I need help with language to use in regard to evolution

I think she means unguided by God, which clearly would be the case if there is no God.

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These are all very helpful additions and distinctions surrounding the various uses of these words in various contexts from differing worldviews. And this is exactly the kind of help I am after in trying to clarify these for an attentive reader. I will most likely have to use footnotes as not all of us at RTB use these consistently with clear distinctions. Thank you, Josh, TJ, George!

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@swamidass,

I don’t know to whom this was addressed, or about whom you are referencing, or what you think it means. If the “she” you mean is our good AJ Roberts, I find it less than necessary: it goes without saying that Atheists would not perceive any “guidance”.

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But sometimes it’s good to be thorough.

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That sounds like a good approach to the nuances of the terminology.

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3 posts were split to a new topic: RTB and the Gebealogical Adam and Eve

I would hope that in the spirit of clarification, you would emphasize to your readers that most evolution selects (Darwinian) and/or fixes (both Darwinian and neutral) already existing heritable variation. IOW, that populations aren’t static and “waiting” for new mutations to occur before evolution can occur.

Is that a reasonable expectation?

I don’t think so. Because…

Although obviously populations aren’t static; what that means is that changes (which is difficult to parse from or distinguish from mutations) will occur through additional mechanisms (sexual selection, recombination, etc.) Obscuring the necessity for “new mutations” seems a bit ludicrous to assert, since mutations are occurring all the time in individuals, and which ones are being fixed in a population is only determined retrospectively.

The pre-existing presence of variation in a population is likely quite broad, especially when one considers the limited assessment of most populations by often sampling very small and/or very skewed sub-sets. I think this concept will be clear. Maybe not in these words, but the underlying, pre-existing variation is captured (I think it is, I’ll double check when I next review for edits.) Thanks.

I’m chiming in a bit late, but hopefully I can contribute a few good points.

I started a thread on this topic which focused just on the science with a very neutral position towards theological and metaphysical questions:

Long story short, random in the context of mutations and evolution is a statistical measurement (e.g. a Poisson distribution). Perhaps the best way to understand what random means in this context is to define what non-random mutations would look like. In the case of non-random mutations we would expect to see the vast majority of organisms producing the same mutation at a very specific base in response to a specific environmental cue. For example, if we exposed bacteria to antibiotics and they adapted through non-random mutations then we would expect a large portion of the bacteria to produce the same mutation in just one generation. Instead, only 1 out of hundreds of millions produce the needed mutation even though one out of ever 3 or so bacteria produced a mutation somewhere in their genome in a single generation.

“Unguided” would reflect the same view. If an organism is guiding mutations then we would expect the same result as non-random mutations. As to a creator guiding mutations, science is silent on that topic. The best science can do is determine if the observations are consistent with their model of random mutations.

Unplanned gets a bit more complicated. I think it would actually be fair to say that mutations are planned just like one can plan a lottery drawing. Polymerases could be better at preventing mutations, but they aren’t. It seems as though they evolved to produce random mutations. There is also the example of the SOS response in E. coli that causes the expression of a error prone polymerase that increases the random mutation rate. I think it would be entirely fair to call them planned random mutations, in a biological sense. Mutations are actually a function of some proteins involved in genetic systems.

In the scientific view, it is about how well the evidence matches your hypothesis. You can build a model of what random mutations should look like, and then see if the observations match that prediction. Does this mean that mutations are not being guided by a deity? No. All we can do is say that the hypothesis is supported, and tentatively conclude that natural mechanisms are probably the cause. Science doesn’t make any philosophically or metaphysically absolute statements. All conclusions are tentative and open to falsification.

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Thank you. I will check it out!

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Thanks very much for chiming in! Substantively!

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One of the experiments that I didn’t mention in my other thread is the Lederberg’s plate replica experiment. This is the other classic experiment that defines random mutation in biology:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC169282/

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This one of the topics I enjoy, so excuse the over-exuberance. The SOS response and its discovery is actually a good way of seeing how the scientific community deals with questions of random and non-random mutations.

There were a series of experiments where scientists grew bacteria with a damaged lactase gene on plates containing very minimal media that contained lactose. What they were looking for is mutations that fixed the lactase gene and allowed them to grow. What they saw was way more lac+ colonies than they expected, as if the presence of the lactose increased the number of lactase converting mutations. This could indicate non-random mutations.

However, the story wasn’t that simple. As it turned out, starving E. coli trigger what is called the SOS response. Certain proteins can sense DNA damage, and when this happens it derepresses a whole host of genes.

image

DNA damage activates RecA which cleaves LexA that is bound to the repressor regions of SOS gene promoters. Some of those SOS genes are error prone polymerases that increase the mutation rate in addition to proteins that increase the recombination rates. Therefore, the reason they saw more lac+ conversions was due to more random mutations.

There was real interest in the initial results, and there were many who legitimately thought that it could point to non-random mutations. However, this didn’t turn out to be the case. Scientists aren’t dogmatically opposed to non-random mutations. Rather, random mutations is what the evidence points to.

There are also examples of somatic hypermutation. This is where certain regions of the genome are prone to higher rates of mutation. This is especially helpful in B-cells where the genes responsible for antibodies see an increase in mutations compared to other parts of the genome. This allows antibodies to quickly evolve better antigen binding sites. Is this a case of non-random mutation? It’s in a gray area. Regions outside of the antibody gene also see an increase in mutations, but there is an obvious advantage for the antibody genes seeing an increase in mutations.

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Thanks, I’m actually familiar with both of your examples, but they’re very helpful in this context of understanding random/non-random mutations.

Regarding somatic hypermutation: B cell proliferation also increases in immune response not just mutational rates, correct? This provides somatic hypermutation enough chances to get it right, right?

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Please forgive me if my posts seem condescending. I have no idea what your background is on these subjects, so I went for the most basic explanations.

If I understand your post, that is correct. The more strongly a B-cell binds to the antigen being presented by the T-cell the stronger the signal it is given to divide and produce antibodies. Therefore, variations in antibodies that improve antigen binding are selected for and improve antigen binding over time.

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And, it’s important to keep in mind that somatic hypermutation is not that specific. It also is associated with a lot of lymphoma genesis/leukemogenesis.

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Yep, but way off topic if we start sharing everything we know about somatic hypermutations.

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In a previous post I mentioned that part of the function of polymerases is to create mutations. Here is an interesting paper that led me to that conclusion:

A quick summary for those who don’t know sciencese. They allowed a polymerase to copy DNA using larger and larger bases. As the size of the bases increased there was a reduction in the number of mutations and an increase in enzyme effeciency which indicates that mutations are due to a loose fit between the polymerase and the incoming

If perfect fidelity is advantageous it would seem to me that polymerases would evolve that feature, but they haven’t. Instead, the active site is just loose enough to allow for mutations. Of course, this is in E. coli so it may not apply to all other species, but it is an interesting finding.

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I think the drift-barrier hypothesis accounts for this. It is not that polymerases are actually somehow selected to cause mutations, but rather improving their replication fidelity beyond a certain point would require unrealistically enormous population sizes because the fitness gains from reducing the mutational load when the mutation rates are already so low would be effectively invisible to selection.

I’m not “sharing everything I know.”

I’m just heading off attempts to insert teleology where there’s no evidence to support doing so.

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