God-did-it can be used to explain anything and everything. It is scientifically useless.
That’s because many of the commenters here are trained scientists who have tested or are testing hypotheses in their various areas of research. It’s how science works! Get with the program or butt out.
I have done that already using data from several studies and falsified several aspects of your poorly defined hypothesis.
For example, you claimed that new genetic information (in the form of new promoters, transporters and metabolic pathways) cannot be produced today since God was done with creation. I showed you contradictory findings from several sources including the LTEE, which documented the formation of new promoters and a new metabolic pathway.
Here is a relatively recent paper documenting the de novo evolution of a maltotriose transporter in a particular yeast species:
According to you these events must no longer happen since God is done with creation, but they are still happening, thus, falsifying your version of the hypothesis of God-guided evolution.
@Jordan do you now see why its hopeless having any meaningful conversation with this guy. He wants us to use the LTEE as a model experiment for the origin of life, even though that experiment is completely unsuitable for that task. In the LTEE, E.coli is used, an organism that has resulted from billions of years of biological evolution. The bacteria has highly evolved biomolecules, and molecular systems none of which were present in prebiotic times. The same applies to PACEEs. The LTEE needs preexisting life to commence, so it can’t give you mechanistic hypotheses or solutions to how that preexisting life emerged in the first place.
In addition he can’t seem to differentiate between experiments that simulate natural evolution and those that use artificial selection. Protein engineers steer the evolution of biomolecules or enzymes towards achieving specific goals like improved function or stability, while Lenski’s LTEE simulated evolution in the wild which is aimless, so as long as the LTEE continues to simulate natural evolution (with no specific evolutionary outcome) we will only get what evolution can brings out. Furthermore, when he says:
He doesn’t realize two things. First, Lenski’s LTEE is not specifically a protein evolution experiment, which protein engineers focus on: Anything can evolve in the LTEE, and on any scale be it at the molecular or organismal level. Second, Lenski’s LTEE was set up to provide answers to questions about the mechanisms and patterns of evolutionary change in biology, which contrasts with protein engineering that uses already known evolutionary mechanisms (like mutations and selection in directed evolution experiments) to make novel peptides or proteins.
Wrong. If God directly dictated our evolutionary outcomes, that’s artificial selection.
Again this is not applicable to GULOP. In the absence of dietary vitamin C, you will die due to its inactivity. It’s a terrible design flaw.
GULOP fits both descriptions. It is a sinister design in the absence of dietary vitamin C, because its inactivity does away with endogenous biosynthesis of vitamin C, preventing survival, reproduction and development. In the presence of adequate vitamin C, it sits in our genome without helping us solving our nutritional need for vitamin C, a compound necessary for our survival making it a bad design.
This is another lie about me. I have never denied certain features which were deemed as flawed later turned out to be design tradeoffs or optimal ones. Why do you lie so much?
I have consistently brought up GULOP, a star example of a design flaw under your hypothesis, but you don’t engage with it, either due to your cluelessness or sheer dishonesty knowing it soundly refutes the nonsense you are spewing.
indeed. even for a single protein we need a lot of genetic information at the amino acid level. for instance: DNA polymerase required to be large enough to support the replication process :
In the way I explained right there in that very post, which you should read.
Why? As you should know, the vast majority of the data in that figure makes a perfect match to the standard tree, requiring only a single gain or loss for each gene. The number requiring two events (two gains, two losses, or a gain and a loss) is minuscule. Can you explain why that’s so?
No it isn’t, if “special creation” means anything.
But you have a different genome from me. Do we belong to different kinds? How different is “different”? And you can’t even identify a single kind so far.
To the extent that you have managed to be clear, your version rejects common descent. I don’t know to what extent, because you won’t say. I don’t know what else in science you reject, because you won’t say. Your views are certainly evolving: it’s only recently that you’ve began to insist that Genesis 1 is a true account of creation.
As should be clear, you can’t tell much and should not use what you can tell as a guide to reality.
What about it? Parallel losses are only recognizable because most of the data converge on one tree, onto which those losses can be mapped. What’s the creationist explanation for any of that?
Incidentally, the gene losses in the first reference aren’t losses, exactly. They’re transfers from the chloroplast genome to the nuclear genome, which has happened many times for many genes. Mitochondrial genes too.
parallel creation of course. this also shows why there is no real evolutionery prediction in terms of gene content. even if all species were equivalent in terms of their genetic content- evolution had no problem with that.
Population genetics would need to model how all these changes get fixed in different populations to explain Sal’s flower below to eliminate some form of special creation as the cause of the different animal “kinds” in the diagram on the post.
Does that make any sense? Why should that gene be created in some species in the nucleus and the same gene in another species in the chloroplast? What sense does it have to put chloroplast genes in the nucleus at all? Some designer.
Population genetics certainly models fixation, so I don’t know what you’re trying to say there. And how do you know those animals are “kinds”? What tells you that?
I did indeed. So why should those gains and losses fit so well on the tree diagram?
Thanks for the nice reference. Also has a very interesting discussion of evolution on rugged fitness landscapes enabled by recombination between different genes.
What do you mean they fit well? How did all those changes originate and then get fixed in separate populations? There are also genes in the diagram unique to the separate “kinds”. I am simply borrowing the word “kinds” from Genesis 1 which means separately created animals.
If you have to ask, you understand nothing. They fit well if they require only one change to happen in order to explain the distribution of the character on the tree.
They didn’t originate and get fixed in separate populations, mostly. They originated and got fixed each in a single population. That’s why they fit the tree.
Sure. That’s because they evolved in those “kinds”. We know how new genes arise: duplication of existing genes or recruitment of non-coding sequences. We know how they’re lost too. And you have no evidence for separate creation of these “kinds” you can’t even identify. Is the “kind” Mus musculus? All rodents? Glires? Mammals? You have no clue.
Are you claiming there was only one gene lost in each case?
If you could model fixation of these changes your claim might be more then vacuous.
You don’t have a clue how many new genes arise. Especially ones without historic sequence similarity. You also don’t have a detailed model how new genes arise from duplication and variation.
Yes. Each case is a single gene. That’s the raw data the diagram is counting. Many genes of course show the same pattern, but the gains and losses are independent of each other.
For a person who claims to know population genetics, you seem confused about what it models. Whatever are you talking about?
You are unfortunately the one without a clue. Known mechanisms are adequate to explain the data. Nor is it clear what you mean by “historic sequence similarity”. Now, what’s true is that if a gene originated from junk DNA sufficiently long ago, that DNA in related species will no longer be similar enough to detect homology. So?
The difference include many genes. How do you know the gains and losses are independent?
I am talking about the waiting time of fixation. This needs to be reconciled.
With all due respect I don’t think you understand the magnitude of the problem evolution faces here. Known mechanisms don’t even come close to explaining the data. The only reasonable explanation is a mind was involved in generating these sequences. Copying information is very different then generating it de novo.
Obviously I don’t know on the basis of that diagram. But it’s the way I bet based on what I know of evolution. I bet that if you put more species into that figure the gains and losses would be redistributed over all the new branches. Genes supposedly unique to humans would be seen as shared among apes, or monkeys, or primates, etc. Genes supposedly unique to chickens would be seen as shared among galliforms, galloanserans, neognaths, birds, archosaurs, etc. Different changes would be seen to happen at different times.
More word salad. Try again.
Please show your work. And notice that once again you confuse the origin of species with the origin of mutations.