Fifteen University of Delaware Undergraduate Researchers to present posters at the  EXPERIMENTAL BIOLOGY MEETINGS
in Washington, DC, April 28 - May 2, 2007

Fifteen students and four faculty attended the Experimental Biology Meetings in Washington, DC. Nine students participated in the Undergraduate Poster Competition sponsored by the American Society for Biochemistry and Molecular Biology.  In that national competition, two students received Honorable Mention for their projects. Five students presented posters at the Undergraduate Poster session sponsored by the American Physiological Society.  All students presented their work in the regular scientific sessions. In addition, two students were selected to present talks on their work in Symposium Sessions. Prior to the trip, the participating students refined their posters based on feedback from a practice presentation on campus.

Click on any picture to enlarge.

Prof. Hal White  Chem & Biochem
Prof. David Usher Biol Sci
Prof. Gary Laverty, Biol. Sci.
Dr. Seung Hong, Biol Sci
Ashley Anttila, Biological Sci
Aly Bourreza, Biochemistry
Corrine Decker, Biological Sciences
Vivek Desai, Biological Sciences
Charles Drummer, Biological Sci.
Joseph Feng, Biochemistry
Caitlin Haag, Biological Sci.
Lindsay Higdon, Biological Sci.
James Kelleher, Biochemistry
Patrick Knerr, Biochemistry
Evan Lebois, Biochemistry

Gregory Madden, Biological sci.
Justin Moses, Biological Sciences

Sarah Swain, Biochemistry
Wen Allen Tseng, Biological Sci

Ready for departure from UD Friday afternoon.

Participants in the ASBMB Undergraduate Poster Competition.

UD students at the Poster Award Ceremony

UD students at the ASBMB Undergraduate Poster Awards Ceremony

University of Delaware Student Poster Presentations and Abstracts.

Effects of the sodium-hydrogen exchange inhibitor EIPA on chloride secretion in permeabilized monolayers of chick renal proximal tubule cells

Ashley Anttila, Sighvatur S. Arnason1, and Gary Laverty

University of Delaware, Biological Sciences
1 University of Iceland

In voltage-clamped cultured monolayers of the chick renal proximal epithelium, parathyroid hormone and the cAMP agonist forskolin stimulate a positive short circuit current (ISC) that is sensitive to chloride ion (Cl-) substitution and to Cl- channel blockers, suggesting a stimulated net Cl- secretion. However, this ISC response is also blocked by the Na+/H+ exchanger (NHE) inhibitor, 5-ethylisopropyl amiloride (EIPA), indicating a possible interaction between these two transport pathways. To further study these interactions, we generated current-voltage curves (I/V curves) on permeabilized monolayers (10 µM amphotericin B to the basolateral side). Control and EIPA (100 µM) pre-treated monolayers were subsequently treated with 1.0 µM forskolin followed by the Cl- channel blocker NPPB. I/V curves were generated after each addition. Forskolin stimulated ISC (intercept of I/V curves) by 19.4 + 3.1 µA/cm2 (n = 7), and EIPA almost completely blocked this effect (0.96 + 1.27 µA/cm2, n = 5). On the other hand, forskolin decreased the I/V curve slope (conductance) by 19 + 4% in controls, but increased it by 17.18 + 4.4% in EIPA treated monolayers. Similarly, NPPB had opposite effects on slope with and without EIPA. These data suggest that forskolin may both activate a Cl- secretion pathway and simultaneously inhibit a conductance associated with NHE, and that these two transport components may be linked. Supported by NSF IBN 03433478.

Ashley also presented her research to a packed audience in the American Physiological Society's Symposium on Epithelial Transporters.

