Any issues getting through airport security?
Looks to be an interesting project though.
3 Likes
It’s a digital thermometer.
2 Likes
It doesn’t work with young earth zealots, but I’m not trying to convince them. I’ve given up assuming good faith on their part long ago: they know full well that they aren’t telling the truth. But the people I am interested in communicating this to are Christians who are confused and perplexed about the whole subject, and as far as I can tell, the things I’ve had to say in this respect have been helpful. And many of them have the same misconceptions and fight-or-flight reactions to concepts such as methodological naturalism as well.
It communicated things clearly to me right at the start of my A level physics course when I was sixteen years old. My physics teacher started off the very first class by asking us to define physics, and when none of us were able to come up with a simple answer, he described it as “the art of measurement.” It’s a bit of an over-simplification but it hammered a very important point home right at the outset: measurement is absolutely fundamental to the very essence of science.
So on, it’s not something that requires advanced degrees and extensive experience. It’s the core fundamentals. It’s the basics. It’s beginner stuff. It’s FizzBuzz territory. It’s stuff that every school leaver with the most rudimentary level of scientific literacy should be expected to know cold.
7 Likes
Evolutionary theory teaches that there is mainly NOT survival of the fittest. Strange enough. Genes related te fitness have low heritability.
https://www.nature.com/articles/hdy1987113
https://www.sciencedirect.com/science/article/abs/pii/0169534787900966
https://www.pnas.org/doi/10.1073/pnas.97.2.698
Perhaps not completely true but nice to know.
To be honest, your question surprised me a bit. Once the surprise wore off I realized my own biases were probably at work. So, thanks of the question!
The quote in question:
Perhaps another way to put it is that, as a scientist, I am curious just how far this regular, reproducible structure of the cosmos extends . . .
–Dennis Venema, " At the Frontiers of Evolution: Abiogenesis and Christian Apologetics"
For me, as a scientist, this hits the nail on the head, but now I understand why it may not be obvious to non-scientists, nor should it be obvious. It’s not a difference in intelligence, just a difference in experience. First, science is curiosity. Why is a thing so, and how did it get that way? That’s the beginning of science. The beginning is not, “Well, I have to remember to only look at the natural”. The next step is to look for what we can reliably measure. It’s empiricism, and it is described by Venema as “regular, reproducible structure”. Next, we come up with a hypothesis which is asking how far into the cosmos this measurable mechanism extends.
Methodological Naturalism is more of a hoity-toity philosophical term. In my experience, science is more about pragmatism. We use empiricism because it’s the most pragmatic way of approaching a question, and it has been shown to be a very successful way of answering questions about the physical universe. As others have noted, science is not some ultimate truth or ideology that’s meant to answer all questions. It’s as Venema describes, a question born of curiosity as to how far observable processes extend into nature.
4 Likes
I would agree that Darwin should have put more stress on success of reproduction instead of survival.
You also stated that it is relatively “easy” for enzymes to change function. So it seems like we have a pretty solid evolutionary pathway. Random sequences produce selectable and easy to reach functions, and then changes to that selected function are easily reached by subsequent changes.
Yes, for that specific structure. However, no one thinks that modern beta-lactamases emerged from random sequence, so it’s completely irrelevant. Modern beta-lactamases evolved 2 billion years ago, and were themselves preceded by almost 2 billion years of evolution. No one thinks that the highly optimized protein folds seen in these beta-lactamases were the product of sudden emergence from random sequence. There is absolutely no reason why Axe’s study should be a model for all protein function as it relates to random sequence.
There are more studies with extremely high chances of function emerging in random sequence.
That’s work Axe should do if he wants to make the claims he seems to want to make.
True, with the caveat that if he was referring to survival of a population rather than an individual, then reproduction would be the mechanism of the populations success. I would have to look at the context of what he wrote. No doubt Darwin would be pleased to see how his ideas have been refined and expanded, but remaining recognizable.
Addendum:
“The phrase ‘survival of the fittest’ is often incorrectly attributed to Darwin. In fact, it was coined by the philosopher Herbert Spencer in response to reading Origin of Species five years after the first edition was published. Alfred Russel Wallace, whose own theory about the mechanics of evolution was almost identical to Darwin’s, wrote to Darwin in 1866 with a lengthy criticism of Darwin’s term ‘natural selection’ and pleaded with him to minimise confusion by adopting ‘Survival of the fittest’. Darwin introduced the phrase in a few places in his works from 5th edition of Origin in 1869. However, he never abandoned the term ‘natural selection’ and only saw ‘survival of the fittest’ as a synonym or auxiliary phrase to help make his meaning clear to his readers.” Survival of the fittest | Darwin Correspondence Project
3 Likes
I don’t know if we humans degenerate at this moment. However sometimes, it seems to be.
