Greetings all.
I decided to break away from my Phylogeny research (still at it BTW) and respond to this comment.
I do so because it’s along the lines of a question I’ve wanted to ask here, which lead me to PS to begin with (and I still haven’t gotten to).
I know this is off-topic, and should go in a separate thread, but I have a few questions about this:
First off, can you direct me to something I can read up on regarding these being “refuted scientifically”?
Second: I’ve been wanting to read examples of what evolutionists would consider as the “best examples of beneficial mutations”. Perhaps information to my first question would answer that. What do I mean by “best”? Well I’m pretty open-minded about that, however “gain of function” mutations would be good examples, or any which demonstrate overcoming apparent IC. But really, whatever each consider “best.” It’s possible everyone has their own favorites. Perhaps someone has put together a top-N list?
You’ll first have to specify what you mean by a “gain of function” mutation. Or by “beneficial mutation” in general, for that matter. To me, the existence of beneficial mutations is so obvious and non-controversial. It’s like asking for evidence of the existence of nitrogen. So I suspect the issue is more with your understanding of “beneficial” than with any lack of evidence of which you are aware.
I’m not sure what arguments @Faizal_Ali is referring to, but it sounds like “some ID proponents” are making the error that @jeffb is making here, which is to interpret “gain of function” as something beneficial or creative. That’s not how the phrase/term is used by biologists. A gain-of-function mutation is defined in comparison to a loss-of-function mutation and that’s really all there is to it. Some GOF mutations are horrific (HTT expansion in Huntington’s disease is a classic example, but see also various cancer-causing gene fusions). Some gain-of-function mutations have dominant negative effects (see N19 or N17 mutations in small GTPases), wherein the “gained” function exerts a negative effect on the normal versions of the protein. All we mean when we say “gain of function” is that there is a new or simply changed activity for the mutant protein, as opposed to simple erasure of the protein as a factor. This is never associated with any claim or comment about fitness.
This, BTW, is one of several good reasons to avoid the practice of asking questions of “evolutionists.” Gains of function and “beneficial mutation” don’t have answers that are specific to people who understand evolution. One can be a YEC and, with a little effort to become informed, know all of this.
Using new techniques for resurrecting ancient genes, scientists have for the first time reconstructed the Darwinian evolution of an apparently “irreducibly complex” molecular system.
The research was led by Joe Thornton, assistant professor of biology at the University of Oregon’s Center for Ecology and Evolutionary Biology, and will be published in the April 7 issue of SCIENCE.
How natural selection can drive the evolution of complex molecular systems – those in which the function of each part depends on its interactions with the other parts–has been an unsolved issue in evolutionary biology. Advocates of Intelligent Design argue that such systems are “irreducibly complex” and thus incompatible with gradual evolution by natural selection.
“Our work demonstrates a fundamental error in the current challenges to Darwinism,” said Thornton. “New techniques allowed us to see how ancient genes and their functions evolved hundreds of millions of years ago. We found that complexity evolved piecemeal through a process of Molecular Exploitation – old genes, constrained by selection for entirely different functions, have been recruited by evolution to participate in new interactions and new functions.”
Behe responded to this with a big “NUH-UH!” as always but could provide nothing to refute the sound scientific research.
WOODS HOLE, Mass. - It sounds like a “Just So Story” - “How the Insect Got its Wings” - but it’s really a mystery that has puzzled biologists for over a century. Intriguing and competing theories of insect wing evolution have emerged in recent years, but none were entirely satisfactory. Finally, a team from the Marine Biological Laboratory (MBL), Woods Hole, has settled the controversy, using clues from long-ago scientific papers as well as state-of-the-art genomic approaches. The study, conducted by MBL Research Associate Heather Bruce and MBL Director Nipam Patel, is published this week in Nature Ecology & Evolution .
Insect wings, the team confirmed, evolved from an outgrowth or “lobe” on the legs of an ancestral crustacean (yes, crustacean). After this marine animal had transitioned to land-dwelling about 300 million years ago, the leg segments closest to its body became incorporated into the body wall during embryonic development, perhaps to better support its weight on land. “The leg lobes then moved up onto the insect’s back, and those later formed the wings,” says Bruce.
One of the reasons it took a century to figure this out, Bruce says, is that it wasn’t appreciated until about 2010 that insects are most closely related to crustaceans within the arthropod phylum, as revealed by genetic similarities.