Chemical Complementation of Androgen Receptor Mutations Associated with Androgen Independent Prostate Cancer

Aly Bourreza and John T. Koh

Department of Chemistry and Biochemistry,

Prostate cancer remains the second leading cause of cancer death in men.  As prostate tissue is dependent on androgens for growth and homeostasis, anti-androgens, such as flutamide and bicalutamide (Casodex®), used alone or in conjunction with chemical castration have been used in the treatment of prostate cancer for decades.  However, as many as 30% -40% of patients treated with anti-androgens become resistant to anti-androgens within five years of treatment.  The prevalence of androgen receptor (AR) mutations that caused flutamide resistance led to the adoption of bicalutamide as the drug of choice for prostate cancer treatment six years ago, however new bicalutamide resistant mutants, W741C and W741L, have recently been identified in the clinic. Bicalutamide acts as an agonist with these mutants.  It is believed that anti-androgens can be synthesized in such a way that they remain functional antagonists in mutant forms of the androgen receptor.

  The novel compounds were synthesized based on the crystal structure of anti-androgen resistant AR mutants.  The androgenic and anti-androgenic effects of novel compounds in competition with synthetic androgen R1881 is evaluated using ARE-luciferase reporter gene assays.  In addition, anti-androgen resistance can be simulated in vitro by culturing LNCaP cells in the presence of anti-androgens for extended periods of time.  Based on structural models we predict that these second generation AR antagonists will be resistant to AR mutations associated with anti-androgen withdrawal syndrome. Funding provided by  the Howard Hughes Medical Institute Undergraduate Science Education Program.

B2-Crystallin Regulation of the Lens Cytoskeleton

Corinne Decker, Kevin Duprey,
Yan Wang, and Melinda K. Duncan

Department of Biological Sciences

The vertebrate lens is composed of epithelial cells and fiber cells, both of which contain crystallins, proteins necessary to maintain the high refractive index of the lens. Mice and humans harboring mutations in bB2-crystallin develop cataracts that have been proposed to be caused by aggregation of mutant βB2-crystallin. However, we have found that mice harboring the Phy mutation of the bB2-crystallin locus develop cataracts associated with profound fibrosis of the adult lens epithelium, expression of abnormally high levels of asmooth muscle actin (aSMA), and the loss of F-actin from lens fiber cells. Although bB2-crystallin expression in the lens initiates at birth, these observations suggest a role for bB2-crystallin in lens cytoskeletal organization. Consequently, we undertook a developmental study of this phenotype. While newborn and 2 week-old crybb2Phy mice exhibited normal lens morphology with no differences in aSMA or F-actin distribution, 4 week-old mutants lost F-actin from the lens fibers and upregulated aSMA expression in the epithelium. The distribution of the intermediate filaments CP49 and filensin was not altered. Upregulation of aSMA in the lens epithelium is associated with epithelial-mesenchymal transitions coupled with the loss of epithelial marker Pax6 and aberrant expression of fiber cell marker cMaf. Remarkably, mutant lens epithelial cells which appear fibrotic maintain Pax6 and do not upregulate cMaf. Overall, these data suggest that bB2-crystallin plays critical roles in the cytoskeletal organization of the lens and suggest that the pathologies seen in bB2-crystallin mutant lenses are not simply due to protein aggregation. Funding provided by grants from the Howard Hughes Medical Institute and the NIH.

CD44 and Posterior Capsular Opacification

Vivek D. Desai and
Melinda K. Duncan

Department of Biological Sciences

Posterior capsular opacification (PCO) is an undesirable wound healing response in which the residual lens cells remaining in the eye after cataract surgery proliferate, migrate into the visual field, and synthesize extracellular matrix molecular similar to those found in scar tissue, damaging the patient’s vision. PCO arises from epithelial mesenchymal transition (EMT) of lens epithelial cells. In other systems, CD44, a receptor for hyaluronan, has been identified to mediate changes in cellular proliferation, migration and cell identity leading to EMT. We hypothesize that the hyaluronan receptor CD44 is involved in EMT of lens cells. CD44 is expressed in the adult lens fiber cells and not in the lens epithelial cells; it is first detected in the newborn lens fiber cells. RT-PCR demonstrated that the “canonical” version of CD44 is the major CD44 splice variant in the lens. In adult mice, CD44 is not expressed in the lens epithelial cells immediately after the cataract surgery, however, its expression highly up-regulates in the lens epithelial cells 1-day following the surgery, therefore CD44 could be an early marker for EMT. α-SMA, an early marker for EMT, is up-regulated in both the WT and CD44 KO lens 2-day after surgery, thus CD44 is not essential for EMT in the lens epithelial cells. Our immediate future work is to study the molecular mechanisms regulating CD44 expression in the lens. Funded by the Beckman Foundation.

