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Author Topic:   Evolution starting with a single bacterium
digitall
Inactive Member


Message 1 of 56 (104495)
05-01-2004 5:40 AM


Someone told me that evolution of antibiotic resistant bacteria is non existent. Antibiotics resistance would be already available in the pool of bacteria. Bij adding antibiotics only the resistant ones would be able to survive and reproduce. The only way to refute this argument is imo to start with a single bacterium and look for surviving ofspring in a selective environment.
Has this ever been observed and is there any information about this subject ?

Replies to this message:
 Message 2 by Rrhain, posted 05-01-2004 6:15 AM digitall has not replied
 Message 4 by digitall, posted 05-01-2004 10:35 AM digitall has not replied

  
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:
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compmage
Member (Idle past 5153 days)
Posts: 601
From: South Africa
Joined: 08-04-2005


Message 3 of 56 (104507)
05-01-2004 9:04 AM
Reply to: Message 2 by Rrhain
05-01-2004 6:15 AM


Good to see you back here again Rrhain.

Freedom, morality, and the human dignity of the individual consists precisely in
this; that he does good not because he is forced to do so, but because he freely
conceives it, wants it, and loves it.
- Mikhail Bakunin, God and the State, from The Columbian Dictionary of Quotations

This message is a reply to:
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digitall
Inactive Member


Message 4 of 56 (104519)
05-01-2004 10:35 AM
Reply to: Message 1 by digitall
05-01-2004 5:40 AM


Rrhain,interesting do you have a source for the E.coli and T4 phage experiment.

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 5 by Rrhain, posted 05-02-2004 4:36 AM digitall 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

  
Guest
Guest


Message 6 of 56 (106746)
05-09-2004 8:21 AM


quote:
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.
How does explain evolution? Isn't that a bit close minded?
How do you know they aern't designed to behave that way? Just to fool you. After all they did it.

Replies to this message:
 Message 7 by crashfrog, posted 05-09-2004 8:38 AM You have not replied

     
crashfrog
Member (Idle past 1466 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


Message 7 of 56 (106748)
05-09-2004 8:38 AM
Reply to: Message 6 by Guest
05-09-2004 8:21 AM


How do you know they aern't designed to behave that way?
Because if they were designed to do it, they all would do it, not just some. Rrhain told you as much, already.

This message is a reply to:
 Message 6 by Guest, posted 05-09-2004 8:21 AM Guest has not replied

Replies to this message:
 Message 8 by scot-free, posted 06-10-2004 10:58 AM crashfrog has replied

  
scot-free
Inactive Member


Message 8 of 56 (114131)
06-10-2004 10:58 AM
Reply to: Message 7 by crashfrog
05-09-2004 8:38 AM


A can of worms ...
Greetings crashfrog
You have a long track record, and I haven't got it. Probably you do have more articulate answers than this:
quote:
unregistered: How do you know they aern't designed to behave that way?
Because if they were designed to do it, they all would do it, not just some. Rrhain told you as much, already.
If you would design them then I assume you may take this road, if possible. But would this be an option? Is design free to make any decision or is it restricted to a close set of rules in order to let it exist as observed?
The observations presented by Rrhain are amazing but the conclusion opens a can of worms. The responsiveness and immediate reactions doesn't fit to the change rates to be observed in other relations. Regarding resistence I guess there must be other mechanisms working more actively than standard mutations.

Searching the truth requires both skepticism and faith.

This message is a reply to:
 Message 7 by crashfrog, posted 05-09-2004 8:38 AM crashfrog has replied

Replies to this message:
 Message 9 by AdminNosy, posted 06-10-2004 11:10 AM scot-free has replied
 Message 10 by crashfrog, posted 06-10-2004 2:21 PM scot-free has replied

  
AdminNosy
Administrator
Posts: 4754
From: Vancouver, BC, Canada
Joined: 11-11-2003


Message 9 of 56 (114134)
06-10-2004 11:10 AM
Reply to: Message 8 by scot-free
06-10-2004 10:58 AM


Not a welcome visitors topic
I will close this. If someone wants to carry it on they may propose a new topic.

This message is a reply to:
 Message 8 by scot-free, posted 06-10-2004 10:58 AM scot-free has replied

Replies to this message:
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crashfrog
Member (Idle past 1466 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


Message 10 of 56 (114170)
06-10-2004 2:21 PM
Reply to: Message 8 by scot-free
06-10-2004 10:58 AM


Probably you do have more articulate answers than this:
There's not a lot to articulate. The behavior of the organisms falsifies a hypothesis that they responded to the pathogen via innate metabolic capabilities, because if they had, they all would have done it, because (according to your hypothesis where mutation did not occur) the organisms are all clones of each other.
Because only a few survived, we know it was because they weren't clones like the rest; because we know they weren't clones, we know that mutation occured. Again, what's to articulate? The only design hypothesis that is tenable is the hypothesis that the designer designed one inital orgainism, and all other organisms are its decendants through evolution. A hypothesis that the observed behavior of these bacteria is the result of a specific, non-mutative metabolic design is falsified by the fact that the vast majority of bacteria died.
The responsiveness and immediate reactions doesn't fit to the change rates to be observed in other relations.
Nonsense. Selection is practically instant. The mutation in question almost certainly occured in the first phase of the experiment, where you grew the bacterial lawn, before you added the pathogen (along with a bazillion other mutations that, as it turned out, weren't selected for.)
There's plenty of time for evolution to work, here. Hundreds of generations and millions of individuals.
Like Ned said this isn't a Visitors topic. If you want to discuss further open a new topic.

