That’s easy to test.
You did not answer my original and important question. What makes you think that the resistance (in the original culture, that is) was due to a mutation? I am not asking for an assumption or guess.
What else do you think it was?
I thought the aza experiment was an excellent complement to the KOs in zebrafish. What would make the paper sound conclusive to you? I guess the answer doesn’t matter if you don’t know anything about DNA methylation or eye development. Or genetics. Or evolution.
Really? Irrelevant? That would mean that when they prepared the initial culture the very real possibility is that resistant bacteria were already present due to pre-exposure. How then do you conclude that they randomly mutated without pre-exposure??? That would be a direct contradiction to your conclusions of randomness and evolution.
Great for the Lederbergs. I am happy for them and their gift of science to genetics and disease control. But I see nothing for evolutionists to crow about.
You’re obviously still not understanding. The experiment demonstrated that the ancestral population did not have any resistance, as random mutations that then occurred in the cultures prior to exposure to antibiotics were what bestowed resistance. Please, do some reading about what the Lederbergs actually did instead before replying again.
It seems to me that there is no such thing as absolutely zero resistance, because there is a level of antibiotic concentration so low that any organism can strictly survive and reproduce in it’s presence. It comes in degrees.
To my knowledge, all organisms have some very low level of intrinsic resistance that makes them able to survive in the presence of some antibiotic, provided the concentration is low enough. That concentration might be as low as one molecule pr. cell, or perhaps even lower.
But that implies that all mutations that affect antibiotic resistance merely tune it up or down.
The same would be true for basically any poison, toxin, pollutant, or what have you. There is some concentration of nervegas so low you can survive it, some level of radioactivity so low it doesn’t measurably affect you, some concentration of snake-venom so low it won’t affect you, etc. etc.
Now of course, that just means if you want to test for whether spontaneous mutants yield increased resistance, you use a concentration of antibiotic large enough that it normally kills all cells without those mutations. That way you know, since the only difference between the cells that die and the cells that survive, is those mutations, then that is the only (sensible) explanation for the increased resistance.
Well, you walked right into that one. Now you are forced to prove that they were mutations in the first place. Please do not respond again until you have done that.
What is your alternate hypothesis? We know mutations happen and we know the physical mechanism by which they happen.
What is your hypothesis and supporting evidence for a different mechanism?
Why am I having to repeat myself? If you don’t think they were mutations, please propose an alternative event that induced resistance.
There are too many things you do not know, meaning your beginning assumptions may be wrong.
- You do not know that perhaps the non-resistant strain of bacteria is the actual mutated variety and that perhaps the resistant strain was the archetypal variety. In other words, the large body of non-resistant material was in fact the mutation, not the other way around.
- You do not know that perhaps the resistant strains in the original culture had at some previous point already been in contact with antibiotics (or their ancestors had been in contact) and had mutated.
- You do not know that perhaps this type of bacteria commonly exists in nature as a mix of resistant and non-resistant strains.
- You do not know that perhaps a latent, hidden resistant gene naturally resides in this bacteria’s chromosome thus giving it a leg up in terms of survival as long as the exposure to antibiotics occurs at a normal level found in nature and not an overwhelming “antibiotic wash” as in Lederberg’s lab.
They started with a single bacterial cell. If resistance was present in that original cell then it would be present in nearly all of the offspring. Instead, they only found resistance in 1 out of hundreds of millions or billions of bacteria. Also, the resistance was hereditary and was kept even in the absence of antibiotics. Since the Lederberg’s did their experiments we have learned a lot about DNA, and we can now map those mutations as they happen.
See above. Also, the resistant bacteria came from the same place on the parent plate which was covered in bacteria that had not seen antibiotics. This means the resistance is clonal and not caused by the antibiotics. The mutation happened on the plate where the bacteria had not seen antibiotics.
The rest of the scientific community disagrees, and for good reason.
Then why were only 1 out of billions of bacteria resistant to antibiotics? Remember, all of the bacteria came from a single and very recent ancestor. All of the bacteria in the experiment were grown from a single bacterium.
Regardless, the single parent of the entire population did not have resistance and did not have the mutations found in subsequent generations. Those mutations arose without the bacteria being exposed to antibiotics during their expansion from a single ancestor.
We do know that. The experiment started with a single bacterium.
With modern technology we can map the mutations that produce antibiotic resistance. Your scenario also doesn’t explain why the resistant bacteria come from the same region of the parent plate.
- You do not know that perhaps a single bacterium will always provide a mix of resistant and non-resistant strains as it grows. And you may be entirely wrong to call this normal activity a random event.
It’s not so much about resistance as it is how much function can the bacteria lose and still replicate. How much of their cell wall can be disrupted by beta-lactams before they can no longer reproduce, or how much of their protein transcription can be interrupted before it becomes a problem. Basic chemical equilbrium is also important for determining if the antibiotics even bind to their targets to begin with.
Yes, we do know that. We know the mutations that produce antibiotic resistance.
You will need too produce evidence that actually shows we are wrong.
I did not question that part. And these “mutations” may be a very normal part of replication. Not random.
Sorry, but I do not. There may be something you have overlooked and as usual (sorry to say), jumped to evolutionary conclusions too fast.
Then why don’t all of the bacteria in the experiment have that mutation? Why do we only find the mutation in 1 out of billion bacteria? Also, why does this mutation happen in bacteria that were not being exposed to antibiotics?
You haven’t been able to point to a single thing we have overlooked in this experiment. All you have done is invent fantasies of how genetics works.
Not necessary for survival. This bacteria will probably naturally replicate and provide only the number of resistant strains (be they ever so small in number) to survive in nature (as opposed to a lab).
Probably? What is the mechanism that decides which replication out of billions produces a specific mutation? What about all of the mutations that happen throughout the bacterial genome in the same fashion that run run the gamut from lethal to deleterious to neutral to beneficial? It’s not as if mutations happen at one base. They happen throughout the genome.
We can also watch mutations happen with just polymerases and DNA and no other proteins involved. When we use PCR to copy DNA we often get mutations, and all that is present is the polymerase (the protein that copies DNA) and the DNA bases needed to build new DNA strands.