Discipline: Biological Sciences
Constance B. Staley - Bennett College
Co-Author(s): Mariama D.S. Ibrahim, East Carolina University, Greenville, NC; Morgan L.Thornton, University of North Carolina at Asheville, Asheville, NC; Dr. Rasheena D. Edmondson, Bennett College, Greensboro, NC; Dr. Akamu Jude, Joint School of Nanoscience and Nanoengineering, Greensboro, NC; Dr. Misty Thomas, North Carolina Agricultural and Technical State University, Greensboro, NC; Dr. Joseph L. Graves Jr. Joint School of Nanoscience and Nanoengineering, Greensboro, NC.
In a 2018 report from the World Health Organization, a pandemic occurrence of antibiotic resistance has been suspected to cause infectious diseases across 22 countries. In the past several decades, research studies have revealed the occurrence of antimicrobial resistance due to misuse, overprescribing, and rapid the evolution of resistance to antimicrobials. However what accounts for the persistence of resistant clones in the absence of the antimicrobial? Compensatory mutations allow for resistance to persist in a microbial environment deprived of a certain antimicrobial (metal or antibiotic). The Graves’s Laboratory has shown that E. coli can evolve resistance to Fe2+. In addition, these strains also acquired resistance to other metals (Ga3+ and Ag+) and traditional antibiotics (e.g. ampicillin, rifampicin, and tetracycline) which are associated with mutations in a number of genes in these bacteria.
To test whether Fe2+ resistance would persist in the absence of excess iron, the Fe2+-resistant populations were cultured in standard DMB medium without additional iron. It is predicted that deprived of Fe2+ these populations should lose iron (and correlated resistances). However, should compensatory mutations arise, some and possibly all resistances should persist in the population. Here we will report genomic data comparing the Fe2+ – selected bacteria to their progeny grown in the absence of excess Fe2+. Our research is ongoing. This research will aid in potentially unveiling compensatory mutations, and the mechanisms of action of these mutations behind the ever-spreading resistance to traditional metals and antibiotics.
Funder Acknowledgement(s): This material is based in part upon work supported by the National Science Foundation under Cooperative Agreement No. DBI-0939454. Any opinions, findings, and conclusions or recommendations expressed in this material are those of the author and do not necessarily reflect the views of the National Science Foundation.
Faculty Advisor: Dr. Joseph L. Graves Jr., firstname.lastname@example.org
Role: I used experimental evolution to culture Fe2+-resistant populations in standard DMB medium without additional iron. I also performed minimum inhibitory concentrations (MIC), contamination checks with Eosin Methylene Blue agar, DNA extraction, and DNA library prep for DNA sequencing.