Research in the Unckless lab

Examples of adaptation to the external environment are as old as (or older than) the theory of evolution by natural selection itself.  Whether it be Darwin’s finches, the peppered moth, coat color in mice or jaw morphology in fish, our basic texts are full of such examples.  Receiving much less attention, even today, is adaptation to the internal environment, whether it be pathogens or elements within one’s own genome.  A broad definition of conflict includes intragenomic (e.g., transposable elements, meiotic drive elements), intergenomic (e.g., cyto-nuclear), and interspecific (e.g, host-parasite interactions). Our goal is to shed light on how often adaptation occurs in response to these conflict-driven challenges to populations, and the genetic load of such conflict.

Our research is currently focused on two empirical systems as well as theoretical investigations that aim to compliment the empirical work.  The goal is to take a holistic approach to these systems, integrating field study, laboratory experiments, genetics, genomics and theoretical work to understand the system from ecology and evolution down to genetic mechanisms.

Empirical work

The evolution of Drosophila immunity

Though immune system genes are among the fastest evolving in the genome, the effector molecules of the humoral immune system, the antimicrobial peptides (AMPs) are the exception.  AMPs, if anything, show lower rates of adaptive evolution in Drosophila which led to the hypothesis that most evolution involved changes in copy number, not protein sequence.  We found evidence that balancing selection might play a much stronger role in the evolution of AMPs than previously expected and that gene duplication might lead to the resolution of conflict between balanced alleles.  We are now using a variety of approaches to understand the forces maintaining diversity in both amino acid sequence and copy number in Drosophila AMPs.

Viruses of Drosophila

We recently discovered Drosophila innubila Nudivirus (DiNV), the first DNA virus associated with Drosophila, that infects several species from across the genus in North America.  A similar virus was recently found in Drosophila collected in Europe and Africa.  The virus is a double-stranded circular DNA virus from the relatively poorly characterized Nudivirus family.  The closest relative of DiNV infects the rhinoceros beetle (Oryctes rhinoceros) and has been used as a biological control agent for decades.  Two species, which are sister to each other but are allopatric (D. falleni in temperate Northern environments and D. innubila in the Sky Islands of the Southwest), carry strains of the virus that show about five percent nucleotide divergence.  In both species, the virus is found at considerable frequency in wild-caught flies (up to 40%) and cause significant reduction in fertility and survivorship. 


Sex-ratio meiotic drive in Drosophila affinis

Another major area of empirical research is a genomic and population level analysis of the meiotic drive system in Drosophila affinis.  Sex-ratio males, those carrying a driving X chromosome, sire nearly all daughters because the driving X disables Y-bearing sperm.  Important work by Robert Voelker and colleagues in the 1960s and 1970s found that a) XO males (those lacking a Y) are fertile, b) a driving X chromosome produces nearly all daughters when in XY males, but nearly all females when in XO males, c) the Y outcompetes the O in the absence of the driving X, and d) a second driving X is not suicidal when paired with the O, but drive is much weaker.  We aim to elucidate the genomic basis of drive and monitor long-term population dynamics of the two drivers and the Y/O polymorphism.


Theoretical work

As stated above, we are interested in how conflict shapes ecological and evolutionary processes.  Our theory work in this area has focused on sex-ratio meiotic drive. Hamilton (1967) argued that without suppressors, meiotic drive elements on the sex chromosomes could drive populations extinct very quickly.  We have asked the logical next question: if a driver arises in a population, what is the probability that the population saves itself, either by the occurrence of a new suppressor mutation or by recruitment of suppressors from standing genetic variation. A related set of questions involves synthetic gene drive systems such as CRISPR/Cas9-mediated drive.

Other theoretical work has focused on the population genetics of adaptation.  Several ideas for future work include a) dynamics of coevolution using Fisher’s geometric model of adaptation, b) evolution of tolerance vs. resistance in defensive symbionts and c) the role of defensive symbionts in host community interactions.  As is always the case in research, we fully expect these studies to lead in new, but as yet unknown, directions.