Discussion of everything related to the Theory of Evolution.
I apologise for my long abstention from this forum, but illness has taken it's toll.
However I am somewhat better now so may I perhaps continue to engage and no doubt irritate.
I did say I would put out some information on antibacterial resistance so here it is for any further discussion.
Antibiotic resistance is often used to show that the development of this resistance in humans is a result of random evolutionary forces that natural selection uses.
However what does the empirical evidence actually show?
In the book “Bacteria versus Antibacterial Agents – an Integrated approach”
http://books.google.co.uk/books?id=mayr ... 8.&f=false
Page 243 has this to say.
As far as ribosomal protection is concerned the book goes on
There is the third mechanism not considered by the book
Some bacteria produce enzymes that neutralize antibiotics groups to a specific site on the antibiotic. This modification reduces the ability of the antibiotic to bind to ribosomes, rendering it harmless to the cell.
The interesting question here is, where do these antibacterial properties come from?
Are they the result of blind random mutations that natural selection can select from.
Here is what the data reveals.
http://www.ncbi.nlm.nih.gov/pmc/article ... ool=pubmed
Tetracycline antibiotics: mode of action, applications, molecular biology, and epidemiology of bacterial resistance.
So the question naturally is, where do these genes comes from?
It goes on
So Bacteria don’t appear to be evolving new genes at all, they are acquiring previously existing antibiotic resistance genes through lateral gene transfer.
It goes on further..
So there is nothing new about antibacterial resistance, for it now appears to have been in nature all along.
In fact Streptomyces uses these methods to protect itself from its own antibiotics.
The idea that antibiotic resistance is so readily used to show that the development of this resistance in humans is a result of random evolutionary forces, actually runs counter to the empirical evidence.
What the empirical evidence shows is that, it is the direct clinical intervention that induces the acquisition of these natural occurring mobile genetic elements in tetracyclines that produces the resistance.
So this is not mutations selected by natural selection but (although unintended) artificial selection.
In fact this paper makes an sound empirical observation.
Another point to keep in mind is this.
Even if a mutation occurs in the ribosome that may provide an advantage to the bacterium, it would come at a cost. Ribosomal mutations, while providing antibiotic resistance for the organism, slow the process of protein synthesis, slow growth rates, and reduce the ability of the affected bacterium to compete in an environment that is devoid of a specific antibiotic.
Furthermore, a mutation that confers resistance to one antibiotic may make the bacterium more susceptible to other antibiotics.
These are deleterious effects and are completely inconsistent with the evolutionary model of natural selection acting on random mutations.
What I find quite amusing is this statement you will find on wikipedia.
Please notice that while this statement acknowledges that antibotic resistance results from pre existing genes that are transferred, it is followed by a simple doctrinal statement that these genes have evolved via natural selection.
This is not science but simple philosophy, no different to a creationist statement like “God created the world in 6 days”
Now that the Olympics and paralympics are over I am able to put away my armchair and pop corn and continue.
One of the reasons I was amused at the wiki statement that a gene evolves via natural selection has to do with their understanding of what a gene is.
Their definition is
This is not exactly correct and at least 5 years out of date, but let's stick with it for the moment.
Now lets see the description of Natural Selection according to this same wiki.
Remember of course, there has to be a functioning entity or biological trait for NS to act upon, and the only mechanism according to any branch of Darwinian evolutionary theory is some random occurrence that produces a function.
Now the gene codes for amino acids that the cell needs to use. (we are not even going to discuss how this coding sequence could have come about.)
Here is what wiki records about amino acids.
In the simplest sense, expressing a gene means manufacturing its corresponding protein, which is a sequence of amino acids.
So according to wiki, we have biological traits coded by genes that are randomly built without any purpose and are then naturally selected through some gradual non random process by which they get stabilised in a population.
However, nearly 50% of these amino acids cannot be selected by the cell that the genes have coded for, because they aren't there to select from. (the body doesn't make them)
So in order for this selective process to occur, there has to be a fully functioning digestive system so that when the food gets eaten, the nutrients travel down into the stomach and then intestines. These organs break up and dissolve the food into small pieces that can be absorbed by the blood stream. Most of these small particles travel from the intestines to the liver, which filters and converts the food into nourishment that the blood stream delivers to the cell. How these nutrients pass into the cell of course is another area we are not even going to go into for now.
So the obvious question is :
Which came first?
The genes that code for the proteins using the amino acids that the body can make.
The genes that codes for the entire digestive tract that provides the cell with the amino acids that body can't make but which the body cannot do without.
Isn't it obvious that that the whole show has to be in place before any of these individual parts can functionally operate.
