The University of Toledo Department of Bilogical Sciences
WOLFE HALL (Room 3246) Saturday, April 3, 2004| Chart | Abstracts 3rd URS | 3rd URS Photos | UT Biological Sciences |
(click on the presenter name for abstract)
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Time |
Speaker |
Presentation Title |
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9:00 |
Dr. Patricia Komuniecki |
Welcome |
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9:05 |
Plenary Lecture- "Recent Progress in the Search for the Molecular Basis of Cancer", Dr. William Taylor, Department of Biological Sciences, University of Toledo |
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9:50 |
Coffee Break |
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10:00 |
"Generation of Novel Alleles of mua-10 in Caenorhabditis elegans" Advisor: Dr. John D. Plenefisch, Department of Biological Sciences, The University of Toledo |
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10:20 |
"The Investigation of Resistance Breakage Capabilities of W260 by Means of D1 Binding Activities" Advisor: Dr. Scott Leisner, Department of Biological Sciences, The University of Toledo |
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10:40 |
"Testing the Interactions between LLS1 and its Candidate Partner Proteins Using BacterioMatch© Two Hybrid System" Advisor: Dr. John Gray, Department of Biological Sciences, The University of Toledo |
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11:00 |
"Regulation of NF-kB Transcriptional Activity by the DNA-Binding Protein, DEK" Advisor: Dr. Brian Ashburner, Department of Biological Sciences, The University of Toledo |
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11:20 |
"Stroke and the Plastic Brain: Are Cortico-Motoneuronal Connections from the Ipsilesional Dorsal Premotor Cortex Unmasked Following Stroke Affecting Primary Motor Cortex Connections?" Advisors: Dr. L. Cohen and Dr. F Hummel, National Institute of Neurological Disorders and Stroke, NIH |
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11:45 |
Pizza lunch |
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12:10 |
Awards ceremony |
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Abstract 9th URS
Casey Darrah
“Generation of Novel Alleies of mua-10 in Caenorhabditis elegans”
Advisor:
Dr. John D. Plenefisch, University of Toledo
The free living soil nematode Caenorhabditis elegans is a model organism widely used for studying development. Previous studies have identified a number of genes essential for cell-cell and cell-matrix attachment. My research centers on mua-10, one of these genes, that is located on the X chromosome and is required for muscle-cuticle attachment in the head region. The one presently know allele is recessive, and causes separation of hypodermis from cuticle in less than five percent of homozygous organisms. This suggests that the known allele is not null. New mutations are being generated using EMS exposure followed by non-complementation screening. I have screened well over two thousand organisms, and have tentively identified one new allele of mua-10 that appears to have a higher penetrance. Further mating will be used to verify this new allele, and additional rounds of mutogenesis will lead to the discovery of still more alleles.
Joel Davidson
“Testing the Interactions between LLS1 and its Candidate Partner
Proteins Using BACTERIOMATCH Two Hybrid System”
Advisor: Dr. John Gray-The University of Toledo
Disease lesion mimics are a large class of plant mutants that show spontaneous cell death in the absence of pathogen. LLS1 (lethal leaf spot 1) in maize is one such disease lesion mimic. LLS1 codes for pheophorbide a oxygenase (PaO) which catalyzes the conversion of pheophorbide a (pheide a) to a red chlorophyll catabolite, an important step in chlorophyll degradation. LLS1 was found to exist in an approximately 400 KDa complex in gel filtrations studies. We are studying the LLS1 protein compex in order to further characterize the events involved in pheide a removal. My work tests candidate protein partners of LLS1 using the BacterioMatch Two-Hybrid System. Since LLS1 localizes to the chloroplast (an endosymbiont), a bacterial system may be more suitable for detecting protein-protein interactions. The BacterioMatch system tests the interaction between a bait fusion protein containing a DNA binding domain and a target fusion protein containing a transcriptional activating domain. The interaction of bait and target proteins initiates a cascade of events which leads to the transcription of reporter genes. Arabidopsis thaliana LLS1 was cloned into the Bait vector, while other candidate partners were cloned into the Target Vector.
Steve Driver
“Stroke and Plastic Brain: Are Cartico-Motoneuronal Connections
from the Ipsilesional Dorsal Premotor Cortex Unmasked Following Affecting Primary Motor
Cortex Connections?”
Advisors: Dr.