“Prior to that, based on morphology, everyone had classified insects in the myriapod group, along with the millipedes and centipedes,” Bruce says. “And if you look in myriapods for where insect wings came from, you won’t find anything,” she says. “So insect wings came to be thought of as ‘novel’ structures that sprang up in insects and had no corresponding structure in the ancestor – because researchers were looking in the wrong place for the insect ancestor.”
Abstract: The origin of insect wings has long been debated. Central to this debate is whether wings are a novel structure on the body wall resulting from gene co-option, or evolved from an exite (outgrowth; for example, a gill) on the leg of an ancestral crustacean. Here, we report the phenotypes for the knockout of five leg patterning genes in the crustacean Parhyale hawaiensis and compare these with their previously published phenotypes in Drosophila and other insects. This leads to an alignment of insect and crustacean legs that suggests that two leg segments that were present in the common ancestor of insects and crustaceans were incorporated into the insect body wall, moving the proximal exite of the leg dorsally, up onto the back, to later form insect wings. Our results suggest that insect wings are not novel structures, but instead evolved from existing, ancestral structures.
Agreed. I’ll add the caveat that the whole simplistic conversation (in creationist contexts) about “beneficial mutations” has an essentialist flavor that is wildly misleading. If @jeffb and other creationists just learned that from this thread, and incorporated it into their thinking, this would be a step forward. A mutation is only “beneficial” in a particular context, which means in a particular genome and under particular environmental conditions. One of my favorite papers in our journal on this topic (of adaptation and its genetic underpinnings) is below and it’s about adaptations to cold in woolly mammoths. Calling these mutations “beneficial” seems useful and helpful in the context of extreme cold, but that’s all. We may reasonably assume that the opposite is the case in other environments. And so, outside of the small and simplistic world of creationism, discussions of mutation, adaptation, and “benefit” must (and do) avoid the implication that a mutation is or can be inherently “beneficial.”
I had a feeling I might need to clarify my question.
First, I understand the concept of beneficial mutations: They are within a context, and can even include loss-of function which lends itself towards a selective advantage. But loss-of-function-beneficial-mutations aren’t very interesting.
I intentionally said that I was being open-minded about “best examples.” I get that that can be subjective. That’s why I said each person may have a different ‘favorite’.
I’m trying my best to make this a simple question. I’m just curious to see what kind of novel things mutations have accomplished. If you don’t personally have any of your own favorites, that’s fine, perhaps someone else does.
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 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.
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”
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:
One mechanism for creating new genes is the gene fusion model that involves reorganization of existing genes, such that fragments of different genes fuse together resulting in novel functionality. Comparative genomics have provided support for the origin of new genes by fusion. Among these, one class includes fusion of entire domains from different proteins that results in the novel protein performing functions of both the domains. Examples of evolution of new genes by this mechanism include the origin of tRNA synthesases ([Berthonneau and Mirande 2000](javascript:;); [Eswarappa et al. 2018](javascript:;)) and fatty acid chain desaturases ([McCarthy and Hardie 1984](javascript:;)). This mechanism for the formation of new genes was also observed during experimental evolution studies in Pseudomonas fluorescens , where fusion of different domains of a desaturase and a di-guanylate cyclase resulted in the generation of an adaptive phenotype ([Farr et al. 2017](javascript:;)). The second class among the gene fusion models includes nonspecific chimeric formation where different fragments of different genes fuse together. Origins of adh-jingwei and adh-twain genes in Drosophila species are examples of this category ([Long and Langley 1993](javascript:;); [Jones et al. 2005](javascript:;)).
A second mechanism of origin of new genes, especially observed in but not limited to bacteria, is from extracellular mobile elements that includes phage DNA and conjugative elements (transposons and plasmids) ([Treangen and Rocha 2011](javascript:;); [Wiedenbeck and Cohan 2011](javascript:;); [Blount et al. 2012](javascript:;); [Jerlstrom Hultqvist et al. 2018](javascript:;)). These mobile elements often result in immediate innovative changes in a one-step genetic event and hence are an important source of generating novelty. Examples of evolution of novel genes by contribution of these mobile elements include the evolution of metabolic pathways ([Pal et al. 2005](javascript:;); [Homma et al. 2007](javascript:;)), diversification of cell-envelope surface structures, synthesis of lipopolysaccharides, and novel regulatory interactions ([Nakamura et al. 2004](javascript:;)).
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.