Regulation of Lipid Metabiolism in

Charles E. Drummer, IV1, Justin DiAngelo,2, Morris Birnbaum2.
2 Department of Endocrinology, University of Pennsylvania, Philadelphia, PA 19104, USA 1University of Delaware, Newark, DE 19716, USA.

Until recently it was believed that insulin was the main regulator of lipogenic gene expression.  However, it has been shown that nutrients themselves play a role in the regulation of these genes and that many lipogenic genes contain carbohydrate responsive elements (ChRE) within their promoters.  These response elements were used to identify ChRE-binding factors that mediate lipogenic gene expression, including carbohydrate responsive element binding protein, ChREBP.  We examined the role of the Drosophila homolog of ChREBP, Mio, in the regulation of fatty acid synthesis, triglyceride storage and lipogenic gene expression.  Using the Gal 4/ UAS system, we created transgenic flies that expressed a MioRNAi knockdown construct.  We assayed triglyceride levels in larvae lacking Mio in their fat bodies and used RT-PCR to examine Fatty Acid Synthase (dFAS) and Acetyl-CoA Carboxylase (dACC) expression. We observed a decrease in larval triglyceride levels in 2 independent transgenic lines.  Consistent with a decrease in triglycerides, we also observed a decrease in dFAS and dACC expression.  We concluded that Mio is necessary for regulating triglyceride storage as well as lipogenic gene expression. Supported in part by the HHMI EXROP Program.

Protein Kinase C (PKC)-mediated Actin Disruption Regulates [Ca2+]i Responses to Mechanical Load in Osteoblasts

Joseph Joshua Feng1, Andris Kronbergs1, Victor P Fomin1,
Peter V Usatyuk
2, Viswanathan Natarajan2,
and  Randall L Duncan1

1Biological Sciences, University of Delaware
2Department of Medicine, University of Chicago

Osteoblasts respond to mechanical load with a rapid and transient increase in intracellular free Ca concentration ([Ca2+]i) that is essential for load-induced bone formation. PKC is also rapidly increased during mechanical stimulation and we postulate that PKC regulates the [Ca2+]i response through alteration of the actin
cytoskeleton. Using fura-2 loaded MC3T3-E1 preosteoblastic cells, we examined the [Ca2+]i response to hypotonic swelling (HS) during phorbol ester (PMA)-induced PKC activation. PKC activation potentiated the peak [Ca2+]i response to HS by 57% compared to HS alone. A significant increase in the rising slope of the transient was also observed. PKC inhibition with 1 μM GF109203X reduced the peak [Ca2+]i response to 32% below HS alone peak levels. Voltage sensitive calcium or mechanosensitive channel block with nifedipine (10-6M) or gadolinium (5x10-6M),
respectively, abrogated the effects of PKC on the HS-induced [Ca2+]i increase. HS alone increased actin stress fibers in MC3T3- E1 cells. However, PMA (10-6M) disrupted of the HS-induced actin organization. Osteoblasts pretreated with actin cytoskeleton stabilizer, phalloidin, failed to exhibit the PKC potentiation of HSinduced [Ca2+]i. These studies suggest that PKC regulates the [Ca2+]i response to mechanical load in osteoblasts by reorganization of actin and through control of channel activity. Supported by NIH/NIAMS AR43222

Fluid Shear Stress Alters ahnak Expression and Association with the L-type Voltage Sensitive Calcium Channel in Osteoblasts

