Conclusion
Our data indicates that the mutation for resistance to T2 is almost certainly not a result of exposure to T2 (the probability that our results were due to chance alone is approximately 0.01%). We recorded a dramatic, consistent increase in the number of colonies on re-spread plates as compared to the plates that were not re-spread, which is consistent with pre-existing mutations in the stock populations.
Analysis of Potential Error
The only data set that was well outside the bounds of expected/ average data was Mohsan’s data set. All of his numbers were greatly exaggerated, suggesting that he ended up plating more cells than anyone else. However, the consistency of his numbers across different sections of the experiment make a dilution error on his part doubtful, which leaves several possibilities. The two most likely of these possibilities are that he either received a higher concentration of E.coli in his original sample, or when drawing from his original sample, he allowed it to settle, and drew from the more concentrated bottom region.
Cullen and Neelo had identical data sets, which is a source of worry. However, as they were both working from the same source, it is not outside the realm of possibility, as the mutation frequency and original concentration would have been nearly identical.