RNA Therapeutic Lab Report

Satisfactory Essays
Introduction: Mutation within cell populations are seldom.1 The mutS gene in E.coli takes part in the repair and recombination of DNA.2 When mutS was deleted from E.coli in a previous study, the mutation rate increased when compared to the wild type strain.2 Rifampicin is known for its inhibition of RNA Polymerase production.3 Without RNA Polymerase, RNA is incapable of production and thus protein synthesis ceases within the cell, resulting in cell death. We hypothesize that since mutS repairs recombinant DNA within E. coli, the deletion of the mutS gene will increase the mutation rate of E. coli.
Method: 100 mL of undiluted wild type and △mutS strains of E. coli were applied to separate Rifampicin (+) plates. We prepared 10 mL of wild type and △mutS strains in test tubes along with three 90 mL test tubes containing water for each strain. We then performed a serial dilution by pipetting 10 mL of wild type strain into
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Although the data did not support our hypothesis, it is widely believed that the data was skewed due to an unexpected mistake. The error may have been due to a distribution error prior to the experiment where the ΔmutS and wild type strains were mislabeled and thus all data resulting from the experiment was reversed for both strains. If the data was merely flipped, then our hypothesis still stands true in terms of validity. Due to the deletion of the mutS gene, the bacteria has lost an essential component that repairs mutated recombinant DNA. This will indirectly show a greater number of colonies representing the mutated surviving bacteria.2 The wild-type strain of E. coli still has its mutS gene present and thus reparations to the mutated DNA occurs normally. As seen in the wild-type plates, lower number colonies were present since not enough bacterial colonies were mutating to gain resistance against the rifampicin
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