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Author Topic:   Evolution starting with a single bacterium
Rrhain
Member
Posts: 6351
From: San Diego, CA, USA
Joined: 05-03-2003


Message 2 of 56 (104502)
05-01-2004 6:15 AM
Reply to: Message 1 by digitall
05-01-2004 5:40 AM


Yes, it has. Go to PubMed and look it up.
On a simpler scale, but demonstrating the same thing, here's an experiment you can do in the privacy of your own bio lab. It doesn't cost much and you can get the materials from any reputable biological supply house.
Take a single E. coli bacterium of K-type. This means the bacterium is susceptible to T4 phage. Let this bacterium reproduce until it forms a lawn. Then, infect the lawn with T4 phage.
What do we expect to happen? That's right, plaques should start to form and, eventually, the entire lawn will die. After all, every single bacterium in the lawn is descended from a single ancestor, so if the ancestor is susceptible, then all the offspring should be susceptible, too.
But what we actually see is that some colonies of bacteria in the lawn are not affected by the phage.
How can this be? Again, the entire lawn is descended from a single ancestor. They should all behave identically. If one is susceptible, then they're all susceptible. If one is immune, then they're all immune. This can't be an example of "adaptation" because if one could do it, they all could do it.
But since there is a discrepancy, we are left with only one conclusion: The bacteria evolved. There must be a genetic difference between the bacteria that are surviving and those that died.
Indeed, we call the new bacteria K-4 because they are immune to T4 phage.
But we're not done. Take a single K-4 bacterium and repeat the process: Let it reproduce to form a lawn and then infect the lawn with T4 phage.
What do we expect to happen? That's right: Absolutely nothing. All of the bacteria are descended from a single ancestor that is immune to T4 phage. Therefore, they all should survive and we shouldn't see any plaques form.
But we do. Plaques do, indeed start to form. How can this be? Again, all the bacteria in the lawn are descended from a single ancestor that was immune to T4 phage, so they should all behave identically. If one is immune, then all are immune. There must be something else going on.
Something evolved, but the question is what. What evolved? Could it be the bacteria experiencing a reversion mutation back to K-type? No, that can't be it. Suppose any given bacteria did revert back to wild. It is surrounded by K-4 type who are immune to T4 phage. As soon as the lawn is infected, those few bacteria will die and immediately be replaced by the offspring of the immune K-4 bacteria. We would never see any plaques forming because the immune bacteria keep filling in any holes that appear.
So if it isn't the bacteria that evolved, it must be the phage. And, indeed, we call the new phage T4h as it has evolved a new host specificity.
There is a similar experiment where you take bacteria that have had their lactose operons removed and they evolve to be able to digest lactose again.
You might want to look up the information regarding the development of bacteria capable of digesting nylon oligimers. It's the result of a single frame-shift mutation.

Rrhain
WWJD? JWRTFM!

This message is a reply to:
 Message 1 by digitall, posted 05-01-2004 5:40 AM digitall has not replied

Replies to this message:
 Message 3 by compmage, posted 05-01-2004 9:04 AM Rrhain has not replied

  
Rrhain
Member
Posts: 6351
From: San Diego, CA, USA
Joined: 05-03-2003


Message 5 of 56 (104701)
05-02-2004 4:36 AM
Reply to: Message 4 by digitall
05-01-2004 10:35 AM


digitall responds to me:
quote:
Rrhain,interesting do you have a source for the E.coli and T4 phage experiment.
My bio text. Life: The Science of Biology by Purves/Orians. This experiment is often done in high schools and intro bio labs in college.
But in response the direct question about evolution of antibiotic resistence in bacteria:
Robinson DA, Enright MC.
Evolution of Staphylococcus aureus by large chromosomal replacements.
J Bacteriol. 2004 Feb;186(4):1060-4.
PMID: 14762000 [PubMed - indexed for MEDLINE]
Conjugative transfer and replacement of hundreds of kilobases of a bacterial chromosome can occur in vitro, but replacements in nature are either an order of magnitude smaller or involve the movement of mobile genetic elements. We discovered that two lineages of Staphylococcus aureus, including a pandemic methicillin-resistant lineage, were founded by single chromosomal replacements of at least approximately 244 and approximately 557 kb representing approximately 10 and approximately 20% of the chromosome, respectively, without the obvious involvement of mobile genetic elements. The replacements are unprecedented in natural populations of bacteria because of their large size and unique structure and may have a dramatic impact on bacterial evolution.
Iwasa Y, Michor F, Nowak MA.
Evolutionary dynamics of escape from biomedical intervention.
Proc R Soc Lond B Biol Sci. 2003 Dec 22;270(1533):2573-8.
PMID: 14728779 [PubMed - indexed for MEDLINE]
Viruses, bacteria, eukaryotic parasites, cancer cells, agricultural pests and other inconvenient animates have an unfortunate tendency to escape from selection pressures that are meant to control them. Chemotherapy, anti-viral drugs or antibiotics fail because their targets do not hold still, but evolve resistance. A major problem in developing vaccines is that microbes evolve and escape from immune responses. The fundamental question is the following: if a genetically diverse population of replicating organisms is challenged with a selection pressure that has the potential to eradicate it, what is the probability that this population will produce escape mutants? Here, we use multi-type branching processes to describe the accumulation of mutants in independent lineages. We calculate escape dynamics for arbitrary mutation networks and fitness landscapes. Our theory shows how to estimate the probability of success or failure of biomedical intervention, such as drug treatment and vaccination, against rapidly evolving organisms.
Jaffe K, Issa S, Daniels E, Haile D.
Dynamics of the emergence of genetic resistance to biocides among asexual and sexual organisms.
J Theor Biol. 1997 Oct 7;188(3):289-99.
PMID: 9344733 [PubMed - indexed for MEDLINE]
A stochastic, agent based, evolutionary algorithm, modeling mating, reproduction, genetic variation, phenotypic expression and selection was used to study the dynamic interactions affecting a multiple-gene system. The results suggest that strong irreversible constraints affect the evolution of resistance to biocides. Resistant genes evolve differently in asexual organisms compared with sexual ones in response to various patterns of biocide applications. Asexual populations (viruses and bacteria) are less likely to develop genetic resistance in response to multiple pesticides or if pesticides are used at low doses, whereas sexual populations (insects for example) are more likely to become resistant to pesticides if susceptibility to the pesticide relates to mate selection. The adaptation of genes not related to the emergence of resistance will affect the dynamics of the evolution of resistance. Increasing the number of pesticides reduces the probability of developing resistance to any of them in asexual organisms but much less so in sexual organisms. Sequential applications of toxins, were slightly less efficient in slowing emergence of resistance compared with simultaneous application of a mix in both sexual and asexual organisms. Targeting only one sex of the pest speeds the development of resistance. The findings are consistent to most of the published analytical models but are closer to known experimental results, showing that nonlinear, agent based simulation models are more powerful in explaining complex processes.

Rrhain
WWJD? JWRTFM!

This message is a reply to:
 Message 4 by digitall, posted 05-01-2004 10:35 AM digitall has not replied

  
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