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Journal of Undergraduate Research

Keywords

biofilm binding, Yersinita pestis, Yersinita pseudotuberculosis

College

Life Sciences

Department

Microbiology and Molecular Biology

Abstract

Yersinia pestis — the causative agent of the deadly bubonic plague, which killed over one-third of Europe in the 14th century – spreads quickly from person to person due to its ability to create a biofilm, characterized by bacterial adhesion to themselves and surfaces. The bacteria infects fleas and forms a biofilm in their midgut, which causes the flea to both feed more often and cough up bacteria biofim into each new host. In this way, the formation of a strong biofilm is essential for the rapid spread of the bubonic plague. In my experiment, I analyzed which genes would most hinder or help the bacteria Yersinia pestis to create such a biofilm, by studying mutants of the most recent relative of Y. pestis, Y. pseudotuberculosis. The mutants (csrB::Tn5, barA::Tn5, uvrY::Tn5, and rcsB::Tn5) were created through transposon mutagenesis, and the name of each gene (csrB, barA, uvrY, rcsB) corresponds to the gene that was interrupted, thus rending it functionless. By studying these mutants and comparing them to the wild type strain, I can deduce which of these four genes inhibits biofilm production, stmulate biofilm production, or has no effect. Previous research in my lab showed qualitative results (by growth on congo red agar) that suggested the csrB mutant creates a strong biofilm, in comparison to the wild type. The csrB mutant appears dark red, whereas the wt appears almost white, suggesting that the csrB takes up more dye than the wt and thus creates a stronger biofilm. My goal in this project is to quantify those earlier findings.

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