No I think you are mixing Acquired immunity with Mutation hypothesis. That is what they are discussing. My idea never even reaches the Acquired immunity level, because I do not believe in it.
Yes great suggestion. We can work together. Maybe we wonât beat up on each other so much then.
Exciting times to get into the field and apply for grant money. xD
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No sermons right now please. (Although I love sermons, and I love to be convicted by the Lord, I do not necessarily consider you his replacementâŚsorry.)
Thanks, I appreciate that. Okay, so I take it we both agree that there is such a thing as DNA. If not, please correct me.
I am however not sure whether you agree that DNA has any influence on the phenotypic attributes of the cell(or organism). Can you clarify?
Yes of course.
So far so good. Would you also agree that one of the attributes that DNA influences is resistance to antibiotics?
Good. That tells me these bacteria are determined to survive. âDeterminedâ is the operative word.
Do you accept that mutations are constantly happening in bacterial genomes - some with beneficial effects, some with negative effects, and most with no measurable phenotypic effect?
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The mutation hypothesis is random mutations, exactly as you describe. That is the hypothesis supported by the results of their experiment, and they are exactly the results you described for random mutation. Letâs go back to your previous post:
âIf these mutations were truly random then the ratios returned would be 1 E-5, 1E-6, 1E-11, 1E-2, 1E-8, 1E-13. They would be all over the place. That would properly describe randomness.â
Letâs look at how this would play out in a liquid culture. If we start with just a few bacteria and applied those rates to different cultures, what would we see when those cultures grew for a while? If the rate were high, like 1E-5, then the mutation would happen in an early generation and we would end up with a lot of resistant bacteria. If the rate were slow in another culture, like 1E-13, then the mutation would happen in one of the last generations, or not at all. This would mean we get a lot of variation between different cultures, right?
So what did Luria and Delbruck get when they ran this experiment? Exactly what is described above. Some cultures had a lot of mutatns, some cultures only a few, and some cultures none at all.
Look at pg 504 in the paper below. There is a table that exactly matches your description of randomness.
Careful there. Why would they do this? Your conclusion is starting to sound deterministic.
Iâm beginning to think this will be your response no matter what evidence is presented. Am I wrong?
Only an intelligent mind with a knowledge of the world and its dangers could label one âbeneficialâ and another âdeleteriousâ. Randomness could not do that. I truly am not trying to be difficult when I say this.
I am asking whether you agree with it.
Is it your understanding that one of the attributes phenotypic attributes that DNA affects, is antibiotic resistance?
Supposing you agree that my DNA, which I inherited from my parents, in part determines how tall I am, what color my hair and eyes are, and so on, could antibiotic resistance not also be one of those attributes?
Then what would you call a mutation that destroys a protein the bacteria needs to survive and replicate? Also, why couldnât randomness produce such a mutation?
I want to answer but very carefully. Yes, I agree that we found in our discussion that the bacteria under investigation did indeed display antibiotic resistance after x number of replications.
Yes, it is us humans that label things as âbeneficialâ and âdeleteriousâ. Those are labels we use to describe how some things behave. I may decide to label a dog as âwildâ or âunrulyâ. The dog does what it does regardless of what I label it, however.
In the same way, particular DNA mutations we label as âbeneficialâ and âdeleteriousâ. We do not dictate to the mutations how to behave, they do what they do, we merely describe those effects with our labels. What matters here is that their effects are real, regardless of what we choose to call or label them. The DNA mutations really do have those effects, however.
By accident? I suppose.
So why do you think that random mutations could not interrupt a vital DNA sequence and lower the fitness of the bacterium harboring that mutation? Do we say lightning isnât random because it strikes people and harms them?
Forgive me, but I am overcome with a certain degree of amazement at the numbers. They tell me that determinism must be eliminated first if possible. If not possible, then I am not sure where to go quite yet.