Student Profile

Degree received: Minnesota State University, Moorhead, Cellular and Molecular Biology major, B.S., 2019

Research: Influenza is a virus that can infect many species, but in order to cross species barriers it has to overcome a number of obstacles. One of these obstacles is the host antiviral immunity. Interferon-stimulated genes (ISGs) are expressed in response to viral infection and make up a large component of the antiviral immune response. I am investigating the function of interferon-stimulated genes in the cross-species transmission barrier of influenza.

Degree received: The Ohio State University, Chemistry major, B.S., 2017

Research: My work will focus on applying co-culture techniques to study host-pathogen interactions in a variety of settings. As a member of Ryan Hunter's Lab I studied how airway epithelial cells responded to infection by Pseudomonas aeruginosa under anaerobic conditions. I applied bulk RNA sequencing to study how P. aeruginosa virulence and the accompanying host response was affected by the presence and absence of oxygen, as well the impact of the normal versus cystic fibrosis epithelial environment. Going forward in the Willett Lab, I will be applying my experience with co-culture systems to investigate key genes utilized by Enterococcus faecalis to colonize the gastrointestinal tract as well as key virulence factors used when it adopts a pathogenic lifestyle.

Degree received: University of Illinois at Urbana-Champaign, Molecular and Cellular Biology, B.S., 2018

Research:   The emergence of drug resistance in Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis, presents a threat to both developed and impoverished countries around the world. My work is largely focused on characterizing antitubercular drug activity in Mtb, more specifically, pyrazinamide and pyrazinamide analogs. While pyrazinamide is an important first line therapeutic in tuberculosis treatment, its exact mechanism is unclear. My research employs various in vitro techniques to study changes of fitness in drugs using genetics-based approaches such as transposon mutagenesis and targeted knockouts. The goal of my research is to elucidate the molecular mechanisms of an effective, yet uncharacterized, pyrazinamide analog in the hopes of better understanding pyrazinamide/pyrazinamide analog activity in Mtb.

Degrees received: Rensselaer Polytechnic Institute

Research: 

Phillip will be investigating the use of induced pluripotent stem cells (iPSC) in generating induced regulatory T cells (Tregs) as a cellular therapy for Graft Versus Host Disease. This process involves genetically modifying iPSC to increase their stability and propensity to differentiate into functioning Tregs and verifying the generated Tregs using genomic, proteomic, metabolomic and functional
assays.

Degrees received: University of California, Davis

Research:

The Soudan Underground Mine in the Vermillion Range in northern Minnesota provides a unique opportunity to study the deep terrestrial biosphere that has been relatively unaffected by photosynthetic activities. The lowest level of the Soudan Underground Mine, which reach a depth of 713 meters, has access to 2.7-billion-year-old banded iron deposits with brine waters that are metal-rich, anoxic, and devoid of detectable organic carbon. Studying how microbes survive in the mine could help to understand the adaptations required to make a living in such unique conditions and how the microbial community, in turn, affects the geochemistry of the mine. The goal of my research is to enrich, isolate, and identify the microorganism that are playing a role in the metabolic cycling in the mine. Additionally, I will be studying the cytochrome-carrying prophage region of the Deltaproteobacterium Desulfuromonas soudanensis strain WTL, that was previously enriched from electrodes in the mine, to identify the role of horizontal gene transfer on the proliferation of cytochrome diversity in metal-reducing bacteria.

Degrees received: University of Wisconsin Milwaukee

Research: The epiphytic bacterium Methylorubrum extroquens is able to grow on reduced one carbon compounds, such as methanol. Doing so, however, presents a metabolic paradox. Methanol, and other one carbon compounds, are metabolized via a high flux oxidative pathway that produces formaldehyde as an obligate intermediate meaning formaldehyde is both a central metabolite and a potent stressor. Consequently, methylotrophs experience, and cope with, high intracellular concentrations of formaldehyde. My PhD research seeks to combine modern genetic techniques and classical bacteriological methodologies to focus on understanding and characterizing the regulatory mechanisms that allow M. extorquens  to mount a formaldehyde specific stress response and maintain cellular homeostasis despite the presence of elevated formaldehyde.

Degrees received: Colorado State University

Research:

Cystic Fibrosis is a genetic disorder that affects ~70,000 people worldwide. This disease is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) and is characterized by the accumulation of thick, sticky mucus in the lower respiratory airways. This accumulation allows for chronic microbial colonization and infection of the lungs leading to a decreased lifespan. By studying this microbial colonization and its dynamic interplay within itself as well as with the host, I aim to elucidate what role bacteria are playing as major pathogens in this disease as well as the role of the host immune response.

Degrees received: University of Michigan, Ann Arbor

Research: My research is focused on investigating innate immunity to Mycobacterium tuberculosis (Mtb) infection focusing on myeloid cell populations. Utilizing mouse models, single cell RNA sequencing, and fluorescent/barcode labeled Mtb strains, I aim to elucidate different cell phenotypes between infected and bystander populations. I also have interests in investigating the mycobacterial genetic requirements for surviving the macrophage response.

