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Antibiotic Resistance - Coggle Diagram
Antibiotic Resistance
Materials and Methods
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After 72 hours, the mice were killed and tissues extracted from their thighs were analyzed
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An additional study was performed by taking different mutant strains of E. Coli and plating them on solid media, using the lacZ strain as a control
To illustrate how the lexA strain plays a role in the SOS response, measurements were taken of the growth and persistance of the lexA mutant strain after being expose to 40 ng/ml of ciprofloxacin
To see if lexA is required for additional mutations, both the lexA and lacZ E.C. strains were exposed to 650 ng/ml of ciprofloxacin
To illustrate how the cross-link repair pathway is initiated by the antibiotics, sensitivity rates were measure prior to exposure and after exposure.
Finally, to illustrate how LexA cleavage will initiate resistance, several polymerases were examined.
Discussion
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Ciprofloxacin and rifampicin are some of the most important and widely used antibiotics on the market
Researchers are concerned that all antibiotics available to treat bacterial diseases have known resistant strains
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This experiment showed that if LexA cleavage was inhibited, so was bacterial resistance
Increasing mutation rates could be caused by various recombination pathways that are employed to repair DNA damage caused by antibiotics
Finally, it was discovered that substitution mutations require derepression of all SOS-regulated polymerases.
Researchers hope to further investigate how the prevention of LexA cleavage forming might be a useful strategy in combating antibiotic resistant strains.
Results
After examining the second set of mice injected with the rifampicin, it was found that while the infection was slowed by the rifampicin, the lacZ also showed significant levels of resistance while the lexA did not
After examining the solid agar plates with E. Coli mutant strains and lacZ as the control, it was discovered that within 24 hours time, ciprofloxacin killed 99% of the bacterial cells
After examining the thigh tissue, it was found that the tissue injected with the lacZ strain showed significant levels of resistance while the tissue injected with the lexA strain showed no resistant mutants
After exposing the lexA strain to 40ng/ml of ciprofloxacin, results showed that lexA was moderately sensitive to more concentrated doses of ciprofloxacin. However, compared to the lacZ strain, lexA showed a higher rate of mutation.
After being exposed to 650 ng/ml of ciprofloxacin, results showed that if LexA cleavage is not present, E. coli show slower rates of resistance.
Results show that the cross-link repair pathway showed no signs of sensitivity or mutation rates, even when compared to the control strain.
After examining the various polymerases, results showed that deleting a single LexA-repressed polymerase had the same effects as inhibiting LexA cleavage. According to these results, derepression of these polymerases is responsible for LexA cleavage initiates substitution mutations.
Introduction
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Antibiotic resistance threatens the progress that the medical community has made since discovering Penicillin
Bacteria become resistant to these antibiotics by mutating their genes that encode for topoisomerases
The hypothesis was that since it is thought that ciprofloxacin causes repair pathways using RecA-ssDNA filament formation, ciprofloxacin may cause the mutations that grant resistance
This experiment attempts to show that interference with LexA autoproteolysis prevents E. Coli from mutating and becoming resistant to ciprofloxacin
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Citation (CSE - Name,Year)
Cirz RT, Chin JK, Andes DR, de Crécy-Lagard V, Craig WA, Romesberg FE. 2005. Inhibition of Mutation and Combating the Evolution of Antibiotic Resistance. Waldor M, editor. PLoS Biology. 3(6):e176. doi:https://doi.org/10.1371/journal.pbio.0030176.
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How this topic fits into my grant proposal: I believe this topic, Antibiotic Resistance, and the data in this paper perfectly illustrate the complexity and the concern of antibiotic resistant strains becoming more prevalent. I would like to continue with this line of research and apply for a grant to further investigate the mechanisms by which bacteria become resistant.