As Lynch and Gabriel around 1993 mentioned, populations that are small and have no sexual reproduction are prone to genetic load: the accumulation of deleterious mutations. By asexual multiplication, you can’t get rid of deleterious mutations in your offspring by exchange for more beneficial sequences from another individual. And every individual has its own deleterious mutations occurring. So, you have to hope for some beneficial mutations for yourself. However, deleterious mutations are more common than beneficial mutations. So waiting doesn’t help that much. Fortunately, humans are there in large numbers and we multiply sexually. Sexuality is important since this gives that beneficial mutations from different parents have the ability to combine by recombination and give healthy offspring. However, we haven’t been there in large numbers in the past and some parts of our genome don’t take part in the recombination process. These are the Y-chromosome (which we all derive from our fathers) and the mitochondrial DNA which we have from our mothers. Since these chromosomes don’t recombine, they accumulate more deleterious than beneficial mutations, so they degenerate. Could be rapid in small populations and slow in larger ones. This is called Mullers ratchet. In scientific literature, typing Mullers ratchet gives information about the problem. It is not solved yet. Maybe a bit inconvenient.
As some of my (female) colleagues put it in the title of a paper, there are many ways to die but only one way to arrive.
5 Likes
Which ones?
Again, why? Your argument here boils down to, functional proteins are rare because I think functional proteins are rare. 10^20 does indeed sound like a very large number, but the number of possible proteins is much, much larger. There are 10^195 possible proteins of length 150 AA. One independent functional protein every 10^175 sounds like a very small number. So which is it? Relying on intuition when it comes to very large spaces of very high dimensionality is a bad idea: most of us just don’t have enough experience to have developed such intuition. What we need is evidence. Given that specific catalytic functionality can be found at a rate higher than 1 per 10^3 for short peptides, I think the burden of proof is on those arguing that the rate overall is many orders of magnitude smaller.
Yes, I’m familiar with Muller’s ratchet (I am a population geneticist, after all). The relationship of the ratchet to mt and Y DNA is more complicated than you suggest, however. Regarding the Y, yes, deleterious mutations do accumulate in the Y, especially early in the history of a new Y within a species. Two things limit their impact, however. One is that the Y is homologous to the X, since they started as the same autosome, which means that damage to the Y copy of a gene still leaves a functional X-linked copy. (The fact that there are the two homologous copies is one of the many things that makes sense in light of evolution and doesn’t otherwise.) Thus, Ys tend to degenerate and shrink while Xs remain fully functional. The other is that a different form of recombination can develop within the Y, based on gene conversion. In humans, this takes the form of gene exchange between the arms of the chromosome, enabled by large palindromic stretches of duplicate DNA on the two arms. Thus, recombination does occur, albeit at a slower rate.
Different considerations apply to the mitochondrion. While there is an overall tendency for genes to migrate from the mitochondrion to the nuclear genome, that’s a very slow process and not enough to evade the accumulation of new deleterious mutations. However, the population size is not actually small, even if there are few individuals of that species carrying the mitochondrion. That’s because the population within each individual is large. There is very strong evidence that strong purifying selection operates on mtDNA even at the level of a single human. How much of that occurs within cells, as different copies of the mitochondrion compete with one another, and how much occurs through competition between cells, and how the selection operates, is still being worked out. See, for example, https://www.annualreviews.org/doi/full/10.1146/annurev-genom-121420-081805
5 Likes
That’s a lesson we learned in astronomy – numbers can get very large; double-check and don’t expect numbers that ‘feel right’.
Probably veering off topic – someone in a biology course asked if we could make a patch for the Y chromosome so it’s not so tiny. Assuming some way to achieve it, would there be any benefit to doing that?
2 Likes
Astronomy has the large numbers, but it doesn’t have the high dimensionality. There are vastly more paths connecting two proteins in protein space than one might intuit, making one’s intuition unreliable about how hard it is for evolution to overcome selective barriers between states.
It’s not clear what the benefit could be, since we’re adapted to having the Y we’ve got. It would just start degenerating again anyway.
2 Likes
I would call this the biologic version of the multiverse argument. However, in biology, its defeated. In biology, we don’t see that functions are gained around every corner. If we dig, biology is always more precisely regulated than we thought before. We see that specific functions that needs to be done in different parts of biology, in many occasions the number of different solution is clearly limited. Functions that emerged independently. Convergent evolution. That’s highly unlikely if there were 10^20 solutions available.
