We have an observed and known natural process that produces tree-like structure in populations. Out of the nearly infinite number of ways you can organize species into a tree there are only a tiny, tiny fraction that would be consistent with the process of common descent and evolution. For example:
Just to recap, there are 1x10^38 possible ways of organizing 30 taxa into a tree. There are a tiny, tiny fraction of those trees that would be consistent with evolution. We observe those trees.
The process is not random. We have common ground here.
What other process would produce this tree-like structure, and why?
Nothing we know of in the material world. That is why we cannot eliminate common descent as a possibility. The problem is there is evidence of more going on in the pattern.
At this point, I have to ask how you think science works. In science, should we refuse to make any conclusions even if we have multiple independent lines of supporting our hypothesis? It seems you are arguing against the basic idea of doing science. Should we refuse to accept forensic science and DNA fingerprinting because God could have planted the DNA? We could dream up a supernatural explanation for every single natural process.
This comes up so often in these kinds of discussions. @Colewd, I’m curious about something. Have you ever investigated the differences between things which exhibit “common design” versus things which arise from “common descent”? Some people think that just because both can potentially be illustrated by tree structures, then the two must surely appear indistinguishable. But they are not indistinguishable.
I’ve sometimes used vehicle parts to illustrate common design. Somebody invented power steering, a new design. Perhaps it was first released to the public on a particular model of vehicle at a particular manufacturing plant. But soon it got installed on many models at multiple factories, not just at that first factory. Very soon the invention probably got licensed to many companies. It is very unlikely that there would be a “nested trees” hierarchy to how the power steering system got distributed on more and more vehicles with each model year. Indeed, the pattern doesn’t look at all like the common descent trees which appear in living organisms where reproduction occurs. Features in motor vehicles don’t “propagate” through the “populations” in patterns similar to what one sees in living things where evolutionary processes perpetuate “common descent” over many generations.
When I make pasta sauce, I don’t stop at oregano and basil. I like to add just a little pinch of parsimony.
If you want to make a conclusion that is fine. In the case of the tree of life the scientific explanation does not completely agree with the pattern observed. Homoplasy is a problem if mechanism is considered. This is the opportunity Winston Ewert is going after with his dependency diagram.
If mechanism is not considered then common descent works as a possible explanation for the tree.
What I consider interesting is testing the likely hood of common ancestry without considering an outside mechanism. I thought the discussion w John and Josh was very interesting.
Homoplasy is an expected source of noise, but the noise is well below the level of the phylogenetic signal. There is (almost) never a perfect correlation in science, and biology is no different. If you think that r-squared of 1.0 are the only acceptable result, then there is a lot of science that you will need to throw out.
We will see how that works out for him. As of now, he is getting a lot of false positives due to spotty annotation. He should be comparing actual DNA sequence instead of the names people give to DNA sequences.
This is a good question and has been discussed extensively on other blogs. If we assume for arguments sake that biology is designed it uses the basic components of the universe (atoms and molecules) as its basic components. These are fixed as what is used to create the diversity we see. The closest to this type of design is software and that is what Winston Ewert was arguing that gene maps follow a dependency graph (used for software design) closer than a tree. I hope he returns. I think I will ping Paul Nelson.
Wheres the model?
It’s a bit dated (is Netscape even around anymore?), but Theobold discusses this very thing in his 29+ Evidences of Macroevolution:
Sometimes I wonder if ID/creationists are allergic to Google:
That’s really all Bill et al. have left…
Bill, please think for a moment. There are some organisms alive with certain genes, which are not found in other organisms. That means there is some circumstance under which those genes are not required for life, otherwise those organisms without those genes could not be alive, yet they are.
The explanation is obvious: whatever it is those genes do is conditionally beneficial. Conditionally means only under certain conditions are they beneficial. And they’re probably not essential even under those conditions.
An easy to understand example is an enzyme that breaks down a novel substrate, like those genes that break down nylon oligomers. They’re beneficial to the organisms that have them if there is nylon in the environment, because then they can use nylon waste products as a carbon source. If the nylon disappears, the genes are no longer beneficial. But the organism can clearly still survive even if it loses these genes, as it can get carbon from other chemicals in it’s surroundings.
Another easy to understand exampe is antibiotic resistance genes. If an antibiotic is present, having a gene that somehow combats this antibiotic is beneficial. If the antibiotic is not present, then then gene is superfluous and can potentially be lost again to deletion mutations.
And so on and so forth. All that is required for gene loss is that the genes are only conditionally beneficial and have not become absolutely essential to the organism. Many, many genes are only conditionally beneficial in this way, in part due to many levels of redundancy and the ability of other genes to compensate for their loss, in part because they only have rather narrow functions aimed at specific environmental challenges. So if or when those challenges disappear, so does the need for those genes.
This very same thing has also been observed in the LTEE where there has been some gene loss, because in the simple flask environment of the experiment, genes that are beneficial for E coli inside mammalian guts have no use in the flask.
No, the other way around. Once the mechanism is considered, homoplasy is readily explained. Once in a rare while, a mutation will happen in parallel independently in multiple lineages.
Is it even possible for you to say something that isn’t diametrically opposed to demonstrable fact?
I agree and there has been gene duplication.
What we have not seen is the generation of a novel enzyme sequence and there are very good mathematical explanations why we would not from cell division alone.
The first step in establishing a mechanism is to model it. Not a toy model but a model that shows a functional sequence can be generated. There are 10 million organized amino acid sequences in human cells. Dawkins tried this with weasel but it required the target sequence to be available. I asked how we would model the generation of 300 english characters. T said gene duplication then random variation. With 300 characters the odds are about 8000 to one that that the first 3 mutations would start to break down the sequence.
I see >5000 papers on generation of novel enzyme sequences. They’re called catalytic antibodies.
They typically have been found at frequencies of more than 10^-8. There’s no problem.
Catalytic antibodies are a fine model, and a far better model than words. Functional sequences abound.
So now build a model that uses this mechanism for more complex protein families.
Perhaps start by acknowledging he demonstrated your claims were false.
What claim did he demonstrate was false?