Caitlin Haag, Ying Shao, and Randall L Duncan

Department of Biological Sciences

Mechanical strains encountered through everyday activities are necessary for skeletal development and function, yet the cellular mechanisms necessary for this response are unknown.  The earliest reaction to mechanical strain caused by fluid shear in osteoblasts is a rapid increase in intracellular calcium that occurs through activation of the L-type voltage sensitive calcium channel (LVSCC).  This calcium influx is necessary to induce bone formation, in vivo.  The actin cytoskeleton of osteoblasts also responds to mechanical strain with an increase in formation of stress fibers.  Ahnak, a 700kD protein has been found to interact with both the LVSCC and the f-actin of the cytoskeleton.   We propose that ahnak bridges the cytoskeleton to the LVSCC and that fluid shear will alter the expression of this protein in a time dependent manner.  We found that ahnak protein levels rapidly decreased in osteoblasts within 1 hour of the onset of fluid shear.  Ahnak levels returned within 6 hrs of shear onset, suggesting that ahnak is rapidly degraded and synthesized or is stored in discrete locations within the cell.  Cell fragmentation studies to identify ahnak storage sites within the cell will be correlated with cytoskeleton disruption and immunofluorescent imaging to determine changes in ahnak localization during application of shear.  Supported by NIH/NIDDK grant DK058246 and Howard Hughes Medical Institute.

Caitlin is pictured with her father.

The Effect of Bcl-2 on Apoptosis
in the Developing Chick Embryo Brain

Lindsay Higdon and Deni Galileo

Department of Biological Sciences

During brain development neurons migrate along radial glia to their final destinations.  Interactions between radial glial substrates and neuronal integrins facilitate migration.  Integrin-substrate interactions have been shown in other systems to induce expression of Bcl-2, a protein that suppresses apoptosis (programmed cell death). Bcl-2 is expressed in the early chick optic tectum (midbrain) where it is hypothesized to promote neuronal survival, but its role has not been demonstrated.  Thus, a replication-competent retroviral vector expressing Bcl-2 was injected into the optic tecta in vivo to increase Bcl-2 levels and characterize the effects on tectal architecture formation.  We have been characterizing Bcl-2 expression patterns by immunostaining infected and un-infected tectal cryosections.  To determine the extent of viral spread we will also immunostain the sections for the viral gag protein. We are also developing an in vitro model that will investigate cell contact mediated survival by using time-lapse microscopy. We have finished constructing a replication-incompetent retroviral vector that encodes Bcl-2 and the marker gene lacZ, which should result in discrete infected cell clones (arrays) with higher numbers of surviving marked neurons. We will infect a group of tecta with this virus and another group with a lacZ-only expressing virus. We will then count and compare the number of cells per clone produced from each virus type. We predict the number of cells per clone with Bcl-2-expressing virus will be greater than control clones. This will implicate Bcl-2 in mediating cell survival during brain development. Supported by the Howard Hughes Medical Institute Undergraduate Program .

Lindsay won honorable mention for her work in the ASBMB Undergraduate Poster Competition. She is pictured with Don Smith, a judge in the competition.

Regulation by Cholesterol of the Gene Expression of
Spot 14 in Adipocytes

James Kelleher and David Usher

Department of Biological Sciences

Thyroid hormone responsive Spot 14 (THRSP) is a transcription factor localized to the liver and adipocytes.  In addition to sensing triiodo-L-thyronine (T3) and glucose levels, previous studies have indicated the expression of Spot 14 is regulated by liver X receptor (LXR), a transcription factor activated by cholesterol.  The known target genes of Spot 14 are specific to lipogenesis, suggesting it as a biochemical control point in the accumulation of lipids.  In adipocytes, however, the regulation and function of Spot 14 have yet to be investigated.  In this study, 3T3 L1 mouse adipocytes were depleted of cholesterol and/or supplemented with an LXR agonist or T3 in order to examine the regulation of Spot 14.  Gene expression of these treated cells was measured through quantitative PCR for Spot 14 and its hypothesized target genes.  In what appears to be through independent mechanisms, the expression of Spot 14 increased with both the additions of T3 and the LXR agonist, whereas the cholesterol depletion had the opposite effect showing a decrease in the mRNA.  The proposed target genes fatty acid synthase (FAS), ATP-citrate lyase (Acly), and phosphoenolpyruvate carboxykinase (Pck1), all enzymes involved in the synthesis of fatty acids, demonstrated a similar, yet T3 dominant response.  In a related study perilipin, a protein found on the surface of large lipid droplets, was also analyzed.  The expression of this gene exhibited a cholesterol dependent response similar to that of Spot 14.  The results from this study provide further indication of the cholesterol-mediated role of Spot 14 in the storage of lipids. This research was funded in part by the Howard Hughes Medical Institute Undergraduate Science Education program