Marvelous. Great stuff! It’s all about the mechanism to prevent mtDNA breakdown, timing and place. what I missed was: purifying selection for what function?
However, Mullers ratchet seems not only to be a problem for Y-chromosomes and mt-DNA but also for autosomes.
When we were young, we learned about recombination. I thought that recombination occurs manytimes almost everywhere. This was wrong. It seems that recombination occurs at recombination hotspots. For instance regulated bij PRDM9. There seem to be tenthousands of hotspots and the areas between them are tenths of thousands bp long. Areas between hotspots recombine seldomly. And entire genes or large parts of genes are part of haplotype blocks. When these large clusters of sequences don’t recombine, they seem to be vulnerable to Mullers ratchet. Additionally to that, it makes it very difficult for genes within such a block to be build up from beneficial mutations that were created by different individuals.
1 Like
I had a great discussion with a PhD physicist a few years ago. As we considered QM happenings in the heat death of the universe, he proposed that would be the basis for cosmic recombination, and I had no objection other than that there could not be an infinite number of these in the future. Kind of like multiverses. What does the physicist do when confronted with the impossibility of there being an infinite number of things?
An abstract for everyone’s consideration:
2 Likes
We see new functions arising quite often during the course of evolution. Your claim is that these apparent gains of function aren’t real because they’re impossible. Your original argument was that they’re impossible because of Axe’s study, but Axe’s study doesn’t actually tell us whether they’re impossible or not. Then you shifted to the argument that they’re impossible because catalytic activity is impossibly rare in random sequence. Now that you’ve seen that that isn’t true, you’ve shifted to simply declaring that new functions aren’t being gained – despite the studies (which have been pointed out to you) that show precisely how new functions could have been gained by a small number of mutations in earlier proteins. You’re not even making an argument at this point.
This is quite wrong. For example, when we dug, it turned out that transcription was much less precisely regulated than we had thought.
Just how many examples of convergent evolution are there at the molecular level?
Purifying selection for the existing function. That’s the definition of purifying selection.
I’m familiar with recombination hotspots – in fact, I’m an author on several of the early papers showing that they exist in humans, and one of my former officemates discovered the role of PRDM9 in regulating them. They’re real and they absolutely do not imply that Muller’s ratchet should be at work in human autosomes. By no means does all recombination occur in hotspots; haplotype blocks can be and are broken. More importantly, there are so many haplotype blocks in the human genome (~150,000) that they have little practical effect on mixing up either deleterious or beneficial mutations, both of which are uncommon. All they do is add a little granularity to the process. Also, PRDM9 itself evolves rapidly, so that on evolutionary time scales hotspots move to new locations repeatedly.
3 Likes
That’s not a problem – it’s the counting that is a problem. Depending on the nature of the universe in terms of extent, there can be an infinite number of things or an ludicrously large number of things but still finite. Last I checked, this was still up for grabs.
And that despite examples given.
Okay, for the non-biologists here, what is a “recombination hotspot”? Is that related to mutational hotspots?
2 Likes
Take a diploid organism, like me for example. I have two copies of each chromosome, one inherited from my father and one from my mother. I passed on one copy of each chromosome to my son. Only I didn’t pass on either my mother’s or my father’s copy, but rather a mosaic of both of them. The process of creating those mosaic is recombination, in which replication of a chromosome switches back and forth between parental copies. It occurs very roughly once per chromosome arm per generation. It’s one of the great innovations in the history of life and its origin is largely a mystery.
It turns out that recombination does not occur uniformly across each chromosome. Instead, some little stretches are much more likely to have recombination occur there – those are hotspots. In most mammals, the hotspots occur because a protein named PRDM9 binds to a particular DNA motif and recruits the recombination machinery to start working there. (It’s rather more complicated than that – not all motifs are active hotspots, I believe. But that’s the basic story.)
An interesting twist in the story is the recombination hotspots tend to destroy themselves over time, thanks to something called GC-biased gene conversion, which tends to replace the existing DNA where recombination occurs. GC-biased gene conversion eventually erases the PRDM9 motif, eliminating the hotspot. Eliminate enough hotspots and there’s now pressure for PRDM9 to change to recognize a different motif, and so there is selection pressure for that gene to evolve rapidly.
Side note: PRDM9 is part of an irreducibly complex recombination system: knock out the gene for that protein (at least in mice) and reproduction fails. Only it’s not really: dogs (among a number of other species) don’t have a functioning PRDM9 gene and yet they manage to carry out recombination and reproduce just fine.
5 Likes