Each of these faculty guide undergraduate research with support from K-INBRE. But, more than just guiding research, these faculty are active mentors with each student.
Dr. Virginia Rider
We are interested in understanding the action of female sex hormones in normal target cells and disease. A major focus of our research is to clarify the mechanisms involved in preparing the uterus to accept an embryo. The maternal cells that interface with the fetal placenta are of particular interest. The proliferation (increase in number) and differentiation (conversion of stroma to decidua) of these cells is regulated by progesterone and estradiol. We are studying how these hormones stimulate two different but related processes in the same cells.
The autoimmune disease systemic lupus erythematosus (lupus) occurs 10 time more often in women than men. Ongoing research in our laboratory suggests that the female sex hormone, estradiol, alters the expression of genes involved in T cell activation. The mechanisms by which estradiol exerts these effects are being delineated.
Current Students: Juli Ward, Guannan Xiao, Alex Talbot, , David Ramsey, Sierra Foster, Zack Krumsick.
Contact Information: phone 620.235.4739 / fax 620.235.4194 / e-mail
Dr. Dan Zurek
My lab is investigating a potent antimicrobial protein from soybean with the ultimate goal of producing a novel antibiotic. Antibiotic resistance is an enormous and rapidly growing problem among numerous human pathogens formerly easily controlled by existing drugs. Discovery of new antibiotics is essential. Research has focused on isolating new medicinal compounds from rare tropical plant species, but little attention has been paid to crop species which can be grown in quantity.
We have cloned a gene from soybean (Glycine max L.) encoding an enzyme possessing glucanase activity, potentially capable of degrading bacterial and fungal cell wall structures, resulting in abatement or termination of microbial growth. It has shown considerable activity against several species of gram negative bacteria (E. coli, Enterobacter aerogenes, and Proteus vulgaris) as well as against Charcoal Rot (Macrophomina phaseolina), a significant fungal pathogen of soybean, corn, cotton, and many other plant species of agronomic importance responsible for hundreds of millions of dollars lost to American farmers annually. Analysis of purified recombinant protein from a yeast expression system is underway to quantitate the efficacy of this protein as an antimicrobial agent.
Contact Information: phone 620.235.4746 / fax 620.235.4194 / e-mail
Dr. Peter Chung
We have been interested in understanding how activated macrophages discriminate between normal and tumor cells and what is involved in that discrimination. Our approach has been to study the response of simian virus 40 (SV40)-transformed mouse fibroblast cells to activated macrophage-mediated cytotoxicity. Although SV40-transformed cells are tumorigenic, they are universally resistant to activated macrophage-mediated killing. However, a single subclone, F5b, was identified, which exhibits the unique phenotype of being sensitive to the tumoricidal activities of activated macrophages; while a sister clone, F5m, maintains the typical SV40-transformed phenotype of resistance.
Understanding the mechanisms by which tumor cells are resistant to macrophages may lead to the development of therapies which can overcome this resistance. Such a therapy could enhance the effectiveness of macrophages to reduce the occurrences of metastasis and to reject tumors.
Our laboratory, through collaboration with Kansas State University, is currently working with these tumorigenic cell lines, and one of our main goals is to identify, through cloning and expression, the putative gene(s) believed to be responsible for susceptibility to macrophage-mediated cytotoxicity. Preliminary molecular data suggests CD81 (a tetraspanin that may be used as a marker in tumorigenic cells) may be involved in differences in monolayer growth seen between the sister clones, F5b and F5m. Ongoing research with both nucleic acids and proteins will hopefully shed light into the mechanisms behind this activity.
Contact Information: phone 620.235.4736 / fax 620.235.4194 / e-mail
Dr. Phil Harries
Virus infections pose a serious health threat to both plants and animals. In order for such infections to exert their negative effects, however, viruses must be able to move from cell-to-cell and spread within their hosts. My lab will focus on studying the methods by which viruses hijack plant cells to facilitate their movement. In particular, we will focus on the potential role of the host cell cytoskeleton which can serve as tracks along which cellular cargo (including invading viruses) can travel. Tomato bushy stunt virus (TBSV) has been shown to require the host cytoskeleton for its spread but the mechanism underlying this requirement is unknown. We will examine the potential association of TBSV proteins with various components of the plant cell cytoskeleton using both microscopy and biochemical techniques. A greater understanding of the mechanisms of virus movement may lead to methods for slowing or stopping virus spread in important crop plants.
Contact Information: phone 620.235.4864 / fax 620.235.4194 / e-mail
Dr. Mandy Peak
Recognition of foreign antigens in the human immune system is primarily performed by the B and T cell receptors. The genes encoding the antigen-binding receptors are produced in a functional form during specific stages of lymphocyte development through a specific DNA rearrangement process referred to as V(D)J recombination. This results in somatic rearrangement of the gene segments that encode the variable regions of B-cell and T-cell receptors. Two lymphoid specific proteins, RAG1 and RAG2, initiate V(D)J recombination by introducing DNA double-strand breaks between each selected gene segment and their bordering recombination signal sequence (RSS) in a two step mechanism, in which the DNA is first nicked followed by hairpin formation. Mutations in either RAG protein that disrupt catalytic activity result in fatal immunodeficiency diseases, including SCID.
Our interests continue at the molecular level and we utilize biochemical methods to further interpret the protein-DNA interactions of RAG1 with the RSS. We will employ photo-crosslinking assays to determine the DNA nucleotides in the RSS heptamer that interact with RAG1 in the presence and absence of RAG2. Overall, these studies will provide important insight into the V(D)J recombination reaction, specifically that significant interaction of the RSS heptamer with RAG1 and to further elucidate the function of RAG1 and RAG2.
Contact Information: phone 620.235.6541 / fax 620.235.4194 / e-mail
Dr. Xiaolu Wu
Research efforts in my lab focus on the highly pathogenic avian influenza virus H5N1, also known as bird flu virus. Different with other influenza virus strains that cause season flu with a mortality rate at 0.1%, influenza virus H5N1 is highly lethal in humans and has a mortality rate of over 60%. Currently, the transmission of H5N1 is limited to direct contact with infected poultry. However, due to the high mutation rate of influenza virus, it is predicted that the appearance of mutated H5N1 strain which may transmit from human to human and lead to a global pandemic is a just a matter of time. Experts estimate that 7 million to 1.5 billion people worldwide would die from such a pandemic. Moreover, there is no effective vaccine against this virus for human, and appearance of drug-resistant strains of H5N1 indicates that novel therapeutic treatments are urgently needed. My lab aims to screen libraries of small compounds to identify potential inhibitors against H5N1 infection. We have set up a tissue culture system in which human 293T cells are employed to generate surrogate influenza viruses that can be safely used in research. We are currently working on testing the effect of the compounds on viral infectivity with luciferase assay. Identified compounds will form the bases for optimization and validation for drug discovery.
Contact information: phone 620.235.4036 / fax 620.235.4194 / email