| dc.description.abstract | Anthrax is caused by Bacillus anthracis, a deadly gram-positive bacterium that could be used as a potential bioterrorist weapon. B. anthracis has virulence factors that contribute to its deadly nature by helping the bacterium evade destruction by the host immune system. One of these factors is a protease subunit called ClpX which was shown to be essential for virulence in animal models. Loss of ClpX also resulted in decreased resistance to antimicrobial peptides, an essential part of innate immunity. However, it is not yet understood why the loss of ClpX results in a loss of resistance to antimicrobial peptides in B. anthracis. More recently, we have seen that B. anthracis lacking ClpX has aberrant cell division resulting in mini-cell formation. Mini-cell formation can occur when there is too much expression of cell division proteins such as FtsZ. Interestingly, ClpX regulates FtsZ expression in bacterial species such as E. coli. For these reasons, we hypothesized that loss of ClpX would lead to overexpression of FtsZ and to mini-cell formation. These mini-cells may be contributing to decreased resistance to antimicrobial peptides. To test this hypothesis, we overexpressed FtsZ using an inducible vector in B. anthracis and exposed the cells to increasing concentrations of an antimicrobial peptide called LL-37. However, we found that after exposure to antimicrobial peptides with increased levels of FtsZ B. anthracis did not exhibit the same phenotype as the ClpX mutant. Thus, our results suggest that the rise in FtsZ levels may not be a key factor in the loss in B. anthracis resistance to antimicrobial peptides in the ClpX mutant. | |
