Biology Department

Jennifer R. Powell





Campus Box 0392


McCreary Hall
300 North Washington St.
Gettysburg, PA 17325-1400


The Powell Lab


BA Hendrix College, 1997
PhD University of California, Berkeley, 2003

Academic Focus

molecular genetics, microbiology, innate immune responses, oxidative and cold stress responses

Research Focus

Innate Immune Response

Animals are exposed to a stunning variety of microorganisms; some are beneficial while others have the potential to cause disease. The innate immune system is an evolutionarily ancient method of defending against potentially pathogenic microbes. To engage an innate immune response, a host organism must recognize that some microbial pathogen is attempting to cause an infection. However, we currently have only a limited understanding of how this occurs. To explore the molecular mechanism of infection recognition, we searched for receptors in the nematode C. elegans, which is an established model for studying host/pathogen interactions. We identified a G-protein coupled receptor called FSHR-1 as an important component of the C. elegans innate immune response to a variety of bacterial pathogens. The receptor FSHR-1 defines a new signaling pathway that acts in the nematode intestine, the major site of infection by ingested pathogens. FSHR-1 regulates the transcription of pathogen-response genes that likely act to kill bacteria and fight infection. It is also required for the oxidative stress response associated with pathogen defense, and for the learned avoidance of pathogenic bacteria. Additional molecular genetic characterization of the function of the FSHR-1 receptor and the microbial components that activate it will help us better understand how C. elegans and other animals recognize and respond to infection.

Cold Shock Response

In addition to pathogens, animals encounter a wide variety of abiotic stresses during their lifetimes, including predators, limited food availability, and changing environmental conditions. We have found that C. elegans exposed to a severe but limited-duration cold shock reallocate lipid stores from their intestine into mature oocytes. This cold stress response massively upregulates the normal process of vitellogenesis, utilizing the vitellogenesis machinery to deplete the intestine of all detectable lipids and resulting in the premature death of the cold-shocked adult worm. Despite this apparent severe cost to fitness, this lipid reallocation is actually an example of terminal investment because the resulting embryos are more likely to survive and hatch following a subsequent severe cold stress than control embryos from non-cold-shocked mothers. Thus, the stressed mother sacrifices herself to benefit her offspring in anticipation of future similar environmental stresses. This cold shock response in C. elegans is a rare example of cytoplasmic terminal investment in a well-studied genetic model system, allowing future characterization at the molecular genetic level.

Courses Taught