You are here:

Genetics/Characteristics of E. Coli

Advertisement


Question
Hello Mr. Stecklein,

Long time, no see.  My experiment is going pretty well, especially after that blunder I made in the first trial.  Even though I have data recorded in tables, I need to put them into charts to make conclusions about the results.  Also, I still need to finish my experiment, I have three trials left.  Along with this experiment I have to do a research paper that contains information about my two mini-topics, which are E. Coli and electricity.  There are some characteristics of E. Coli that are not explained in great detail in many other sources, so I would like to ask you a few questions about this bacterium.

1. What is the complete life cycle of E. Coli, from birth to reproduction?  How does it grow and synthesize more organelles?

2. Although I have some knowledge about binary fission, which is the main form of reproduction in E. Coli, how frequently does binary fission occur, and how long does it take to occur?

3. Is the exact size of E. Coli bacteria about 0.5*1-3 micrometers?

3. What predators eat E. Coli?

4. E. Coli exists in the human feces, but what substances does it consume there?

5. Does it have any defenses against other organisms?  An example would be trichocysts in paremecium caudatum.

Thanks alot, as always.  I will try to get my results to you as soon as my experiment is completed.

Sincerely,
Aravind Kannan


Answer
Hi Aravind--

Glad to hear things are going well...

1.  E. coli grows like any other organism.  The life cycle can be described in terms of when they are inoculated into new media.  First, there will be a so-called lag phase in which the organisms will synthesize enzymes and proteins necessary to sustain themselves in new media--i.e., enzymes for carbohydrate and amino acid hydrolysis, etc.  After the microogranisms have the necessary enzymatic machinery, there will be an exponential increase in the number of bacteria (the logarithmic phase).  For the microbiology class I teach, i performed a calculation--I won't put all the math here, but needless to say, I found that starting with a single E. coli cell, assuming division approximately every 20 minutes, it would only take 1.77 days (~42.5 hours) for this single cell to replicate enough to fill the volume of the earth.  Why is the world not filled with bacteria?  Because this calculation made two very important assumptions--infinite supply of nutrients and immediate removal of waste products (neither of which are possible).  After this sharp rise in population, the growth will plateau (the stationary phase)--again, because they are running out of nutrients, metabolic wastes are building up, and physical space is becoming smaller.  Finally, the organisms will begin to die, thus, we observe the death phase.

2.  As you correctly stated, binary fission is the main reproductive method of E. coli (and most bacteria).  This process differs between different species...  For example, a marine microorganism known as Vibrio natrigens will multiply every 15 minutes if grown at optimal temperature and oxygen concentration.  E. coli is closer to 20 minutes (at optimal temperature), and then around 30 minutes for more average ambient conditions.  So what does this mean?  That every 20-30 minutes, E. coli is replicating its entire genome (4,639,221 base pairs) and translating proteins that will be necessary for the resultant daughter cells...

3.  That would be a very good estimate...

3b.  Bacteria do not generally eat eachother, nor do many organisms prey on bacteria.  Instead, bacteria generally suffer from the effects of competitors--some fungi and bacteria secrete soluble substances (like antibiotics) that will inhibit the growth or organisms around it.  Alternatively, things like bacteriophages (viruses that infect bacteria), can destroy bacterial cells as well.

4.  E. coli scavenges nutrients from the lumen of our intestines.  When you consume a meal, enzymes break down the food into things like sugars, lipids, and amino acids (by glycosylases, lipases, and proteases respectively).  These nutrients are suspended in the fluid that will traverse the entire length of the small and large intestines and eventually be secreted as feces.  The bacteria in the lumen of your intestines (primarily the large intestine) simply take nutrients out of this fluid or feces that the body has not absorbed.

5.  E. coli does have several defense mechanisms, many of which contribute to the virulence of pathogenic strains.  I've listed some examples below are some examples.  I won't go into explaining each of them as they are far beyond the scope of your project.  If you have any questions on any particular antigen, please let me know...

***Adhesins***
CFAI/CFAII
Type 1 fimbriae
P fimbriae
S fimbriae
Intimin (non-fimbrial adhesin)

***Invasins***
hemolysisn
siderophores and siderophore uptake systems
Shigella-like "invasins" for intracellular invasion and spread

***Toxins***
LT toxin
ST toxin
Shiga-like toxin
cytotoxins
endotoxin LPS)

***Antiphagocytic surface properties*** (IMPORTANT ONE)
capsules
K antigens
LPS

***Defense against serum bactericidal reactions*** (IMPORTANT ONE)
LPS
K antigens

***Defense against immune responses*** (IMPORTANT ONE)
capsules
K antigens
LPS
antigenic variation

Hope that helps!  Please let me know if you need any more help...

Let me know your final results and conclusions!

Shane

Genetics

All Answers


Answers by Expert:


Ask Experts

Volunteer


Shane Stecklein

Expertise

I can answer general questions in molecular and statistical genetics as well as those relating to general cellular and molecular biology. My primary interests are in cancer biology and immunology.

Experience

I am currently an undergraduate pre-medical student pursuing a B.S. in cellular biology with a minor in chemistry. I work as a research assistant in a molecular biology laboratory investigating the Adenomatous Polyposis Coli (APC) gene--this locus is mutated in over 80% of all colorectal cancers--my individual project is to investigate the interaction of the APC protein with elements of the cytoskeleton (particularly cytokeratin 18) in colonic epithelial cells. Our primary goal is to discern the mechanism by which the nuclear function (or lack thereof) of the mutated protein results in tumorgenic polyps. I also teach undergraduate laboratory courses in chemistry and microbiology at the University of Kansas. Upon completion of my undergraduate degree, I hope to enter an M.D., Ph.D. progam and pursue a career in radiology and nuclear medicine and continue to do cancer research.

Organizations
Tri-beta Honors Society
American Society for Microbiology
National Society of Collegiate Scholars
American Chemical Society

Education/Credentials
B.S. - Cellular Biology /w minor in Chemistry (Honors) (in progress)

Awards and Honors
State of Kansas Scholar
University of Kansas Honor Scholar
Mount Oread Scholar
National Collegiate Scholar

©2012 About.com, a part of The New York Times Company. All rights reserved.