Persister Cells in E. coli

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Bacterial populations form dormant, antibiotic tolerant cells called persister cells. Persister cells are not mutants but phenotypic variants of the wild type ⁵. Persisters are selected to increase chances of survival in fluctuating environments ². Persisters are “phenotypic variants” that “enter a non-growing, dormant state.” The dormant state is distinguished by diminished activity of key molecules. Persisters can be distinguished from normal cells due to their reduced growth rate ². Cells in the persister state are highly immune to bacterial antibiotics, which interfere with processes of key molecules ¹. Persisters may represent the long-looked-for explanation for biofilm tolerance to antibiotics ³.

Section 1

Electron micrograph of the Ebola Zaire virus. This was the first photo ever taken of the virus, on 10/13/1976. By Dr. F.A. Murphy, now at U.C. Davis, then at the CDC.

At right is a sample image insertion. It works for any image uploaded anywhere to MicrobeWiki. The insertion code consists of:
Double brackets: [[
Filename: Ebola virus 1.jpeg
Thumbnail status: |thumb|
Pixel size: |300px|
Placement on page: |right|
Legend/credit: Electron micrograph of the Ebola Zaire virus. This was the first photo ever taken of the virus, on 10/13/1976. By Dr. F.A. Murphy, now at U.C. Davis, then at the CDC.
Closed double brackets: ]]

Other examples:
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Subscript: H₂O
Superscript: Fe³⁺

Overall paper length should be 3,000 words, with at least 3 figures with data.

Section 2

Include some current research in each topic, with at least one figure showing data.

Section 3

Include some current research in each topic, with at least one figure showing data.

Further Reading

[Sample link] Ebola Hemorrhagic Fever—Centers for Disease Control and Prevention, Special Pathogens Branch

References

[(1) Balaban, Nathalie Q., et al. "A problem of persistence: still more questions than answers?." Nature Reviews Microbiology 11.8 (2013): 587-591.] [(2) Balaban, Nathalie Q., et al. "Bacterial persistence as a phenotypic switch." Science 305.5690 (2004): 1622-1625.] [(3) Brown, Breann L., et al. "The Escherichia coli toxin MqsR destabilizes the transcriptional repression complex formed between the antitoxin MqsA and the mqsRA operon promoter." Journal of Biological Chemistry 288.2 (2013): 1286-1294.] [(4) Cheow, Wean Sin, Matthew Wook Chang, and Kunn Hadinoto. "Antibacterial efficacy of inhalable levofloxacin-loaded polymeric nanoparticles against E. coli biofilm cells: the effect of antibiotic release profile." Pharmaceutical research 27.8 (2010): 1597-1609.] [(5) Dörr, Tobias, Marin Vulić, and Kim Lewis. "Ciprofloxacin causes persister formation by inducing the TisB toxin in Escherichia coli." PLoS biology 8.2 (2010): e1000317.] [(6) Fauvart, Maarten, Valerie N. De Groote, and Jan Michiels. "Role of persister cells in chronic infections: clinical relevance and perspectives on anti-persister therapies." Journal of medical microbiology 60.6 (2011): 699-709.] [(7) Gefen, Orit, and Nathalie Q. Balaban. "The importance of being persistent: heterogeneity of bacterial populations under antibiotic stress." FEMS microbiology reviews 33.4 (2009): 704-717.] [(8) Gefen, Orit, et al. "Single-cell protein induction dynamics reveals a period of vulnerability to antibiotics in persister bacteria." Proceedings of the National Academy of Sciences 105.16 (2008): 6145-6149.] [(9) Hofsteenge, Niels, Erik van Nimwegen, and Olin K. Silander. "Quantitative analysis of persister fractions suggests different mechanisms of formation among environmental isolates of E. coli." BMC microbiology 13.1 (2013): 25.]

Edited by (your name here), a student of Nora Sullivan in BIOL168L (Microbiology) in The Keck Science Department of the Claremont Colleges Spring 2014.