This message is a reply to:
 Message 8 by scot-free, posted 06-10-2004 10:58 AM scot-free has replied

Replies to this message:
 Message 12 by scot-free, posted 06-10-2004 6:57 PM crashfrog has replied

  
scot-free
Inactive Member


Message 11 of 56 (114234)
06-10-2004 6:31 PM
Reply to: Message 9 by AdminNosy
06-10-2004 11:10 AM


Re: Not a welcome visitors topic
Sorry that I used th opportunity to pop in ... is there an option to move the subject to another board?
If not, I would appreciate if you leave it open ...

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scot-free
Inactive Member


Message 12 of 56 (114244)
06-10-2004 6:57 PM
Reply to: Message 10 by crashfrog
06-10-2004 2:21 PM


Biologic machines?
Greetings crashfrog
quote:
... because if they had, they all would have done it, because (according to your hypothesis where mutation did not occur) the organisms are all clones of each other.
I am not more than informed layman but it makes me wonder to call a homocygote reproduction cloning. There is so much unknown so far, e.g. so-called junk DNA, that I am cautious to make claims which I don't know for sure. Perhaps others do, so I ask.
The observation is: A set of bacteria is reacting heterogenous stemming from a single cell, though mutation must have occured. Well, I suspect this may be a short cut by eliminating other options too early.
quote:
A hypothesis that the observed behavior of these bacteria is the result of a specific, non-mutative metabolic design is falsified by the fact that the vast majority of bacteria died.
I don't know of a fully fledged theory about this, but I consider a build-in mechanism of adaption to react on external stimuli, but there is no need to react uniform. This ability works not like waiting for random mutations in order to be successful but a straight forward protection. Why doesn't all bacteria react equally? Well, bacteria aren't to be compared to humans, which react individually, nor as machines or robots as being programmed. Just different. They are living ... and I feel we only have inadequate theories what live really is.
quote:
Nonsense. Selection is practically instant. The mutation in question almost certainly occured in the first phase of the experiment, where you grew the bacterial lawn, before you added the pathogen (along with a bazillion other mutations that, as it turned out, weren't selected for.)
There's plenty of time for evolution to work, here. Hundreds of generations and millions of individuals.
Not really convincing. To filter a significant improvement selection only works when the impact comes in. Beforehand mutation must have occured and also significantly in the right way in numbers in order to pass the thresshold to survive the bacillus attack. I doubt your explanation.
quote:
Like Ned said this isn't a Visitors topic. If you want to discuss further open a new topic.
I will go looking for it ...

This message is a reply to:
 Message 10 by crashfrog, posted 06-10-2004 2:21 PM crashfrog has replied

Replies to this message:
 Message 13 by crashfrog, posted 06-10-2004 7:09 PM scot-free has replied
 Message 16 by Coragyps, posted 06-10-2004 11:05 PM scot-free has not replied

  
crashfrog
Member (Idle past 1466 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


Message 13 of 56 (114246)
06-10-2004 7:09 PM
Reply to: Message 12 by scot-free
06-10-2004 6:57 PM


I am not more than informed layman but it makes me wonder to call a homocygote reproduction cloning.
Well, bacteria don't have sex. They do exchange some genetic elements, but in a world without mutation, they're not exchanging anything they don't already both have.
So, if we reject mutation, we necessarily conclude that all these bacteria have exactly the same genetics.
Since they don't, however, we conclude that mutation occured. And why wouldn't it? Reproduction is a chemical process, and it's not perfect. Mutation just means that reproduction wasn't perfect, and why would we expect it to be?
Well, I suspect this may be a short cut by eliminating other options too early.
Too early? We've been through this. No other option is coherent with the observation.
I don't know of a fully fledged theory about this, but I consider a build-in mechanism of adaption to react on external stimuli, but there is no need to react uniform.
They have that built-in, random mechanism of adaptation. It's called "mutation and natural selection." It's the mechanism the experiment proves exists, and it's the same mechanism that does the same thing in all other organisms.
Why propose an additional, unknown, untestable mechanism when we already have one that explains it just as well? How would you determine the difference between your unknown mechanism and the evolutionary mechanism, since the results are exactly the same in every case?
To filter a significant improvement selection only works when the impact comes in. Beforehand mutation must have occured and also significantly in the right way in numbers in order to pass the thresshold to survive the bacillus attack.
Right, the selection happens when we introduce the pathogen. The mutation happens before, when we're growing the lawn. What part of that confused you?
Moreover, given that bacteria reproduce asexually, what makes you think that the mutation that confers immunity needs to happen any more than once? All the resistant bacteria might very well be the decendant of exactly one individual.
I doubt your explanation.
So I see, but the problem is, you don't doubt my evidence or reasoning, you doubt the conclusion. That's the back-ass-wards way to think, and it's what prompted Sherlock Holmes to say "once you have eliminated the impossible, whatever remains, however improbable, must be the truth."
I'm sure you find the theory of evolution improbable. The problem for you is that all other explanations turn out to be even more improbable, or outright impossible or otherwise incoherent with the evidence.
Evolution by natural selection and random mutation is the obvious, and only, explanation for what happened in the dish, twice over.

This message is a reply to:
 Message 12 by scot-free, posted 06-10-2004 6:57 PM scot-free has replied

Replies to this message:
 Message 17 by scot-free, posted 06-11-2004 4:50 PM crashfrog has replied

  
AdminNosy
Administrator
Posts: 4754
From: Vancouver, BC, Canada
Joined: 11-11-2003


Message 14 of 56 (114264)
06-10-2004 10:05 PM


Thread moved here from the Welcome, Visitors! forum.

  
crashfrog
Member (Idle past 1466 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


Message 15 of 56 (114268)
06-10-2004 10:30 PM


What happened to messages 12 and 13?
Oh, never mind, I guess they're back.
This message has been edited by crashfrog, 06-10-2004 09:34 PM

  
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