The Environmental Mutagenesis & Genomics Society has announced the inaugural winners of the EMGS Undergraduate Research Scholarship Program.
Amanda Morin, a student in the Biology Department at the University of Western Ontario, and Meghan Davis, a Biological Engineering student at the Massachusetts Institute of Technology, were selected from a field of applicants by the EMGS Awards & Honors Committee.
The aim of the scholarship program is to improve the participation and engagement of underrepresented undergraduate students in EMGS-related activities by encouraging scientific research by underrepresented undergraduate students and support their attendance at EMGS annual meetings.
Applicants were asked to seek the sponsorship of an EMGS member and to submit a proposal for a research project to be conducted in a in the sponsor’s lab for at least one semester. Morin’s EMGS member sponsor is Kathleen Hill, Ph.D., of the University of Western Ontario. According to her application, Morin’s research project will examine the “compelling evidence for genotoxicity associated with microplastics.” Davis’s EMGS member sponsor is Laurie Boyer, Ph.D., a Biology professor at MIT. According to her application, Davis’s research project “aims to further investigate the mechanism by which doxorubicin causes cardiotoxicity by assessing the impact on DNA damage and regulation, in addition to mitochondrial function and sarcomere organization following treatment leading to the cardiotoxic phenotype.”
Both Morin and Davis will receive financial support ($1,000 for materials and supplies) to conduct their research project, as well as travel support (up to $1,500) to attend the annual EMGS meeting and to present their research findings as a poster and/or platform presentation. The annual meeting is scheduled for Sept. 16-20 in Palm Springs, Calif.
Amanda Morin’s Research Proposal: “There is compelling evidence for genotoxicity associated with microplastics. The Hill laboratory is assessing micronuclei frequencies in wild-caught native fish species of the Great Lakes and our local waterways with associated metrics of microplastics burden. We are also using a brine shrimp model for directly assessing microplastic size and genotoxicity using biomarkers of DNA damage and cytotoxicity. Amanda’s role will be to carry out assays of DNA damage and cytotoxicity in fish tissues collected to date and design and assess genotoxicity using microplastic exposure experiments in our brine shrimp system. Amanda will work with our interdisciplinary team that includes earth scientists who characterize microplastics in the Great Lakes and our fisheries scientists.”
Meghan Davis’s Research Proposal: “Cardiotoxicity is a well-documented impact of numerous drugs and chemicals that negatively impact heart function. One notable example of this are anthracyclines, such as doxorubicin, which are powerful chemotherapeutic agents that are efficacious in combating various forms of cancer. Notwithstanding, their prescription and use are limited by the severe cardiotoxic phenotypes which often present in patients taking these drugs. The cardiotoxic effects anthracyclines and some of their preventative medications are underdeveloped at a cellular level, which impedes the use of cardioprotective drugs in clinic as well as their development. It is currently understood that the cardiotoxicity is dose-dependent as well as cumulative and can lead to lasting detrimental effects. Additionally, the current understanding of doxorubicin’s mechanism includes degrading cardiolipin, increasing reactive oxygen species generation, and causing Tob2b mediated DNA damage. The present study aims to further investigate the mechanism by which doxorubicin causes cardiotoxicity by assessing the impact on DNA damage and regulation, in addition to mitochondrial function and sarcomere organization following treatment leading to the cardiotoxic phenotype. In my work in the Boyer lab, I have worked to develop this characterization – first in vitro and currently translating to an in vivo model. We have shown so far that doxorubicin induced cardiotoxicity is characterized at a cellular level by an increase in oxidative phosphorylation and mitochondrial membrane potential, but not necessarily DNA damage, however we suspect there is a change in the epigenetic regulation seen in our in vivo model. I am incredibly excited to further characterize these nuclear and mitochondrial changes due to chemotherapy treatment as I have seen their impacts in my own life.”