But of course the obvious is not acceptable.
Instead we have these doctrinal statements promulgated with a religious fervour, and any dissent from that view is considered heretical.
The problem with all these just so stories is that they fall apart when the detail is examined.
Wouldn't it be nice to see some real science showing how Natural Selection produces a gene.
But that's hoping for too much, after all what has science got to do with a good story.
This whole idea gets more farcical when we consider what the latest research on genes throws up.
That however is better left for another time.
Let me see if I've got this straight. Someone says to you, "beneficial mutations exist. Example: antibiotic resistance." And your response is, "this bacterium got antibiotic resistance from lateral gene transfer, therefore beneficial mutations do not exist."
That's like saying the grocery store couldn't possibly be selling DVDs because Best Buy sells DVDs. In order to demonstrate that mutation is not responsible for antibiotic resistance, you would have to go through all cases of antibiotic resistance and show how lateral gene transfer is the cause in each and every one of them.
A much better approach would be to look for papers which detail the spontaneous mutation of antibiotic resistance in the lab. If you fail to find such papers, that would be an indication that such mutations do not exist.
It took me about thirty seconds to find such papers. I'm not sure how many you require, but logic says even one is enough to invalidate your argument. I've selected three to reference. The abstract for the first one can be found here:
Unfortunately, the full text is not available online (at least not that I could find) but the abstract gives a good idea of the content. This article reviews the current research on mutations which confer antibiotic resistance. It acknowledges that horizontal gene transfer is responsible for the spread of many mutations, but also references many instances where antibiotic resistance has arisen as the direct result of mutation.
I was able to get a copy of the second source through my public library's subscription to EBSCO. It's an American Scientist article from 11/6/06 called "Free Upgrades, Unfortunately." The article describes a study where the researchers took samples of bacteria from people infected with M. tuberculosis. They did this at two different points in time: once early on in the infection and then again later, when the bacteria had had time to mutate inside the person's body. They found mutations that conferred antibiotic resistance.
"Okay," you might say, "but what if the patients picked up some resistant bacteria somehow? Those bacteria could have spread the resistance to them."
Not only did antibiotic resistant bacteria show up out of nowhere in the patients, they also showed up in the lab. Researchers started with normal M. tuberculosis and exposed them to the antibiotic. They were easily able to produce several antibiotic-resistant strains.
I intended to present this simply as an example of beneficial mutations, but it coincidentally contradicts your assertion that antibiotic resistance always comes at a price. The whole point of this study was not to demonstrate that mutations can cause antibiotic resistance (that's well-established and they completed that task only incidentally as part of their methodology) but to see if antibiotic resistant strains evolved in vivo are as hardy as non-resistant ones. They found that, in many cases, they were.
Now, I realize that citing papers which are not freely available online might seem like kind of a cop-out, so here's one that is available in full-text:
Again, the ability of mutation to cause resistance is taken for granted: the focus of the article is on the technicalities of measuring mutation rates. But there are still copious examples in this article of bacteria acquiring resistance through mutation. These mutations have been observed clinically as well as in the lab. Researchers can actually induce these mutations to order. They can cook up any resistance they want, using nothing more than their knowledge of mutation rates and the rapid reproduction of these organisms.
I will mention something else about the costs of resistance. Though the American Scientist article indicates that there is not always a cost, I don't mean to imply that there is never a cost. Of course there are costs. This is what I have been saying all along: the terms "advantageous" and "deleterious" are highly relative. They depend almost exclusively on context. A bacterium living in an antibiotic-free environment will probably not be as successful if it has a resistance mutation. But as soon as antibiotics enter the environment, suddenly it's a stud, out-reproducing all its fellow bacteria. That is whole point of the combination of random mutations with directional selection: one fuels the variation on which the other acts. And steady mutation rates mean that even alleles which are eliminated from the population can pop up again later.
You are somewhat correct to point out that, clinically, we can never be sure that a mutation has arisen because the conditions are not controlled. But many of these cases of resistance mutations occur in the lab. These are cultures that are carefully kept from contamination. No lateral gene transfer is possible in these situations.
The only possible argument left to you is to contend that these variants are not arising spontaneously but were always there, hidden in the bacterial colonies in such small numbers that they were undetectable until exposure to antibiotics brought them roaring to life. If that is indeed your argument, then I have two challenges to offer:
1) If mutation cannot cause antibiotic resistance, then why do mutagens increase the speed with which resistance-conferring variants arise?
