But the problem is that the actual research did not say "Evolution is random", or even "Evolution is stochastic." They were looking specifically at developmental systems drift. There has been a debate going on within the biological community about how traits change. Specifically, the role of "genetic drift".
"Genetic drift" refers to evolution (i.e. genotype and phenotype changes in a population) in the absence of selection pressure.
Yes, this is what I said. The evidence I see which you for some reason do not is in the significance of random and determined in the end product. The organisms which evolve are not random. The genetic mutations which are a small piece of the process are not the process. While I understand the argument you are making about the definition of random, you are not understanding the argument I (and many others) am making about the significance of the randomness to the process.
Look at a hypothetical example. Suppose you have a bucket of 10 balls and 10 blocks, all different colors. One child pulls out 5 balls and another child pulls out 5 the blocks. The colors are random but the objects are not. So is that a random process? Big deal, they randomly selected the objects and technically they got random colored objects. Who cares? They determined which objects they wanted, that was not random. So you are arguing there is a random component therefore it is a random process. You want to clarify that into, it depends on what you are looking at. Up to there, we agree.
But here's the problem. You and in this case, mijo, continue to use numbers or mutations in your mental models as if all the qualities we are talking about here are equal. Both of you ignored my example of random time but determined selection criteria. The point is, it is not a matter of what you are looking at whether it is a random process or not. It is a matter of which of the processes best represents the whole. You claim it is ideology. It is not ideology, it is a description of the whole over a description of a single part.
Biologists noted change in species over time, with no obvious advantage for the species as a result of that change. Why did that happen? Some people said that these changes occurred because there was some unrecognized selection pressure. Without that pressure, there would be a conservative force that would keep the population stable. Others reasoned that with no selection pressure, there might be random changes in the population to a trait that was no better, but no worse, than the previous state.
The biologists from the OP figured out a way to test the two theories. These nematodes gave them a way to track the changes. If the changes in the population were random, not the result of selection, the traits involved would go sometimes this way and sometimes that way, and sometimes reverse direction, because there was no real advantage for one direction or the other. If the changes provided an advantage, the direction of change would be consistent, as things got a little bit better at each step.
It turns out that most, but not all, of those changes went in a single direction. Developmental systems drift occurs primarily as a result of selection pressure.
Did you then not look at the additional citations I posted showing one determined and random trait evolving in the cave fish? There was no selection pressure on one component of the no longer needed eye. Since it was no longer being actively selected, it disappeared purely by passive random genetic drift. On the other hand, the retina which was biologically expensive to the fish, disappeared through active selection.
The point of that study and of the debate you speak of (which is exactly what I have been posting about) is that genetic drift is not the main process of change the research is revealing.
So does that mean that "evolution is not random?" Well, again, you have to define your terms. In their case, they defined random as not favoring one direction or the other for development of a particular trait. They defined evolution as changes to a trait. Using those terms, "evolution" is not "random". (And actually, they never used the word random, and they never claimed to define evolution. They said stochastic, and they specified evolution of a trait.)
I'm not sure that this is a real paradigm shift at all. I think it's a return to a paradigm that is as old as Darwin. It did challenge a potential new paradigm that said there were other forces besides natural selection that were responsible for changing species' characteristics. This paper says that "genetic drift" is not a significant role.
(Aside: We speak of "natural selection" as a "force" or say it "drives" evolution. We can't help ourselves. We have to talk about causes, and things that do things, but it is an illusion. Natural selection isn't a force, it's a consequence.)
And here is where the paradigm shift is occurring. Because when the mechanisms of natural selection are more and more revealed, it turns out there actually are active forces involved.
More accurately, I think the two should be given different weight depending on what you are describing. Either can lead to misunderstanding of the process. I think insistence on saying that one or the other is "better" either means you are fixated on one aspect, or there's some sort of psychological or ideological bias against the other.
Better is the adjective I am applying to description of evolution. You need the context. I am not fixated on one aspect and neither is Dawkins. Rather the evidence leans heavily in this direction.
Just look at the mechanisms by which microorganisms acquire anti-infective resistance. Whole genes providing anti-infective resistance are spread out among organisms and across species. This is not a matter of sharing genetic soup with random acquisitions. It is an active process of acquiring adaptation. Look at these papers.
High-frequency conjugative transfer of antibiotic resistance genes to Yersinia pestis in the flea midgut
Multidrug Resistance in Yersinia pestis Mediated by a Transferable Plasmid
Streptomycin, chloramphenicol, and tetracycline are used to treat plague, and tetracycline and sulfonamides are recommended for prophylaxis.4 Classically, Y. pestis isolates are uniformly susceptible to the antibiotics active against gram-negative bacteria.5,6,7
We report high-level resistance to multiple antibiotics, including all the drugs recommended for plague prophylaxis and therapy, in a clinical isolate of Y. pestis. The resistance genes were carried by a plasmid that could conjugate to other Y. pestis isolates. This report should serve as a warning of the risk of the spread of resistance in Y. pestis, a species previously considered universally susceptible to antibiotics
That is not random mutation!
CRISPR elements in Yersinia pestis acquire new repeats by preferential uptake of bacteriophage DNA, and provide additional tools for evolutionary studies
We have found in the published sequence data additional evidence for a mechanism by which CRISPRs could acquire phage DNA. Hoe et al. (1999)Down described spacer sequences and organization in a CRISPR of Streptococcus pyogenes. Only one of the five sequenced S. pyogenes genomes, MIGAS, possesses a CRISPR. We performed a BLAST search with the S. pyogenes spacer sequences against the five sequenced genomes and found that seven out of the nine spacers described correspond to a phage-associated sequence, present in at least one of the genomes except that of MIGAS. Phage DNA constitutes up to 12·4 % of the S. pyogenes genome (Beres et al., 2002Down) and is involved in recombination and horizontal transfer of new genes. There may be, in the case of strain MIGAS, a relationship between the presence of a CRISPR and the lack of a particular prophage. One possible explanation for that finding could be that CRISPRs are structures able to take up pieces of foreign DNA as part of a defence mechanism. In this view, it is tempting to further speculate that CRISPRs may represent a memory of past ‘genetic aggressions’. The fact that most of the spacers described in other bacteria have no homologue in the databases could still be explained by such a phage origin, as only a very small number of the existing bacteriophages have so far been sequenced.
The way in which the CRISPR loci appear to evolve in Y. pestis, and the frequency at which they acquire new motifs, at least within the Orientalis group of strains, are such that these loci may provide powerful and easy-to-use phylogenetic tools in complement to MLVA. It may be that the picking up of new spacers is not occurring at a uniform rate across the Y. pestis species, but rather that some unknown conditions are able to trigger an increased activity.
Random processes take on a smaller and smaller role.
That's the core "meme" he needs to protect. He thinks he's clearer than the article writers, you see... and Dawkins. I don't know where he picked up this imagined expertise, but all of those of that ilk seem to have it.