Degrees received: Bethel University, MN

Reasearch:

Tissue resident memory T cells (T RM ) patrol peripheral tissues without recirculating through blood or lymph and play a critical role in front-line protection from viral infections. Recently, the Masopust lab reported the existence of bona fide lymph node resident memory T cells (LN T RM ). Although LN T RM may constitute a significant proportion of memory T cells in human lymph nodes, their function is entirely unknown. My research aims to define the ontogeny, fate, and function of LN T RM . I will investigate the specific contributions of LN T RM to lymph node immunosurveillance, local viral clearance, and orchestration of memory immune responses.

Degrees received: B.S., University of Wisconsin, Stout-Menomonie, WI, 2013

Research:

My research is focused around the idea of anergy in CD4+ T cells. Anergy is a functional unresponsiveness that results from incomplete or altered activation signals. My goals are to find the peptides that are driving CD4+ T cells to become anergic, and characterize their role in infection and autoimmunity.

Degrees received: Florida International University

Research: Title: Molecular mechanisms of PARP inhibitor sensitivity in ovarian cancer

Ovarian cancer continues to be the most lethal gynecologic malignancy in the US, with High Grade Serous Ovarian Cancer (HGSOC) being the most common and most lethal subtype of cancer. Germline deleterious mutations in BRCA1 and BRCA2 are associated with carcinogenesis, are involved in contributing to homologous recombination dysfunction, and can be therapeutically exploited using PARP inhibitors. Despite the synthetic lethal action of PARP inhibitors on BRCA1/2 mutated cancers, drug resistance develops and the majority of patients relapse. In addition, the precise role of PARP inhibition on wild-type BRCA1/2 HGSOCs is unclear, warranting further study on the mechanism of action in ovarian cancers with different genomic backgrounds. The goal of my research is to study the molecular mechanisms of PARP inhibition in HGSOCs containing BRCA1/2 mutations and comparing these responses to wild-type BRCA1/2 ovarian cancers. By studying the differential responses that HGSOCs have on PARP inhibition at the level of the proteome, we can ascertain which type of HGSOCs would benefit most with PARP inhibition with minimal risk of relapse. Finally, studying changes in the proteome upon PARP inhibition will reveal other sets of genes besides BRCA1/2 that are involved in homologous recombination dysfunction.

Degrees received: Creighton University

Research: 

Degrees received: University of Wyoming

Research: I am working to understand the role of steroid hormone receptor signaling (estrogen receptor, ER, and the progesterone receptor, PR) in luminal (ER+) breast cancer (BC) that has acquired both endocrine resistance and endothelial to mesenchymal transition. Specifically,  elucidating the signaling events that lead to expansion of a subpopulation of CD44^high/CD24^low cancer cells, circulating stem cell (CSC) like cells, within endocrine resistant BC. In previous models, ER is thought to be down regulated in endocrine resistance; yet PR, (which is induced by ER), exhibits increased transcriptional activity. To understand what is driving these signaling events leading to a CSC phenotype, I am creating new models of endocrine resistance in multiple cell lines and comparing the signaling components in 2D versus 3D tissue culture conditions. Additionally, these TC models will be expanded to mouse models for in vivo characterization. Learning more about the roles of ER and PR in driving the stem cell-like subpopulation within BC resistance will provide insight into mechanisms of cancer cell plasticity and possible reversal of endocrine resistance. 

Degrees received: B.S., University of Minnesota, Twin Cities, Minneapolis, MN, 2008

Research:

Tissue-resident memory CD4⁺ and CD8⁺ T cells (T_RM) have been identified in many tissues and organs of mice and humans. T_RM reside in barrier (e.g., skin, gut, and lung) and non-barrier tissues (e.g., pancreas, kidney, liver, brain, and SLOs). T_RM are the dominant T cell population involved in immunosurveillance of most organs and upon activation they are capable of in-situ proliferation, producing proinflammatory cytokines, recruiting circulating memory cells and B cells, as well as other functions. These abilities make T_RM important players in monitoring and protecting the tissues they occupy from infection and cancer. Recently, there is an increasing awareness that they also likely promote unfavorable responses such as inflammatory diseases, transplant rejection, allergy, and autoimmune diseases that include inflammatory bowel disease, vitiligo, and multiple sclerosis. If T_RM do have a prominent role in immunopathology, elimination of T_RM in affected tissues may reduce levels of inflammation and close those tissues to routine immune surveillance, allowing for durable remission. My research project is focused on understanding how tissue-resident memory T-cell populations are generated and maintained in peripheral tissues and in developing depletion strategies explicitly targeted against tissue-resident memory T-cell populations. Depletion strategies can be tested in relevant autoimmune and allergic mouse models as well as transplant models in both clean and dirty mice, and will also help elucidate tissue-specific mechanisms of T cell recruitment, retention, and homeostasis.

Degrees received: University of North Carolina, Chapel Hill

Research: 

Memory CD8 T cells provide us with long-term protection against reinfection by intracellular pathogens. The CD8 T cells memory pool is heterogenous; our group has recently defined a rare circulating subset known as long-lived effector cells (LLECs) which are characterized by their expression of KLRG1 and superior control of LM. Months after infection in SPF mice, the LLEC population wanes in comparison to other subsets. However, this does not seem to be the case in “dirty mice,” which have higher systemic pro-inflammatory cytokine levels. My work centers around the hypothesis that LLECs are uniquely able to utilize pro-inflammatory cytokines such as IL-18 for their maintenance.