It would be, except creationists can’t actually answer that question. Because ultimately they have to say that changes in expression and/or changes in morphology aren’t novel, which covers 99.9% of metazoan evolution and means that the ‘corner’ they’ve ‘forced’ us into is common ancestry of all animal life. Which isn’t great for the ‘Young’ part of YEC.
I’d say more often “won’t” than “can’t.” @jeffb, do you see the point here?
I suspect there will be a tie-in to Behe’s latest ridiculous strawman i.e "evolution almost always works by breaking things = DEVOLUTION!". Here’s hoping I’m wrong.
Even if true, it would be a spectacular evasion of the question, since it does nothing to explain what novelty, specifically, is in need of explanation.
What is uninteresting about them? And why does it matter whether they are interesting?
Every single attribute of every single organism that has ever existed on earth is a novel thing that resulted from mutations.
Is that enough for you?
That was an informative video. Thank you.
I pulled that phrase from the original quote here:
BTW, I anticipated that I might get that kind of response: “Define what you mean by…”. Which is why I said the follow:
I’ll also take a moment to reiterate this:
BTW, apologizes to @thoughtful, it looks like I hijacked a good conversation. Speaking of, am I able to move this conversation to another thread? If so how? (I’m still a little new here).
Hey, two things. First, you are a decent chap for noting this!!! Second, it would be great to start a new thread but I think that power lies with @moderators and not with us.
It wasn’t my thread, but yeah I have that problem a lot. If you’re YEC you’ll get lots of replies. Once you’ve been here long enough you can start your own side conversations without approval. Err on the side of linking to a post and starting a new thread if it’s even just a slightly different topic and you’ll do a lot better than I did. You just have to wait for approval on the new thread when you’re new.
I’m not either one of those guys - but would like to see “Jeffb asks for examples of beneficial mutations”
@jeffb are you asking for observable examples?
I’m currently waiting to see if/when scientists will be able to identify whether the newer SARS-CoV-2 variant has gained a specific function to be more transmissible.
The problem, by analogy: You’ve been told that pyramids are built by stacking stone blocks on one another, and you’re asking for evidence of levitating blocks. You have a fundamental misunderstanding of the expectations and predictions of evolution, which is leading you to request forms of evidence that are somewhere between irrelevant and contradictory to the actual theory. That was the reason for my requested definition, to lead you down a path where you came to understand that evolution does not predict what you are asking for.
The studies cited by others are interesting, but they have all unfortunately skipped a step and silently corrected your malformed request to the closest form consistent with what evolution actually predicts, and provided examples appropriate to that. This is distressingly common, and universally results in the creationist replying ‘but that’s not x!’ where ‘x’ is their unstated misunderstanding of evolutionary expectations.
So let’s instead get the expectation stated upfront, so the expectation can be corrected first. Then we can work on examples of those things.
“Best” is rather subjective (what makes one beneficial gain of function mutation, assuming it is the conjunction of these two attributes you find interesting, better than another?), but there are certainly examples known of mutations that are simultaneously gain of function while also being selectively beneficial. Here’s one:
We describe here an experimental example of an origin of a new gene where both of the above-mentioned mechanisms interplay. Our experiments show how phage DNA when fused with an existing bacterial gene results in novel functionality. More specifically, a chimeric gene is formed by addition of a 169-bp fragment of foreign DNA to a truncated lacI gene. When translated into a protein, due to an internal stop codon, this 169-bp region adds only 23 amino acids to the C-terminal of the truncated LacI protein. When expressed, the chimeric protein can suppress temperature sensitivity in a mutant of Salmonella enterica serovar Typhimurium strain LT2 (designated S . Typhimurium throughout the text) at nonpermissive temperatures. The gene fusion results in relocalization of the chimeric LacI protein to the outer membrane, which results in an increase in membrane vesicle formation and suppression of the temperature-sensitive phenotype. Furthermore, the native repressor functions (i.e., DNA binding and inducer response) of the LacI protein are maintained in the chimeric protein, even though they are not needed for the novel function.