L. Cohen and Dr. F. Hummel-NIH
Stroke is the third leading cause of death in the Unitd States, and the main cause of long-term disability among adults. The neuronal plasticity underlying functional recovery, after stroke, is incompletely understood. Animal and human studies suggest a substantial role for the premotor cortex of the affected hemisphere. The dorsal premotor cortex (PMd) is highly interconnected to the spinal cord by direct projections in a similar, but distinct, manner to that of the primary motor cortex (M1). It has been proposed that these connections, which are physiologically less active in the normal brain, may become “unmasked” and functionally active during recovery from stroke affecting the normal M1 pathway. To test this hypothesis we studied patients with focal, sub-cortical, lesions of the cortico-spinal connections originating from M1 (posterior portion of the internal capsule). These small strokes spared the fibers of the direct connections between the PMd and te spinal cord (anterior portion of the internal capsule). The goal of this study was to determine whether redundant cartio-spinal connections, from the dorsal premotor cortex, are utilized during functional recovery following a stroke affecting cortico-spinal connections of the primary motor cortex.
Jessica A. Falk
“The Investigation of Resistance breakage capabilities of W260 by Means
of D1 Binding Activities”
Advisor: Dr. Scott Leisner – The University of Toledo
Crop damage due to viruses produces substantial loses, and researchers study model systems to engineers resistance. Arabidopsis thaliana ecotype Tsu-O is resistant to most Cauliflower mosaic virus (CaMV) strains (including CM1841), but the W260 strain breaks this resistance. Since gene VI product (PVI) is critical for virus-host interactions, PVI is probably involved in W260 resistance breakage. The amino-terminal 110 amino acids [domain 1(D1)] contains the determinant for W260 resistance breakage. The D1s of W260 and CM1841 vary at three amino acids positions (62, 97, 100). Interestingly, D1 of W260 bound more efficiently to full-length PVI than the CM1841 domain. Hence, a different binding of D1 to PVI apparently correlates with resistance breakage. Our hypothesis is that the methionine 97 of W260 D1 is responsible for resistance breakage and for the difference in PVI binding. We generated a D1 clone from a CaMV isolate that does not break Tsu-O resistance, yet it harbors the W260 amino acid at position 100. This construct was tested for interaction with PVI by yeast two-hybrid assays. The D1 bound more efficiently than either CM1841 or W260 D1s. These results support the hypothesis that a different binding between D1 and full length PVI correlates with resistance breakage. However, these data also show that the binding involved in resistance breakage is more complex that expected.
Morgan Sammons
“Regulation of NF-kB transcriptional Activity by the DNA-Binding
Protein, DEK”
Advisor: Dr. Brian Ashburner – The University of Toledo
Nuclear factor-kappa B (NF-kB) is a transcription factor involved in regulation of the immune and inflammatory responses and protection from apoptosis. The TAD (transactivation domain) of the p65 subunit of NF-kB is both a potent transactivator and a target for transcriptional cofactors. The goal of this work is to identify new proteins that can act as either coactivators or corepressors of NF-kB through the C-terminal TAD. A yeast two-hybrid screen with the p65 TAD as bait identified the product of the DEK proto-oncogene as a protein with the potential to interact with p65. DEK plays a role in chromatin remodeling, although DEK can also be found in complex with known corepressor proteins. An in vivo interaction seen through coimmunoprecipitation of p65 and DEK and subsequent Western analysis confirms the yeast two-hybrid screen results. Reporter gene assays show repression of p65 transcriptional activity by DEK in Hela and HEK293T cell lines. Transiently expressed DEK also represses both TNF-a induced p65 transcriptional activation in a dose-dependent manner and the basal transcriptional activity of p65 in non-induced HeLa cells. DEK can also decrease potency of p65 TAD transactivation in reporter gene assays using a Gal4-p65 deletion mutant containing the same region of the C-terminal TAD used in the two-hybrid screen. These results taken together suggest that DEK acts as a corepressor of NF-kB transcriptional activity through an interaction with the p65 TAD. Further studies will attempt to elucidate the molecular mechanism of transcriptional repression of p65 by DEK.
9th URS Photos
| Presenters |
 |
| L>R: Dr. Patricia Komuniecki, Dr. William Taylor, Casey Darrah, Steve Driver, Morgan Sammons, Joel Davidson, Jessica Falk and Dr. Emilio Duran. |
| Winners |
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First place Morgan Sammons |
last updated 29 Dec 2005
please contact brenda.leady@utoledo.edu with comments or concerns