Zinc-triggered Hydrogelation
of Designed β-hairpin Peptides

Patrick J. Knerr, Christopher Micklitsch,
Colin Thorpe, and Joel P. Schneider

Department of Chemistry and Biochemistry

Peptides have been designed which undergo intramolecular folding from random coil to β-hairpin conformation, triggered by specific environmental conditions such as temperature, pH and ionic strength.  These folded, amphiphilic β-hairpins then intermolecularly self-assemble to form a crosslinked, fibrillar network, converting the bulk material from a free-flowing liquid to a self-supporting, rigid hydrogel.  This work reports a new trigger: zinc-induced hydrogelation.  A pentadentate ligand with a strong propensity to chelate zinc was synthesized and coupled to the side-chain of diaminopriopionic acid, yielding a zinc-ligating α-amino acid.  This residue was subsequently incorporated into a 20 residue β-hairpin peptide composed of two strand regions connected by a four residue type II’ β-turn.  Using this approach, a peptide was designed which does not fold and self-assemble until the addition of one or more equivalents of the zinc chloride trigger.  Such a responsive system is of particular interest in the development of sensor technology to detect and remediate toxic levels of zinc pollution in water or soil, as well as in the design of microfluidic devices.  Funding has been supplied by the Arnold and Mabel Beckman Foundation, the HHMI Undergraduate Biological Sciences Education Program and the National Institute of Health.

A Role for N-glycosylation in Differential Growth Control and Drosophila Development:
Phenotypic Analysis of

Evan Lebois and Erica Selva

Department of Biological Sciences

In this study we begin to phenotypically characterize Alg10, an enzyme that adds the terminal glucose residue to the growing dolichol-linked oligosaccharide during N-glycosylation prior to its en masse transfer to a nascent polypeptide.  Genetic and molecular approaches were developed to characterize the alg10 loss of function phenotype during Drosophila development.  While pleotrophic phenotypes were observed in alg10 mutant embryos, clonal analysis of the alg10 mutation in the developing wing yielded a smaller and rounder adult wing phenotype as compared to wild type.  This implicates a potential link between glycosylation and pathways governing growth control.  Both the Insulin receptor (InR) signaling pathway and the Epidermal growth factor pathway acting through c-myc are known to control growth in Drosophila, roles that are conserved in mammals. To begin to address whether alg10 disrupts InR signaling, I examined the genetic interaction between alg10 and an activated form of InR that produced large disordered eyes.  By removing half the Alg10 activity in this background, an enhanced phenotype was observed with an irregular eye surface, fused ommatidia, and patches of necrotic tissue.  This indicates a genetic interaction between alg10 and the dInR pathway and suggests alg10 influences InR mediated growth control.  This work was funded by an HHMI Undergraduate Research Scholarship.

Evan also spoke about his work in the American Society for Biochemistry  and Molecular Biology Symposium on "Extracellular Matrix at the Organism Scale."

Parathyroid Hormone (PTH) Reduces the Elastic Modulus of Osteoblasts through Disruption of the Actin Cytoskeleton

Gregory Russell Madden, Randall Duncan,
Weidong Yang, and  Manisha Malik.

Department of Biological Sciences

Bone responds to mechanical stimulation with an increase in bone formation, in vivo, yet mechanosensitivity is lost upon continued stimulation. Osteoblasts rapidly increase actin stress fibers in response to mechanical loading and we predict that this increase
may induce mechanical desensitization. Parathyroid hormone (PTH) enhances the response of bone to mechanical loads and briefly destabilizes the actin cytoskeleton. We postulate that PTH increases cellular elasticity, and hence mechanosensitivity, through disruption of actin stress fibers. The cellular elasticity of MC3T3- E1 osteoblasts was quantified using atomic force microscopy in ramping mode to establish the stress-strain curve of the cell. We found that PTH treatment for 30 min increased the elasticity of an osteoblast two-fold. Confocal microscopy studies demonstrate that
actin stress fiber formation is increased in MC3T3-E1 cells within 15 min of initiation of fluid shear and that addition of 50 nM PTH prevents this increase in actin organization. These results indicate that PTH increases the intracellular elasticity of osteoblasts by
disrupting the actin cytoskeleton that may explain the PTHenhanced response of bone to mechanical loads. Continuing studies will define the elastic modulus of osteoblasts during fluid shear and cytoskeletal disruption and correlate the elastic modulus with cellular responses to mechanical load. (Supported by HHMI and NIH/NIAMS AR043222)

