Beckman Foundation Scholar Awards

Boston University and UROP are proud to announce that we received a three-year Arnold & Mabel Beckman Foundation Scholars Program Award starting in 2014, which marks the sixth time that Boston University has received a Beckman Award. The current Beckman award will allow six Boston University students to receive generous two-year Scholar awards to conduct independent research. Two Beckman Scholars were selected in April 2015 and we will be selecting two new scholars in April 2016.

Each student named as a Beckman Scholar performs research part-time during two academic years and full-time over two summers. The Beckman Scholar Award consists of a stipend ($4,600 per academic year, $6,800 per summer), a travel and supplies allowance ($2,800), and a mentor allowance for travel and supplies ($5,000). The award also includes a trip to the Beckman Scholars Annual Research Symposium, held each summer in Irvine, CA, where each student will present his or her research to a group of Beckman scholars, mentors, scientists, and administrators. Competition for this award is open to Boston University sophomores who are US Citizens or Permanent Residents and who are majoring in Biology, BMB, Chemistry or Biomedical Engineering. For more information on the award and the application process, please click here.

Beckman Scholars

The 2015 Beckman Scholars are pictured below.


Anastasia Nizhnik

Advisor: Dr. Cynthia Bradham, Department of Biology
Molecular Characterization of Genes Specifying Skeletal Patterning in the Sea Urchin Model

Developmental patterning is a complex process that regulates tissue specification and morphogenesis. The sea urchin larval skeleton provides a comparatively simple model in which to study patterning of developmental events. Skeletal patterning in the sea urchin embryo requires cell-cell interactions between the pattern-containing ectoderm and the skeletogenic primary mesenchyme cells (PMCs). The Bradham lab previously performed a high-throughput screen to identify ectodermal patterning genes. This work identified SVEP and LOX as ectodermally expressed gene candidates for specifying skeletal patterning. SVEP encodes an adhesion protein that had not previously been characterized in the sea urchin. LOX is a gene whose product, lipoxygenase, acts on arachidonic acid to produce HETES, which in turn impacts multiple signal transduction pathways including PI3K, PKC, and Ras signaling. A genetic loss-of-function (LOF) analysis for either SVEP or LOX led to dramatic defects in the orientation of the initial skeletal elements, which are known as triradiates. The purpose of this project is to understand how the genes SVEP and LOX work together to orient the larval skeleton. Our goal is to perform combined LOF for SVEP and LOX to determine if the triradiate orientation defects observed in the individual LOF studies are additive or synergistic. That is, the scholar will investigate skeletal morphology, PMC positioning and triradiate orientation in double LOF embryos (i.e., embryos with SVEP and LOX simultaneously inactivated). The results of this project will establish the function of SVEP and LOX in sea urchin embryonic skeletal patterning.  Understanding the molecular mechanisms underlying skeletal pattern formation in sea urchin embryos will likely uncover conserved patterning genes and their functions. Interestingly, many of the skeletal patterning candidate genes identified in the Bradham lab have been generally implicated in developmental patterning as well as cancer migration and metastasis. Thus, a more complete understanding about how these sea urchin genes function to direct cell migration and skeletal patterning will provide information about developmental processes, and will likely also provide insight into cancer progression.

Nicole Carter

Advisor: Dr. Thomas Gilmore, Department of Biology
Characterization of Transcription Factor NF-κB from Invertebrate Models to Understand the Molecular Basis of Immunity and Symbiotic Relationships

Almost all organisms, including humans, have symbiotic relationships with other organisms, which are essential for the health of both organisms. To cite one prominent example, the health of coral reefs often relies on symbiotic relationships between corals (members of the phylum Cnidaria) and photosynthetic algae, and these symbiotic relationships can be interfered with by external stresses (ocean acidification, warming, etc.). However, little is known at the molecular level about how these relationships are maintained, or disrupted. This project, which is being conducted in collaboration with the lab of Virginia Weis at Oregon State University, seeks to deepen our understanding of the molecular processes that occur during symbiosis in simple marine ecosystems. Specifically, we are using a model cnidarian, the anemone Aiptasia pallida to explore symbiotic relationships involving the anemone and a series of symbiotic algae. Specifically, the project aims to characterize activation of the NF-κB transcription factor pathway in Aiptasia in response to symbiont introduction or escape. NF-κB is well-known for its role in immunity from flies to humans, and based on preliminary results from Aiptasia, it is a reasonable hypothesis that NF-κB is also be involved in host-symbiont or host-pathogen responses in lower organisms. The Gilmore lab has shown that cnidarians including Aiptasia contain NF-κB, but its exact role in marine cnidarians is only poorly understood, NF-κB. For this project, I have cloned the cDNA encoding Aiptasia, and have conducted preliminary experiments towards characterizing the protein, Ap-NF-κB. Using cell- and lab-based model systems, I will characterize effects of environmental stress and the consequent loss of symbiosis on NF-κB activity. Overall, the outcome of this research will likely reveal the evolutionary basis of vertebrate immunity, and provide information on the effects of environmental stress on molecular pathways in sensitive marine organisms.

Information on past Beckman Scholars is available here.