My introduction into the world of insects was completely serendipitous. As a prospective medical student, I sought research experience because it made me more of a well-rounded applicant. Because of my interests in chemical biology, I occupied a position in the Hili Lab in the University of Georgia’s Department of Chemistry. There, I investigated the efficiency and fidelity of T3 DNA ligase in ligase-catalyzed oligonucleotide polymerizations. After publishing my findings, I sought to diversify my research experience. Considering my preference to be advised by someone with incomparable pedagogical approaches, I reached out to the highly decorated Patricia Moore. Luckily, my inquiry was met with an acceptance into her lab. Because it’s affiliated with UGA’s Department of Entomology, this acceptance served as my stepping stone into the world of insects.
As an undergraduate student, I focused on the evolution of DNA methyltransferase 1 (DNMT1) in the large milkweed bug, Oncopeltus fasciatus. Now, I use that work as the foundation upon which my time in graduate school is built. Specifically, I’m interested in the relationship between male fertility and DNMT1. More broadly, there exists an entire class of methyltransferase proteins: DNMT1a, DNMT1b, DNMT2, and DNMT3. They all function to methylate nucleic acid, but differ in the mechanism by which they achieve this epigenetic regulation and, sometimes, in the kind of nucleic acid being methylated.
DNA methyltransferase 2 (DNMT2) is responsible for RNA methylation, but the rest of the aforementioned proteins target DNA. DNMT1 is the protein around which my work revolves and I want to know whether or not it has a subsidiary contribution. It mainly functions to methylate the cytosine base in CpG dinucleotide bridges, but there’s evidence to support another function specific to embryogenesis and gametogenesis. The red flour beetle, Tribolium castaneum, doesn’t have a methylated genome, but requires DNMT1 for viability since a deficiency in the protein compromises their embryonic development, thus leading to a lethal phenotype. Because DNMT1 is believed to have little to no effect in male insects, evolutionary work on DNMT1 mainly used female insects as models. In the brown planthopper, Nilaparvata lugens, and O. fasciatus, DNMT1 is necessary for oogenesis. With respect to spermatogenesis though, there have been claims of DNMT1 having no essential role in the process. However, my lab found evidence to support the contrary. We found that downregulating DNMT1 yields a phenotype of decreased testis size, testis content, and quality of testis structure in O. fasciatus. This proportional relationship between DNMT1 levels and spermatogenic integrity suggests similarity in the function of DNMT1 across the sexes of the O. fasciatus species and, more importantly, further advocates for the evolution of DNMT1 within insect phylogeny.
As of now, I’m extending my work to seek a more causal than correlational relationship. DNMT1-deficient males have a decreased amount of germ cells and those that remain have abnormal structures within their nuclei. This could be indicative of apoptosis, so I’m creating an assay to assess cell death.
When I think about my time as an entomologist, all I can do is smile. I’m not an outside kind of girl, so developing a love for bugs still leaves me in disbelief. My affection for the bugs grew so much that they are now my phone’s background. However, such a memorable research experience wouldn’t be possible if it weren’t for my principal investigator, Dr. Patricia Moore. In collaborating with her, I begin to understand why I’m a better scientist. Under her guidance, the quality of my scientific communication marked by oral presentations and scientific writing continues to improve. Understandably, I will forever be grateful for Patricia Moore.
