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dc.contributor.advisorMcGillivray, Shauna
dc.contributor.authorKouretas, Bella
dc.date5/19/2022
dc.date.accessioned2022-07-22T13:16:04Z
dc.date.available2022-07-22T13:16:04Z
dc.date.issued2022
dc.identifier.urihttps://repository.tcu.edu/handle/116099117/54217
dc.description.abstractThe gram-positive bacterium, Bacillus anthracis, is responsible for the deadly disease Anthrax. B. anthracis is dangerous due to virulence factors, or defenses the bacteria uses to infect a host. We hope to better understand how this bacterium interacts with its hosts by studying the genes necessary for virulence. Bacterial mutants, which have a change in their genetic sequence, sometimes show reduced ability to cause disease in a host. Studying these mutants helps us understand the bacteria's infection method. Previously, our lab created a library of mutants using a technique called transposon mutagenesis and then screened these transposon mutants for phenotypes linked to decreased virulence. This resulted in the identification of 11 transposon mutants that were less effective at causing disease in the nematode Caenorhabditis elegans. To prioritize these mutants, we tested them using a second infection model, the caterpillar Galleria mellonella. G. mellonella is an ideal model due to its optimal size for injection, conserved innate immune defenses, and previous success as an infection model for B. anthracis. We found that only one of these 11 mutants, TN2, had reduced virulence in both C. elegans and G. mellonella. Future research will focus on confirming the genetic change in this mutant and determining the mechanism by which it contributes to infection. This could lead to new antibiotic targets in the future.
dc.subjectAnthrax
dc.subjectGalleria mellonella
dc.subjectBacillus anthracis
dc.subjectvirulence
dc.titleInvestigation of the glycosyl-like 2 transferase family protein and its role in Bacillus anthracis virulence
etd.degree.departmentBiology
local.collegeCollege of Science and Engineering
local.collegeJohn V. Roach Honors College
local.departmentBiology


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