Promotion and inhibition of mutation in pathogens

• Main Author: Maurice Samuel Devaraj
• Format: Article
• Language: English
• Published: Limited liability company «Science and Innovations» (Saratov) 2014-03-01
• Series: Russian Open Medical Journal
• Subjects: directed mutation; Escherichia Coli; drug-resistance; streptomycin; magnesium ion
• Online Access: http://www.romj.org/node/91

This paper presents the research findings of a sequence of three experiments that were used to assess the impact of a cell’s stage in its life cycle on mutatability and its possible mechanism. The first experiment consisted of a modified fluctuation test (Luria-Delbruck) to test for concurrency of jackpot streptomycin-resistant mutant colony in synchronously treated cultures. The second experiment consisted of performing the same test with each set of parallel cultures consisting of different media that included adenosine tri-phosphate (ATP), adenosine di-phosphate (ADP), adenosine mono phosphate (AMP), and adenosine, to see if these compounds, whose levels were modified in bacterial cells during cell division, promoted or suppressed mutation. A third experiment was performed using the same methodology to test the effect of magnesium on the occurrence of the mutant colonies. In the first experiment, the occurrence of jackpot counts of streptomycin-resistant bacteria was concurrent among parallel cultures, indicating that mutation was directed. In the second experiment, ATP and adenosine suppressed mutation, though in different levels. ADP and AMP promoted mutation in different levels. In the third experiment, addition of extracellular magnesium (in the form of magnesium sulphate) promoted mutation, even in the presence of adenosine, which was identified as a mutation suppressor in experiment 2. We conclude that bacterial mutation is a directed response to external stress and that mutatability is dependent on the cell’s phase during the time of external stress. We also conclude that mutation is possible during the cell division process due to the availability of cellular magnesium for ribosomal ribonucleic acid (rRNA) modification. Findings from this research may be used to prevent development of drug resistance, whether epigenetic or arising due to deoxyribonucleic acid (DNA) modification, in several pathogens, especially Mycobacterium tuberculosis through the co-administration of adenosine along with antibiotic treatment.