Greg is pictured with his research advisor, Randall Duncan.

Effect of Calibration Method on Estimation of Central Pressure
at Rest and During Cold Pressor Testing.

Justin Moses, Adam Fullenkamp, and
David G. Edwards

Dept of Health, Nutrition, and Exercise Sciences,
University of Delaware

Non-invasive estimates of central blood pressure (CP) using a radial transfer function would be valuable in physiologic studies since central systolic pressure (CSP) better reflects myocardial demand. However, this technique appears to be dependent on the calibration method. The purpose of this study was to determine the effect of different calibration procedures on CP estimates at rest and during cold pressor testing. Fifteen healthy subjects (age 23.5 ± 2 years) underwent blood pressure measurement in the left brachial artery (BP) and simultaneous recording of brachial and radial artery waveforms in the right arm. The right foot was placed in ice water and measurements were repeated 90 seconds later. The radial pressure wave was calibrated using BSP and BDP (Cuff), diastolic and brachial mean arterial pressure (MAP) determined from the brachial wave (BM), or diastolic and MAP calculated as 1/3PP + DP (CM). CP was estimated for each calibration method from the radial wave via a transfer function. Cold pressure testing increased (p<0.05) BSP (109 ± 2 vs. 127 ± 3 mmHg) and BDP (62 ± 2 vs. 77 ± 3 mmHg). Radial SP varied from BSP by + 9 and + 7 mmHg when calibrated using BM and CM respectively. As a result BM-CSP was 6.1 ± 1 and 4.5 ± 1 mmHg greater (p<0.05) than Cuff-CSP and EM-CSP respectively however all 3 methods tracked the cold pressor response similarly. Estimates of CP using a radial transfer function are dependent on the method of calibration. However, the ability to track changes in CP using a transfer function is not dependent on calibration and may provide valuable physiologic information.

Characterization of SMA Fibroblast Cell Lines
Using Pyrosequencing

Sarah Swain and Vicky Funanage

A. I. DuPont Hospital for Children

Spinal Muscular Atrophy (SMA) is an autosomal recessive disease that is caused by mutation or deletion of the survival motor neuron gene 1 (SMN1).  SMN2, which is 99% identical to SMN1, is present in all patients but is unable to compensate for SMN1.  A base change in exon 7 is responsible for the alternative splicing of SMN2 transcripts.  Full-length transcripts are predominantly produced by SMN1, whereas SMN2 produces Δ7 mRNA and little full-length transcript.  Thus, SMA results from insufficient levels of SMN protein in motor neurons.  The severity of the disease seems to inversely correlate with SMN2 copy number making determination of SMN copy number crucial for clinical diagnosis and prognosis. Genetic diagnosis of SMA involves PCR amplification followed by DraI enzyme digestion analysis.  The disadvantages of this approach include underestimation of SMN copy number and the lack of a true quantitative assessment.  We are developing a Pyrosequencing method that allows sensitive and quantitative determination of SMN copy number using a modified genotyping assay that includes the cystic fibrosis transmembrane regulator gene (CFTR) as an internal standard.  SMN and CFTR are amplified in a multiplex PCR and then analyzed by Pyrosequencing.  SMN copy number can be determined by comparing the peak height of the SMN genes to standard peaks in CFTR.  This research was funded in part by the Howard Hughes Medical Institute Undergraduate Science Education program.

Sarah is president of the American Society for Biochemistry and Molecular Biology. She recieved a $400 travel award from the Society to come to the meetings and present her research.

