Talk:Host Dependency of Mycobacterium leprae
What I liked most about your topic was how you compared M. tuberculosis to M. leprae. I found it most surprising that M. leprae had lost the genes encoding for NADH. When you say that this results in a less efficient aerobic pathway, do you know what levels of oxygen are the best for culturing the bacteria or if the oxygen levels impact how it tends to colonize epithelial cells and nonmyelin producing Schwann cells? I thought that how dead M. leprae cells or the cell wall in itself could still cause demyelination to occur was very interesting! Overall, I thought the topic was really interesting. While it covering quite a few different topics, all were explained very completely.
A couple of minor editing points in your article that you might address.
- In the introduction, the sentence "M. leprae has one of the slowest doubling times of any pathogen; it takes approximately 14 days for the cells to divide", is awkward. You don't need a semicolon when it could be described in two sentences. You do this a couple more times I think (also in the intro "The loss of these genes have caused M. leprae to rely on the host cell to survive; the bacteria needs an extremely specific environment to thrive in.") .
-In the introduction sentence "Many of these pseudogenes correspond to genes found in Mycobacterium tuberculosis that are still functional" the species name needs to be italicized.
- In the first couple of paragraphs of the Mycobacterium leprae genome (2nd section) there appears to be a consistent misspelling of the species name (as well as a lack of italics) for M. leprae.
- You changed your method of citing from numbers in rounded () brackets to author names in rounded brackets and then to author's names in square  brackets. It was confusing, I thought that you were trying to describe the particular name in a certain fashion for a reason.
Now for more relevant ideas on the material:
I think that it would be beneficial to your project if you considered the evolutionary relationship between M tuberculosis and M leprae. It seems possible that M leprae is a divergent form of M tuberculosis given the high percentage of pseudogenes found in M.leprae that correspond with a functional gene in M. tuberculosis. If there is any material about this relationship, I would love to hear some about it.