April 26, 2013

Marin Ryan ‘ 13Hamline UniversityBiology Senior Seminar Abstract:

Exploring Bioremediation Through the Mobilization of Bacteria in Fungal Hyphae

Porous soils appear to be the most at risk for toxification by Polycyclic Aromatic Hydrocarbons (PAHs). To bioremediate these soils, organisms such as bacteria and fungi are necessary to either sequester or degrade PAHs. The movement of bacteria through fungal hyphae was studied in the paper by Kohlmeier et al. (2005) which I will be presenting on. Achromobacter sp. sk1 was found to travel through a network of water films along hydrophilic hyphae. Flagellation appeared to be a prerequisite for moving bacteria through water films, as motility was only observed in flagellated Achromobacter sp. sk1. These results suggest that a working symbiosis of fungal hyphae and bacteria is necessary to move through porous soils and degrade PAHs.

Katie Gelinas ‘ 13Hamline UniversityBiology Senior Seminar Abstract:

Creating an RSPO3 PPM1h Dual Expression Vector using Gateway Cloning Technology

A Transposon based mutagenesis study of colon cancer in mice led to the identification of around 80 commonly mutated genes in colorectal cancer by the Tim Starr lab at the University of Minnesota Medical School. Several of these genes were identified as being commonly mutated together by a statistical analysis of that data, and one such pairing PPM1H and RSPO3 are the subject of further study in the Goldberg lab at Hamline University. These two genes, one, PPM1H, a serine/threonine phosphatase and member of a family of known tumor suppressors, and the other an activator of the Canonical WNT signaling pathway will be dually knocked down and overexpressed, respectively, in order to study their effects simultaneously in Human Colorectal Cancer cell lines. The main focus of this research thus far has been the creation of this dual vector, and that is what my presentation will focus on today.

Hilary Murphy ‘ 13Hamline UniversityBiology Senior Seminar Abstract:

Histocompatability Complex in Autoimmune Diabetes Mellitus Type 1 and Islet Transplantation

The topic I have chosen to research is analyzing the correlation between the major histocompatibility complex (MHC) and type 1 diabetes mellitus (T1D). T1D is an autoimmune disease that results from the destruction of insulin producing beta cells (Raache, 2011). This is driven by T-cell mediated autoimmune destruction of insulin producing beta cells in the pancreas (Tian, 2007). Certain combinations of MHC region genes lead to the T1D susceptibility. The article I have chosen to focus on is the study done by Chen et. al (2007), it states that H2g7 MHC is the primary genetic contributor to T1D in non-obese diabetic (NOD) mice. The study examines how hematopoietically derived antigen-presenting cells (APCs) expressing MHC molecules delete/inactivate autoreactive diabetogenic T-cells, thus implying that hematopoietic chimerization by the APCs expressing dominant protective MHC molecules could possibly help prevent T1D. The main objective of this study is to address what APC subtypes (B-cells, macrophages, dendritic cells) help mediate the range of Type 1 Diabetes protective effects obtained by multiple genes within the H2nb1 MHC halotype and also knowing the engraftment levels they must use to accomplish this. As a side reference in a study done by Beilhack, et.al (2005), transplantation of MHC-matched purified hematopoietic stem cells prevented diabetes development in NOD mice. In order to concentrate on these objectives, there were analyses of NOD mice background bone marrow chimeras where H2nb1 molecules were expressed on different proportions of different APC subtypes. A histological analysis measured the insulitis development on the bone marrow-chimeric NOD mice diabetes free after 26 weeks. There was an analysis of B-cell reconstitution, bone marrow chimerism levels, and the frequency of A14- Tcells. These tests showed a small B-cell effect, but the prevention of T1D was the strongest when about 50% or more of the dendritic cells and macrophages expressed H2nb1 molecules. This depleted the pathogenesis of the T-cells destroying the beta cells in the pancreas. In conclusion, this study demonstrates that expression of MHC halotype H2nb1 on either dendritic cells/macrophages or B-cells can inhibit insulitis and T1D development in NOD mice. This further supports future studies of clinical applications of bone marrow chimerization for T1D prevention, although cotransplantation of donor matched pancreatic islets is very risky .