2) If these variants exist in such small numbers, and they get no benefit from their antibiotic resistance until an antibiotic is introduced to the environment, then how do they survive for so long and occur so frequently? Wouldn't their relative disadvantage/small numbers increase the likelihood that they would, by chance, fail to reproduce and thus remove their alleles from the population? I mean, we might expect that some would survive by chance, but why is it that scientists can generate antibiotic resistance, under controlled conditions, in literally any population of bacteria they decide to test? How do you account for that without steady mutation rates?
Edited to add a third question: how do these preexisting alleles for antibiotic resistance elude researchers who create pure strains from a single bacterium and even sequence the DNA of that bacterium to ensure that the allele is not present in its genome?
To wrap up, your assertion that bacteria never get antibiotic resistance from mutation is astounding given the abundance of evidence to the contrary. You seem very concerned about the latest research, but the fact is that we've known about these beneficial mutations for decades. The latest research is way beyond that, investigating the details of how often these mutations occur, what other effects they have on the bacteria, how the mutations spread once they are introduced, etc.
If arguing with people on the internet helps me understand science, then I will do it. FOR THE CHILDREN.
I'm not touching this trollbait with a ten-foot pole, lol.
I'm not interested in debating the origin of genes with you. As I said previously, I'm only concerned with the issue of beneficial mutations. However, you might be interested in watching (if you haven't already) What Darwin Never Knew. It has some good visuals of the complexity of genomic interactions. The simple answer to your question is that genes are legos made of legos. Nothing is created de novo; it's all built modularly. Do a Google search on "gene origins."
If arguing with people on the internet helps me understand science, then I will do it. FOR THE CHILDREN.
For the sake of clarity, and I have stated this before and will probably have to continue ad nauseam.
My position is not that random mutations do not happen. They do.
Does NS act upon random mutations. Yes I believe that may also happen.
In other words, does evolution (change over time) happen. Yes
Does this mechanism account for species change, let alone the Origin of Species. (remember this is the subject of this thread)
I argue NO
Aside from a lot of adolescent rhetoric (not necessary from you)I see no evidence.
I have also clearly stated about14351-480.html
I went on to state (not to you)
Which is about where you came in.
So let me turn to your question
This is what I have stated.
It appears to me that you are raising straw man arguments here.
The abstract you refer to is certainly not inconsistent with my statements.
In fact if I may refer you to a more recent and complete paper in 2009.
The role of natural environments in the evolution of resistance traits in pathogenic bacteria
This is how the abstract begins
All I have argued is that this resistance is already there in nature. The question is not how did the resistance in humans come about. We know that, well sort of!
The question is how did these genes come about in the first place.
That is what I found amusing about the wiki posit ie that NS is “what done it”.
For that statement to be valid then empirical evidence is required.
But what do we get.
Well antibacterial resistance proves this. (Perhaps not you but others do claim this)
With all due respect it does nothing of the kind.
What it does show is that clinical intervention passes on a resistance that already exists in nature.
That sounds to me very much like artificial selection.
Not a very good one at that, since we are now having to deal with the consequences.
The 5 years out of date comment has to do with the latest Encode definition of a gene. Nothing to do with trollbait.
Ok so you are not interested in discussing the origin of genes with me but you do know the simple answer.
Genes are legos made of legos.
My my, however did I miss that one.
Errr yep I've got it.
I have been accused of lacking imagination, that's what it must be.
Got to keep working at it.!!
So, in other words...you agree that beneficial mutations exist. When you said "Where are the functional phenotypes that random mutation is supposed to have produced in order for NS to select from?" you did not mean to deny that an organism may acquire a beneficial trait from a random mutation. You simply meant that you didn't think beneficial mutations sufficient to account for complex adaptations. By "functional phenotype" you mean the whole mouse trap, not just a piece of it.
It sounds like what you're saying is that natural selection can't account for complex structures like eyes and blood clotting cascades because random mutation can't produce eyes or blood clotting cascades.
This is an argument I can understand. I don't agree with it, but I can understand why someone would take this position. However, your statement that "The random mutations that do occur are invariably deleterious to the organism" seems to contradict the aforementioned argument. Hence my initial incredulity. But if we can agree that a random mutation might confer a benefit for the mutated organism, then we can agree that the variation on which natural selection acts is, at least in part, the result of random mutation.
Then there are three steps to antibiotic resistance. First, the bacteria evolves a gene that confers resistance to some dangerous substance. This substance is "natural" in the sense that it is not man-made (not an artificial antibiotic).
Second, the bacteria encounters the man-made antibiotic. The gene that conferred resistance to the "natural" substance isn't much use against the man-made antibiotic until a random mutation tweaks it in such a way that it confers resistance to that man-made antibiotic.
