My father didn’t retire from Scott. But that’s where I was born, in 1954. I think my parents lived there for a couple of years – they moved to Dow AFB in early 1955.

Did your father’s service reach back far enough to include the mid 40s? My father was in the Air Force 1950 to 54.

Oh, BTW, did he retire at Scott AFB?

You asked:

It seems to me that this is key to your criticism of Skell. So can you tell us what experimentation and insight, that would not also be motivated by other theories, led to the discovery of relatedness? We sometimes forget that evolutionists do not have a monopoly on research into genetic similarities between organisms.

I’m afraid that I don’t understand your question.

If perchance you are trying to say that ideas other than deep common ancestry might conceivably had led to the discovery I describe in my essay, I guess the only thing I can do is point out that such hypotheticals are but armchair musings. The fact of the matter is that ’twas Darwinian ideas, through and through, that actually led to these remarkable discoveries. This fact suffices to make my point (which was to refute Skell’s claims).

Since when is design predicated only on function and utility?

What else is there?

As aside (that I’ll admit, was a motivation for continuing this discussion) – you said on UD that you will be asking Meyer about this essay. If you don’t mind, bring his comments over to this blog. Clive Hayden waits until my comments will not appear on the current comments tab on UD, which sometimes can take a day or more. And that is if he allows my comments to fly. If you want me to participate in a discussion about Meyer’s reactions, it’s best done here.

the evolutionary relatedness

Or in less question-begging terms: the relatedness

of the apicoplast and chloroplast is not something that jumps out at you. You don’t look at a micrograph of a malaria parasite and say “wow! a chloroplast”. It took some very clever insight and good experimentation to discover this fascinating tidbit.

It seems to me that this is key to your criticism of Skell. So can you tell us what experimentation and insight, that would not also be motivated by other theories, led to the discovery of relatedness? We sometimes forget that evolutionists do not have a monopoly on research into genetic similarities between organisms.

In my opinion, a design-based approach misses this completely…because design is predicated on function and utility, and the parasite has nothing that approximates the function of a chloroplast.

Since when is design predicated only on function and utility? And again, by contrast, what was Kohler et al’s approach based on that helped their discovery, and which was unique to an evolutionary approach? Common descent doesn’t count unless it contributes something distinct from general relatedness or similarity between organisms or structures.

On the other hand, the discovery depended directly on shared characteristics, and only secondarily on assumed evolutionary history. Similar discoveries have been made under creationist assumptions as well, which also lead to a theory of common characteristics, due to common design (in the case of Linnaeus’ Systema Natura, due to a divine order).

So research motivated by assumptions of common descent (e.g. under evo theory) can lead to discoveries of common structures and functions, which in turn can lead to significant medical advances. And ID proponents would do well to bear this in mind. But evo theory and even common descent are not necessary for those discoveries, as competing hypotheses can and have also led to discoveries of common structures and functions, which in turn can lead to significant medical advances. If Kohler, Delwiche et al. had been performing their phylogenetic analysis under e.g. Linnean (non-evolutionary) assumptions, how would their research have been any less directed or robust?
I don’t see any evidence from the above that evolutionary assumptions helped them. The key to the discovery was finding a relatedness between two biological structures in different organisms — an area of investigation that began centuries before Darwin and does not depend on common descent or natural selection.

Start with Linnaeus’ taxonomic system, which was based on creationist assumptions and motivations. The article on which this essay is based relies on the system Linnaeus founded. Event the abstract uses it four times: “phylum Apicomplexa”, “Toxoplasma gondii”, etc.

So I’m disappointed to see this essay begin by adopting unnecessarily loaded words like ‘regurgitate’. My estimation of Hunt’s willingness to fairly consider ID arguments has gone down.

As an “ultimate success story” I do think you make a credible case for rRNA. At least I’ll be giving RNA more attention downstream.

So far as ribosomal commitment differences between prokaryotes and eukaryotes, there are the obvious competing interests of managing additional infrastructure (nuclear machinery) that could tip the scales. But this is a very macro scale issue. My own selfish interest goes to changes that occur within smaller groups of more closely related organisms – say within a family like the grasses or legumes. There are plenty of adaptations that higher plants are into (and doing quite well with), and it seems these adaptations play off of RNA regulatory mechanisms in concert with DNA. Epistasis fascinates me, and while one can model some epistatic effects without consideration of RNA, I wonder whether that view is not just too simplistic. The road from genotype to phenotype goes through the forest of RNA. We should not miss the forest for the trees.

Thanks for the comment (and apologies for the slow response). Your questions are intriguing. I wish I could come up with a clever retort to your statement about rubisco. I guess maybe if rubisco were really so clever, it would have seen what its original activity would have led to (high atmospheric oxygen) and figured out ahead of time a mechanism that would not be so poisoned by oxygen.

