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: Afrita Davis, Rebecca Bryon, Dustin Graham, Caleb Burrows, David Ramsey.
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 (620.235.44864) / fax (620.235.4194) / e-mail