They copy themselves already, so there is little reason for us to attempt what you suggest and if we are just copying it then that would not be an example of design anyway.
Besides this is a foolish gap to stuff a god-of-the-gaps argument into. We are rapidly mastering the mechanics of how cells work and have already rewritten portions of DNA and alter viruses for gene therapy. I see no reason why we might not one day design a cell from scratch. I expect it to be a great deal more simple than cells which evolved and I don’t see why that is so significant.
We certainly can make complex machines. That is a reachable goal and thus a chimera to pin the distinction between living organisms and machines on. The real difference in living organism isn’t complexity but the fact that they are a product of self-organization and evolution. That is something that the complexity of our designs will never change.
I think many of us are focusing on different characteristics of each analogy - computer program or language. An analogy isn’t the thing - it has some (not necessarily all) of the characteristics of the thing it is describing.
To clarify my earlier post with respect to design, I wasn’t trying to make an ID argument for DNA. But DNA does exhibit organization, like a computer program. How it got that organization is an open question. I know the second law of thermodynamics argument cannot be used to prove design of DNA, because the earth isn’t a closed system, and even if it was, there can be local decreases of entropy.
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T_aquaticus
(The Friendly Neighborhood Atheist)
83
Sexual selection allows mutations to move towards fixation in parallel with each other. You don’t have to wait for each mutation to fix before another can start moving towards fixation.
Emerged from scratch? Can you actually show that?
You seemed to have confused gene with DNA. They are not necessarily the same thing. You can have a stretch of DNA that is not a gene. However, a handful of mutations in that stretch of DNA can cause the DNA to be transcribed and turn it into a gene. That seems to be the case for the vast majority of human orphan genes I have found. There seems to be a common misperception in the ID/creationist community that these orphan genes emerged from nothing, but they didn’t. They emerged from DNA that wasn’t previously transcribed. You can find orthologous DNA in other primate genomes, such as in the chimp genome.
If you agree that the human genome contains an increase in information, then the mutations that separate humans and chimps are exactly the mutations you are looking for as examples of mutations that increase information.
Regularly, mutation rate is 10^-8. Fixation chance (neutral) is < 10^-4 per mutation and lower for larger populations. Time to fixation is > 100.000 years for each single neutral mutation taken a generation interval of 10 years and much larger for larger effective populations. The chance for more a few concerted mutations to rise and settle is…0.
T_aquaticus
(The Friendly Neighborhood Atheist)
86
I should have said sexual reproduction. A misstatement on my part.
Meiosis unlinks genes from each other so that mutations can move towards fixation independently of one another.
That article is saying the exact same thing I am saying.
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T_aquaticus
(The Friendly Neighborhood Atheist)
87
@Vanengelen
In generation 1 there are multiple neutral mutations that fix in 100,000 years.
In generation 2 there are multiple neutral mutations that fix in 100,000 years.
In generation 3 there are multiple neutral mutations that fix in 100,000 years.
This means there is something like an assembly line of mutations that are continually fixing in each generation, about 100,000 (could be more or less) years after they first appear.
And the chance is 10^-8 times 10^-8 times 10^-8 times etc. etc. etc.
And then, we gave generated information.
T_aquaticus
(The Friendly Neighborhood Atheist)
89
That’s the Sharpshooter fallacy. The probability that mutations will reach fixation is 1 in 1. It is inevitable, just by chance alone much less by selection which greatly increases the probability of fixation. The probability of any set of specific mutations reaching fixation is extremely improbable, but the probability of any mutations reaching fixation is inevitable. The probability of 50 to 100 mutations occurring in a single individual comes with the same improbability, and yet every single person is born with a set of mutations that have probability of 1 in 6 billion to the 50th power.
And the chance that the neighbour codon mutation was deleterious is 20 times higher inevitable.
Yes, of course the variation in noise is immense and therefore we never meet a second unrelated person with exactly the same DNA. But in this thread we talk about information
T_aquaticus
(The Friendly Neighborhood Atheist)
91
Negative selection removes deleterious mutations, so I don’t see a problem here. Care to explain?
You talk about information, but you continually change the definition so that your beliefs about information are never challenged.
I’m not sure I am correctly following the case you are building here. Are you saying that mutations in non coding sequences are deleterious? Non-regulatory sequences? In what way?
