Information's role in evolution.Should we put it more in the picture?

Quite the opposite. The question is how do you define information as it relates to evolution, how do you measure it, and how do you model it. It is not a matter of excluding the idea of information. Rather, it is a question of how one models information in the process of evolution.The problem I think you are having is our disagreement with creationists as to how information is measured in these systems. For example, no creationist has been able to measure complex specified complexity (CSI) in any meaningful manner. I can find the thread later if you are interested, but there was a discussion at Uncommon Descent not too long ago where someone asked the creationists how they would calculate CSI for some very simple evolutionary examples. No one was able to do it, nor could they figure out how it could be done.On the flip side, one can derive information from genomic sequences by applying the theory of evolution. A perfect example of this is the SIFTER algorithm. SIFTER applies the theory of evolution to predict protein function, the functional information of a given sequence. From the paper:

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SIFTER builds upon phylogenomics by employing statistical inference algorithms to propagate available function annotations within a phylogeny, instead of relying on manual inference, as fully described in Materials and Methods. Statistical inference requires a probabilistic model of how the character states (in this case, molecular function) evolve; to this end, we constructed a model of molecular function evolution to infer function in a reconciled phylogeny. Our model takes into account evidence of varying quality and computes a posterior probability for every possible molecular function (from the set of GO molecular function terms) for each protein in the phylogeny, including ancestor proteins. In our model, each molecular function may evolve from any other function, and a protein's function may evolve more rapidly after duplication events than after speciation events.

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The result is an algorithm that can predict protein function with 96% accuracy, even with very little phylogenetic information to work from.So how do creationists apply ID theory to predict protein function?

Your link appears to be broken. Nonetheless, could you explain here how your theory can be used to analyze sequence data? Could you compare two homologous sequences from two species and show us how your theory can be used to measure the information in each sequence caused by neurogenic interactions?

Then please do. Please cite mechanisms by which specific stimuli result in specific mutations, and only those mutations.From everything I have read, mutations that occur in bacteria are random with respect to fitness. For example, mutations which confer antibiotic and phage resistance occur in the absence of either antibiotics or phage. This is the findings made by Luria and Delbruck as well as the Lederbergs (google "fluctuation experiment mutations" and "plate replica experiment" for more info). It's not as if bacteria sense antibiotics in the environment and then make specific mutations in specific genes to counteract the bactericidal activity of antibiotics. Mutations occur throughout the genome, most of which do not confer resistance to antibiotics.

So how does your theory explain detrimental mutations, such as those that cause horrifically painful diseases in young children that then lead to their early death? Epigenetics does not change the genomic sequence, and the mutations that Shapiro et al. speak of are random with respect to fitness. If you think I am wrong, then please cite a paper that demonstrates that mutations are not random with respect to fitness.

But it is not a type of genomic information, which is what we are talking about. How does that observation change the genomic sequence in sperm and ova?

They do change from generation to generation. They change through mutations, but not through epigenetics. Also, HGT is mutation. It is the insertion of foreign DNA into the host genome. These events, just like other mutations, can be beneficial, neutral, or detrimental. The insertion of retroviruses into the human genome are a perfect example. By last count, we have nearly 200,000 of these insertions (most being solo LTR's). Some of them do have beneficial function, but the vast majority are acquiring mutations at a rate consistent with neutral drift (i.e. they are neutral). Only heritable information can drive evolution. That is why random mutations with respect to fitness are important to the process of evolution and why your ramblings are not.Also, the directed nature of protein-protein interactions are a product of their DNA sequence. Change the DNA sequence and you can change how information is handled in the cell. Therefore, the only way to change how a cell processes information is by changing the DNA sequence. This is why random mutations are important to the process of evolution, because they are inheritable.

No, it can't. Epigenetics does not change the DNA sequence. The reasons that chimps and humans are different is because our DNA sequence is different, not because our DNA methylation patterns are different. HGT is random with respect to fitness as exemplified by ERV's found in the human genome. So what are the falsifications? Where it concerns evolution, information is transferred through natural selection. This is the process by which random mutations are filtered through environmental information.

So show us how these engineering systems guide mutations so that they only produce specific beneficial mutations in a given environment, and only those mutations.

Then demonstrate, WITH DATA, what the other way is.

Epigenesis DOES NOT CHANGE THE DNA SEQUENCE. Chimps and humans are different because our DNA sequences are different. Therefore, your theory is meaningless for explaining the differences between species. IOW, your theory is useless as it relates to evolution.

Question to zi ko:With the right empathic input, could a human give birth to a zebra?

Yes, multiple generations as in 3-5 generations, at most. That is not permanent. Epigenetics deals with DNA methylation and histone packaging, not with DNA sequence. They can also pave the way to new combinations that are neutral and detrimental with respect to fitness, otherwise known as random mutations. A change in gene expression is not the same as DNA mutation.

Not until you demonstrate a mechanism by which emotions in the brain can cause specific mutations in sperm and ova. Where is that mechanism?

DNA mutation is NOT epigenetics. The organism does not choose to only produce beneficial mutations. You are making stuff up. And where is the data to back up this claim?

That mechanism has already been established. The flow of information in evolution moves from the environment to the population's genome through natural selection. It has nothing to do with empathy.Edited by Taq, : No reason given.