expression to understand how it is regulated sex-specifically.
Convergent evolution of SEX-LIMITED PIGMENTATION
In recent work with Dr. Amir Yassin (Yassin & Delaney et al. 2016), we report that female-limited color dimorphism has evolved convergently through independent genetic changes to same transcription factor, pdm3, in four species within the Drosophila montium subgroup (D. serrata, D. kikkawai, D. leontia, and D. burlai). I have since then used genome-wide association analysis to identify additional structural variants in these species in the same and different introns of pdm3. My research is aims to understand why is pdm3 a hotspot for convergent female-limited evolution, and if there are there many or few ways to evolve this female-limited trait.
I am currently taking advantage of the replicate origins of female-limited color dimorphism to map and identify pdm3 cis-regulatory elements (i.e., non-coding regulatory regions that direct expression patterns of nearby genes) controlling female color in multiple species in the Drosophila montium subgroup. This work will allow me to generalize whether there are multiple or limited ways to derive female-specific gene expression.
FItness OF SEXually dimorphic ALLELES
Color polymorphisms, where multiple discrete phenotypes exist within one species, are often controlled by a single locus with multiple alleles. Theory suggests that multiple color morphs can be maintained over long time scales if the morphs experience fitness trade-offs, potentially the result of pleiotropic effects of color alleles. Are alleles for female-limited color dimorphism under balancing selection?
Another focus of my research is to determine what the costs and benefits are of light vs. dark pigmentation alleles in Drosophila montium species with sex-limited color polymorphisms. I combine evolutionary fitness and behavioral assays with transgenic techniques to measure how much each allele affects fitness. Knowing the fitness of each color allele in each sex will reveal the possible role of intralocus sexual conflict (or lack of it) in the evolution and maintenance of a sexually dimorphic trait.