So here’s an example of a mutation, specifically an insertion of a piece of DNA originating from the phage genome, into the reading frame a bacterial protein coding gene, resulting in a novel fusion protein that is 23 amino acids longer, which subsequently is simultaneously capable of maintaining the original function of the pre-mutation bacterial gene, while it gains the biochemical function of being transported to the outer membrane(one biophysical gain of function), results in membrane vesicle formation (another gain of function), which confers increased temperature tolerance (which is a beneficial phenotypic effect).
One insertion mutation to a gene, making it larger, giving it two new biophysical functions, that confers a novel beneficial phenotype.
I very much agree. Moreover, it’s intrinsically fun to learn how biology works, independent of the polemics. Don’t miss out.
36 posts were split to a new topic: YEC interest in science
If the issue is “beneficial”, that is defined as an increase of fitness. Not by an increase in “complexity” or by a “gain of function”, or by a mutation being “interesting”. You can construct an example by taking any site in the DNA where there can be a mutation that reduces the fitness. There are a great many such sites, of course. Now we know that at any site, mutations are possible from any one of the four bases to any other one. Now just consider a sequence that contains the base that reduces the fitness there, say in that case a mutation to a C from the original base, an A. Is a point mutation possible that increases fitness? Of course, just consider the mutation from C back to A. End of story. (It also shows that if you think that there is some deep information-theoretic reason why there cannot ever be a beneficial mutation, you are very wrong).
This paper discusses the earlier variant which came to dominate. In contrast with Sanford, the history of COVID accords with the usual model of viral fitness increasing with enhanced transmission and neutral or decreased virulence.
The rate of sequence variation among SARS-CoV-2 isolates is modest for an RNA virus but the enormous number of human-to-human transmission events has provided abundant opportunity for selection of sequence variants. Among these, the SARS-CoV-2 Spike protein variant, D614G, was not present in the presumptive common ancestor of this zoonotic virus, but was first detected in late January in Germany and China. The D614G variant steadily increased in frequency and now constitutes >97% of isolates world-wide, raising the question whether D614G confers a replication advantage to SARS-CoV-2. Structural models predict that D614G would disrupt contacts between the S1 and S2 domains of the Spike protein and cause significant shifts in conformation. Using single-cycle vectors we showed that D614G is three to nine-fold more infectious than the ancestral form on human lung and colon cell lines, as well as on other human cell lines rendered permissive by ectopic expression of human ACE2 and TMPRSS2, or by ACE2 orthologues from pangolin, pig, dog, or cat.
Thank you Rumraket! Yes, this is a good example of what I’m looking for. I’ll read over this one this weekend.
Well I thought you were doing well.
And yes, I see that. I’m finding myself thinking very carefully over every post, including how I ask questions.
Good question. Yes actual observed examples, not hypothetical narratives.
I guess you missed this follow-up that I posted. https://www.nature.com/articles/s41467-020-19818-2 I’m sure there will be more papers on it.
Good catch - pertinent article. I’m sure that with the unprecedented real time scrutiny devoted to this virus, that there will be much argumentation and lessons learned. It is evident, however, that this pandemic is yet another case study which discredits Sanford’s ideas in regards to origins and progression of infectious disease.
In regards to the more recent UK variant in the news, the N501Y mutation, the resulting alteration of the viral spike protein is suggested to have a greater affinity to human ACE2 receptor.
Here is the CDC summary for new variants…
Emerging SARS-CoV-2 Variants
I thought this general article in Vox was decent.
The new UK coronavirus mutations, explained
Analysis is still very preliminary, but there does appear to be an emerging consensus that the alterations of the viral spike protein in the UK and SA strains are raising transmissibility.
Yes, this is the one I was referring to. I was being lazy and didn’t feel like looking up what I was called - N501Y.
It doesn’t discredit Sanford’s ideas as far as I understand his hypothesis. There can be increased fitness in the model in the initial evolution of the strain - Fitness will just decrease eventually as mutations accumulate.
I had read the Vox article earlier. It definitely was the best popular article I’ve read on the subject. I’m definitely trying to keep up anything new written about it. If I find anything of significance I’ll post it.