Third, the bacteria becomes successful because it is immune to the man-made antibiotic. So it freely proliferates and passes its resistance to the man-made antibiotic on to all its friends, and even to other types through horizontal gene transfer.
So. If I understand you correctly, putting forth antibiotic resistance as an example of beneficial mutation is flawed for this reason: the gene that is altered by the mutation was already conferring resistance to dangerous substances, therefore the mutation didn't really confer any benefit; it tweaked a benefit that was already there.
What I don't understand is why you tried to explain this by citing a paper on horizontal gene transfer. That's the third step. Why did you go there, if the real question is where the gene in step one came from?
Maybe you meant that there is no step two? That there are bacteria which are naturally immune to man-made antibiotics because they are immune to natural antibiotics? And that these bacteria spread their immunity through horizontal gene transfer? Which brings us back to the experimentally verified fact that mutation can also cause immunity. In which case HGT is irrelevant.
I'm sorry, but no matter how I try to unpack your argument, it still strikes me as fundamentally illogical. And the only response you can come up with is to cry "straw man" and quote the same flawed argument that I just excoriated. You say that the sources I linked are "not inconsistent with your statements" but you don't explain how. You offer no refutation of the copious examples of antibiotic resistance that have nothing to do with HGT.
Here's another thing I find curious: you say the resistance was already there in nature because this paper says the resistance genes "evolved in non-clinical (natural) environment before the use of antibiotics by humans." But later on in the paper, they mention that although there are some bacteria which produce natural antibiotics and thus already have genes specifically for antibiotic resistance, "some resistance genes may have other functional roles in their original organisms besides antibiotic resistance." In other words, genes that now confer antibiotic resistance may have served a completely different function in the past. "These examples illustrate the concept that a determinant which contributes to the resistance of human pathogens to antibiotics can be involved in central metabolic processes of environmental bacteria in their natural habitats."
So, one of the major points of the paper you quoted is that a gene that was originally used to make a protein involved in metabolism might later play a role in antibiotic resistance. This seems to directly contradict your assertion that all antibiotic resistance is "already there in nature." In fact, it supports the idea that natural selection plays a strong role in the evolution of these genes. Because, as any biologist will tell you, natural selection doesn't work de novo. It takes what is already there and tweaks it. Complex structures don't evolve overnight. You don't need the whole mousetrap at once because the individual pieces may be individually useful for other things.
If the sources I cited were truly consistent with your argument, you should have pulled quotes from them and explained how they supported you. Instead, you cited a new source. Not only does this new source not support your argument, but the parts that you didn't quote actually directly contradict you.
No, seriously. Google "gene origins." It's really interesting.
If arguing with people on the internet helps me understand science, then I will do it. FOR THE CHILDREN.
Please don't take my statement any further than what I have said.
To me the jury is still out.
How does one distinguish between what is a random and what is a prescribed cellular response to outside pressure.
It is for this reason that I argue that random mutations “mistakes” are mostly deleterious simply because of the cell's checkpoint and correction processes. These processes ensure integrity to some already existing template. I am not aware of any biologist that disagrees that most random mutations are deleterious.
Now you go on with your steps to acquired resistance. Allow me for a moment just to
engage with your first step description.(I will deal with the rest as this develops.)
Could you explain please; How does the bacteria “evolve” a gene?
If that is how a gene arrived then could you demonstrate the process.
That is what the scientific method requires.
If you are unable to, then you are treating a hypothesis as a fact.
Now if you recognise you are dealing with a hypothesis that's ok with me, so long as you don't quickly slide from hypothesis to fact, as you appear to be doing.
If I am wrong then please correct me.
btw I will Google "gene origins"
Life: the active situational model on the cell membrane, equipped with a polypeptide-nucleic technology
Polypeptide-nucleic technology: Technological database recorded triplet code of four letters in the DNA-nucleotide carrier, through the device of RNA-IO is implemented in the polypeptide interface.
It is an ancient, several billion years ago the development of brilliant engineering. Engineers - "active models the situation in lipid membranes". Thus, the question of the origin of life, it is a question of the origin of those ancient membrane-engineers!
https://www.facebook.com/photo.php?fbid ... =1&theater
All I'm arguing is proof of concept. If you admit the possibility, that is enough for me.
What pressure is a colony of bacteria being subjected to when you keep them in their optimal environment? How do you account for steady rates of mutation in populations of organisms kept under controlled laboratory conditions?
Scroll up. We already talked about this.
No. It's not germane to this discussion. See "gene origins" above.
We can both agree that a bacterial strain which was previously not antibiotic resistant had genes. Where those genes came from is not important at the moment. You focus on this and completely ignore the larger issue of the irrelevancy of horizontal gene transfer.
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