Sure, I’ll watch it when I have a chance.
In return, could you watch the video in the opening post so we can compare notes? A little reciprocity?
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I am hesitant. The video begins with a clown emoji and after 5 minutes I felt it completely mischaracterized Noble even while using a meme.
I cannot cut and paste the relevant portion of your reference, but it clearly states they have no idea on the mechanism(s) in the study. Generally, when stdying complicated systems which are not well understood, a stochastic approach is often the only one to adopt. Getting into vague statements on fitness for such systems is inappropriate.
I forgot to add that stochastic methods can provide powerful tools for studies of complex systems (including those in biology) and may provide better results than deterministic approach - so the notion of random (and at times treated as noise) or dynamic systems is valid. You need to comprehend my remarks within the context that I have often stated, in that theistic evolution is an invalid notion.
It is worth noting, that the definition now means that even when genetic information is changed purposefully, it is still considered to be a random change with respect to fitness.
If you watch the Dawkins and Noble video and report back on the study Noble references for Lamerkianism, then I will summarize the argument in the book:
We can approach this question in three stages. The first stage is to establish that genomic change is not random with respect to location in the genome… The second stage in the argument is to note that well-documented examples of functionally relevant genomic change already exist… The third stage in the argument is experimental demonstration that the inheritance of acquired characteristics occurs.
But if you agree with @klw about intentional changes still being random with respect to fitness, then it would be a circular or non-falisfiable position Noble is arguing against.
Hi, and @T_aquaticus. I did not say the intentional CRISPR change was random! I said it was still subject to Natural Selection.
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Which I took to mean intentional changes were randomly subject to natural selection (or future fitness).
Because the underlying belief of Neo-Darwinism, that EES is challenging, is that evolutionary genetic changes are random with respect to fitness.
Hence the importance I felt of my random thought with symbiosis.
I don’t know what you mean by “randomly subject to natural selection” as opposed to just “subject to natural selection”. Natural selection results in a non-random transmission of those traits that affect the fitness of the organism (its survival and reproduction).
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It’s the only way I can understand how an intentional genetic change is said to be random with respect to fitness
I am not a geneticist so pardon my crude analogy (and the geneticists on the forum feel free to correct me if I am wrong)…but one could say that a researcher inserts by CRISPR a genetic modification that is not random-with-respect-to-fitness, because he/she knows beforehand the effect such a modification will make to the organism’s ability to survive or reproduce.
If all goes as planned, once the organism is released into the environment, it will be subject to the same natural selection as any other organism. i.e., if the new CRISPR gene was designed to improve the organism’s performance in some way, and if that does indeed prove to be that the modified organism has higher fitness (survival and reproduction) relative to alternate forms in the population, then the CRISPR modification will “be selected for” in the environment, and individuals that have that genetic modification will come to predominate over time in the population.
I think you could say that both the CRISPR modification and the subsequent act of Natural selection are non-random with respect to fitness in this case.
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I did watch the entire video. Unfortunately, these types of discussions don’t lend themselves well to understanding the science. They only talked about vague mechanisms, and they weren’t showing any data or figures in slides. It reminded me a bit of this cartoon:
I don’t say this to disparage either participant. It’s just an inherent problem with surface level scientific discussions.
Talking specifically about Noble’s discussion on Lamarckism, he put forth the idea that extracellular vesicles contain RNA were fusing with germline cells. He seemed to suggest that introducing this RNA would change subsequent phenotypes in some meaningful manner. I just don’t see how this could result in a stable phenotype over many generations. RNA doesn’t last long inside of a cell so it wouldn’t last until someone was born, grew up, and then had children of their own. The RNA would also be diluted out as the single celled embryo divided and grew into a full human being. So how is this supposed to be Lamarckism? At best, it is equivalent to phenotypic plasticity which is alread a part of the modern theory.
I think Noble understands the situation which is why he used vague language to describe these processes. He described them as “the organism makes DNA changes”, or something similar. Replace “a miracle occurs here” with “the organism does it” in the cartoon above and that’s about what it sounded like. He never claimed that these processes produce specific beneficial changes in response to a specific stimuli.
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If I were to pick an analogy, it’s a bit like intentionally buying a lottery ticket. The results of the lottery are still random. I think it would be accurate to say that evolution has selected for mechanisms that produce mutations, but those mutations are still random with respect to fitness. In fact, several of the E. coli lineages in Lenski’s long term evolution experiment evolved higher mutation rates, but those mutations were still random.