As for the question “why so much RNA?” – I guess one place I think I am going is the idea that rRNA is the end-all of life. If we think of success in nature in terms of reproductive success, then rRNA is the ultimate success story. It’s not so much that life needs so much rRNA, but rather that rRNA has taken over (and did, many eons ago) life processes to its own ends.

Do eukaryotes devote fewer resources to the ribosome than prokaryotes? I don’t know. Perhaps so, but I suspect that the difference, if it exists, is not much more than a factor of 2 or 3 (at least in terms of overall demand son the cell).

In a 2007 ‘minireview’, (http://www3.interscience.wiley.com/cgi-bin/fulltext/118546650/PDFSTART) John Hyde writes:

The key gene, named pfcrt for ‘chloroquine resistance
transporter’, resides on chromosome 7, encodes a
49 kDa protein with 10 predicted transmembrane
domains, and exhibits mutations that showed complete
linkage to the chloroquine-resistance phenotype in the
40 laboratory-adapted strains of P. falciparum originally
examined [9]. The polymorphism in this gene
documented to date is considerable, indicative of several
independent origins of drug-resistant alleles. It
encompasses at least 16 single, nonsynonymous nucleotide
substitutions in parasites from field samples, but
only one amino acid change, K76T, located in the first
transmembrane domain, is found consistently in chloroquine-
resistant parasites, although never on its own
[6,10]. At least three other changes (and usually several
more) are always seen in combination with K76T,
relative to the canonical wild-type sequence, possibly
compensating for unfavourable changes in the normal
function of the chloroquine resistance transporter
(CRT) protein induced by K76T and ⁄ or as a response
to pressure from antimalarial drugs other than chloroquine
that also pass through this transporter.

If PfCRT is named after its resistance to chloroquine, and, if the “key” a.a. change is at one site, why are you going on about PfMDR1? Hyde, in the same article, also tells us that MDR stands for “multi drug resistance”, which means that though it might develop resistance to CQ, it also develops resistance to other drugs and, hence its resistance cannot be considered CQ specific.

As to T-URF13, here’s some quotes from an article:

“The plethora of evidence that mitochondrial activity plays an important role in plant reproduction provides strong support for the loss-of-function hypothesis for the mechanism of CMS. The facility with which pollen production is impaired by disturbance to mitochondrial metabolism seems to render the search for other types of mechanism superfluous.” . . .

“Alternatively, one possible loss-of-function hypothesis is that the efficiency of mitochondrial activity is decreased by T-URF13, resulting in an incapacity of the plants to reach a threshold of ATP production required for pollen development (Levings, 1993). . . .

“Despite the general use of the term cytoplasmic male sterility to designate the phenomenon, neither population geneticists nor breeders have ever underestimated the role of the nuclear genotype in the phenotypic expression of CMS. Population geneticists have been confronted with the presence of restorers in the populations studied, often complicating the analysis of CMS systems in natural populations (Charlesworth and Laporte, 1998; van Damme et al., 2004). . . .
. . . In a male sterility-inducing cytoplasm, fertility may be restored by a nuclear gene in two ways. Firstly, the nuclear gene may inhibit production of the sterility protein throughout the plant, or specifically in floral organs or tissues.
This situation is the most frequently reported, generally with a post-transcriptional effect on the male sterility gene mRNA. . . . In recent studies, attempts to identify the male sterility determinant have often been based on the assumption that the restorer genotype affect the amount, or size, of the mRNA produced from the CMS gene . . . Alternatively, the restorer gene may restore fertility by counteracting the physiological effect of the sterility gene product. This is assumed to be the case for the Rf2 of maize Texas CMS. This restorer gene was the first to be identified and encodes a mitochondrial aldehyde dehydrogenase (Cui et al., 1996; Liu et al., 2001; Moller 2001). ‘Physiological restorers’also include genes introduced into the nuclear genomes of male sterile plants to compensate for ‘loss-of-function’ mutations.”

Isn’t it clear that T-URF13 very likely involves a “loss-of-fucntion” scenario, and, hence, shouldn’t be viewed as an evolutionary “development”?

I make a living breeding soybean. So maybe I’m a plant scientist. As such I do consider rubisco a fairly significant protein. And so long as we’re turning some conventional ideas upside down, consider that if rubisco were a cleverer and more ambitious enzyme we might not need so much of it. So if expediency (effectiveness, efficiency – pick your favorite) is to count for something, the RNAs and rubiscos of the cellular world come out at the short end rather than at the top. Sure, you can’t get along without RNA as you can manage without rubisco, but still – why so awful much? It would seem that in the name of conserving energy the cellular machinery would be well served to find either alternate ways to do what RNAs do – or at least make the RNA machinery more efficient. Has anyone looked at the cellular RNA budgets across evolutionary time to see whether RNAs take up fewer resources now than in more primitive cell types?

Have to run, but want to return to this line of thinking… a retro notion if you will.