Elucidating the Role of Junctional Adhesion Molecule-A Homodimerization in Angiogenesis

Wen Allen Tseng
and Ulhas Naik

Department of Biological Sciences

Angiogenesis is the formation of new blood vessels from pre-existing ones.  It is involved in both physiological and pathological processes.  Junctional adhesion molecule-A (JAM-A) is required for the induction of angiogenesis by basic fibroblast growth factor.  JAM-A is also known to form homodimers in vitro and in vivo.  This study intends to determine the relationship between JAM-A homodimerization and angiogenesis.  For this purpose, site-directed mutagenesis was performed on JAM-A cDNA constructs to introduce mutations designed to impair homodimerization.  Our goal is to use these constructs to examine the relationship between angiogenesis and JAM-A homodimerization in a blood vessel endothelial cell model.  In order to confirm that the mutations do, in fact, impair homodimerization, Chinese hamster ovary (CHO) cells were transfected with wild-type or mutant JAM-A constructs.  The cells were then treated with a cross-linker, bis(sulfosuccinimidyl) suberate (BS3), lysed, and subjected to Western blotting for JAM-A.  Putative homodimer bands were seen at roughly twice the molecular weight of monomeric JAM-A.  Dimer bands were detected at similar intensities for both mutant and wild-type JAM-A, indicating no difference in homodimerization.  A different approach may be needed to detect any differences.  This research was funded by the Arnold and Mabel Beckman Foundation and the Barry M. Goldwater Foundation.

won honorable mention for his work in the ASBMB Undergraduate Poster Competition.

Some photos of the trip from various sources.

US Capitol Building

Prepared for departure in front of Mckinly Lab

Evan, Joseph, Allen, James, and Justin at the ASBMB poster competition.

Sarah Swain, Dr. Hal White, and James Kelleher.

Alumni Dinner, Clockwise from left:
Dr. Seung Hong, Dr. David Usher, Mrs Usher, Elisabeth Mari (BS '05) and friend,
Greg Madden, and Caitlin Haag.

Alumni Dinner, Clockwise from front left: Dr. Gary Laverty, Ashley Anttila, Linday Higdon,  Corrine Decker,  Jen Buss (BS '06), Sarah Swain,
Justin Moses, and Aly Bourreza.

Alumni Dinner, Clockwise from left: Charles Drummer, Joseph Feng, Evan Lebois, Allen Tseng, Pat Knerr, James Kelleher,
and Vivek Desai.

Alumni Dinner, Clockwise from front left:
 Michael Skinner (BS '96), Eugene Antiopov (BS '02) and guest, Dr. Hal White and daughters Rachel BA '02 and Anna BA '97, and Lilian Pintea.

Dr. White in his role as judge of posters from non-UD students.

Dr. White with Honorable Mention winners Lindsay higdon and Allen Tseng.

Washington DC Convention Center
Washington DC Convention Center

Mobile in the Convention Center.

Taking a break from the Scientific Session, UD group see some Washington Sights.
Washington DC Convention Center Washington DC Convention Center

Aly Bourreza with Dr. White.

Sarah, Evan, and Joseph at the Convention Center.

Joseph Feng with his poster.

Justin, Lindsay, Pat, Aly,Sarah, Evan, and Corrine at the Lincoln Memorial.

Justin, Aly, Sarah, and Pat at the Washington Monument.

Ashley answering questions after her symposium talk.

The trip to the Experimental Biology Meetings in Washington, DC was organized by the University of Delaware HHMI Undergraduate Science Education Program with additional support from travel grants from the American Society for Biochemistry and Molecular Biology and the Beckman Scholars Program. The HHMI Program, the Beckman Scholars Program, Charles Peter White Fellowships, and the Undergraduate Research Program supported research by the students.

ASBMB Undergraduate Poster Competition in San Francisco 2006
Return to HHMI Undergraduate Home PageUniversity of Delaware HHMI Home Page
Created 19 December 2006,  revised 7 May 2007 by Hal White [halwhite at]
Copyright 2007, Harold B. White, Department of Chemistry and Biochemistry, University of Delaware