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Even though I am an atheist and you are a Christian, I think our views are pretty similar where this is concerned. I know the limits of science and that it can’t begin to answer questions about ontological claims where biology is concerned, or for randomness. While our beliefs may differ, I think there is a general agreement about what science can or can’t say.
Their experiment tested for both deterministic and random mutations. The initial observation that led to the experiment was the emergence of phage resistant bacteria. When the bacteria were exposed to phage the culture cleared, indicating widespread lysis of bacteria that you would expect from phage infection. However, at some point bacteria came back and grew, and they were fully resistant to phage. They considered two main explanations:
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Phage resistance was the result of the bacteria sensing phage and specifically altering their genome to make themselves phage resistant. This would be non-random mutation with respect to fitness. If this were the case, you would expect to see about the same number of resistant bacteria each time you run the same experiment.
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The mutation conferring phage resistance occurred before the bacteria were exposed to phage, not in response to phage. If this were the case, then the mutation could have happened in any generation. If the mutation happened in an early generation then you would get lots of resistant colonies. If it happened in a later generation then you would have fewer resistant bacteria. This means you would expect a lot of variance in the number of resistant bacteria from one experiment to the next.
What they observed was a lot of variance, a fluctuation in the number of resistant bacteria. This is why it is often described as a fluctuation test. Despite not knowing the specific molecular mechanism that produces the mutations, they were able to determine if the mutations happened in response to phage or in the absence of phage.
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I am not a geneticist either , so take that into account. That may be something in the future, and also a real concern for environmental changes and problems if used that way, but at present my understanding its that it is being used for treatment of disease, and modification of genes to produce various products, and those uses seldom produce better fitness. Most crops are unable to sustain themselves in the environment without help from farmers, and the genetically modified bacteria produced to say, produce a drug, are less fit that the wild strain. It is being given a hard look at being used to eliminate mosquitos and prevent malaria, but for the aforementioned concerns, has not been used yet.
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Yes, well of course if a genetically modified crop has reduced fitness compared to the wild types, and is only being kept around through active intervention from a farmer, then the process would no longer be considered “natural selection” but “artificial selection”.
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The quote below from a review is insightful and emphasises my point that the complexity of these systems requires stochastic treatments - this goes beyond ontological randomeness:
*Molecular biology is breathtaking in its seemingly unbounded potential for intricacy and *
*complexity. Genomes contain as many as billions of DNA bases, encoding tens of thousands of *
*genes, expressed in diverse spatio-temporal patterns, and acting within thousands of different cell *
*types. In principle, the space of potential patterns, from genomes, to expression programs *
*(reulons), stable cell types, or histological patterns, while not infinite, is enormous, although only
a miniscule fraction of it is realized. A major effort in molecular biology is to discover those
systems, and to decipher how their organization leads to biological function: how regulatory
sequences and molecular signal encode expression patterns; how expressed genes support cellular
functions; how cells partner to maintain tissue homeostasis and so on.
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Some degree of foresight is a strong line to draw. An organic system’s (imperfect) error correction mechanisms wouldn’t get there, but that is the issue I see Noble considering.
(or the purposeful behavior that led to symbiosis)
Cool! I’m sure you found Noble to be entirely respectable and never treated Dawkins like an idiot.
I’ll look into this. Thanks so much! I will get to that section of Noble’s book as soon as I am able to.
What do you mean by this? All behavior could be defined as having “a purpose”. That is a non-informative statement because any-and-all behaviour involves organisms “doing things” for various reasons. It’s just the definition of behaviour.
So, it is not a question about whether a behavior is “purposeful” or not from the perspective of an organism, rather what Noble needs to demonstrate for Lamarckism to hold (I think what the topic of this thread is circling around) is whether behaviours can cause non-random (beneficial) mutations in the genome that are subsequently passed on to the genomes of progeny in a way that increases their fitness. As far as I understand it, Noble has not presented any research that demonstrates this. The bacteria flagella scenario he referred to was shown to be explained by conventional means of random mutation and natural selection…
Are you aware of any other evidence of the rate of beneficial mutations increasing as a result of behaviour? I think that’s what one needs to challenge the existing Neo-Darwinian framework.
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