T_aquaticus believes that non coding regions collect mutations that after some time make from a non coding sequence a functional gene. Over time, one by one these neutral but for the future beneficial mutations are brought together. I argue against this unscientific idea that in these non coding regions more mutations occur that are detrimental for the aimed new function. It is collecting noise. Junk. The chance that a mutation leads to an potential in the future detrimental aminoacid is 20 times higher then that it leads to the aimed beneficial aminoacid. Simply because there are 20 different aminoacids. When there is no selection. Time doesn’t help. If T_aquaticus believes that a functional gene appears in one moment or in the course of generations, the improbability is the same. And that is immense.
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T_aquaticus
(The Friendly Neighborhood Atheist)
96
It’s not a belief. It’s an observation. The human orphan genes you are talking about are regions of the genome that differ by a handful of mutations compared to the chimp genome. In the human genome these regions of DNA are transcribed and possible translated into proteins, often quite short peptides. So it is those handful of mutations that are responsible for the conversion to genes in the human genome.
Where is your evidence that these mutations are deleterious? Heck, where is the evidence that even a majority of these human orphan genes have beneficial function? That is still very much a question.
That assumes that a single amino acid change is deleterious. This is falsified by the massive number of viable and beneficial homologous proteins that differ in amino acid sequence but still have the same beneficial function.
That seems to be an unfalsifiable claim since we have the mutations that did just that. It would seem that even if you saw these mutations happening right in front of your eyes that you would reject them as evidence for evolution.
Thank you for your comments, I have only a few minor remarks left.
There is a difference between observations and conclusions that are drawn from research. Scientists have found genes that are unique for humans. The have found sequences in animals that have some degree of similarity. Of course, there are, since there is always something with some degree of similarity. That’s the observation. Some years ago, I followed a very nice presentation at a congress of the nobel prize laureate pääbo. He showed clearly that you need ancient DNA to properly draw conclusions of phylogenetics. The conclusions that are drawn from DNA of only present creatures about phylogenetic relationships are certainly wrong. He showed that the use of ancient DNA completely changed phylogeny. However, when we don’t have ancient DNA, we can’t correct and the models are certainly wrong.
I mentioned more articles. It’s already for some years that it is clear that humans have unique genes. Not only these smaller peptides.
You missed the points with regards to deleterious mutations. If there are mutations that changes a sequence in the direction of a functional beneficial protein, then by chance, there are far more options for mutations that don’t lead to that aimed functional protein in the future, but are contradictory and therefort in potence deleterious.
Of course in some parts of a protein, the exact aminoacid does not matter. For that place, several different aminoacids are OK. For that place, there are no beneficial nor deleterious point mutations. This is not part of our conversation and this does not influence my argument that there are far more in potence detrimental compared to beneficial mutations. And non-functional sequences collect noise, not for the future necessary mutations. That would be teleology.
In one sentence, you say that I have an unfalsifiable claim, and that my claim is falsified. They can’t both be true. However, they both can be untrue. And I think, they are.
T_aquaticus
(The Friendly Neighborhood Atheist)
99
The observation is that the orthologous DNA (with shared synteny) shared between species only differs by a few mutations. The claim is that these genes had to come “from nothing”. Obviously, this conclusion is falsified by the presence of the very similar orthologous DNA. Moreover, we can determine the mutations needed to produce the candidate gene.
You need DNA from extinct species in order to properly place the extinct species in a phylogeny. We have DNA from modern species which does allow us to place them in a phylogeny.
So what point are you trying to make?
Deleterious mutations are removed by natural selection.
You are continually changing definitions as each are falsified. That is what makes the ID/creationist information argument unfalsifiable.
Gregory Winter, George Smith, and Frances Arnold shared the 2018 Nobel prize in Chemistry.
What they have done is to really speed up evolution
These quotes are from the official site:
“This ensures that the enzyme template in each round has at least some rudimentary starting activity under the conditions used in that round.”
“This is possible as long as the enzyme that is chosen as a starting point has at least some low level of activity for the intended reaction, i.e. some level of catalytic promiscuity (Figure 4, reviewed in e.g. 43-46). An inactive scaffold is not a suitable choice; directed evolution requires some low level of activity. Even a very low activity level towards the intended reaction provides a starting state to optimise through evolution. Often just a few mutations are required to boost up the new activity.”
“If an enzyme has a low level of activity for an intended reaction, but much higher activity for a natural one, it may be fruitful to first lower the natural activity before starting the directed evolution efforts towards the new intended reaction.“
These brillant scientists were able to extremely speed up evolution. Never new functions emerged.