Something from nothing, life from death, and progress through degradation are not part of ID. Somehow I don’t think that detracts from ID in the least.

To vainly attempt to get across to you, I point out to you that ID is concerned with the ‘build-up’ of information, not its degradation. Degradation is simply a class of processes that brings about important results biologically and elsehwere (microchips are ‘etched’, for example). But, as “Joseph” points out, we here at ID are interested in the progressive end of evolution. Microevolution is ceded by most, but macroevolution—which is progressive evolution—is what we refute.

You’re bringing an aracane argument to UD and trying to use it as a sledgehammer. It won’t work. You say cms is still being studied . . . . . but, of course, since it has agricultural applications and ‘Big Ag’ is interested. But there is simply no interest in Turf13. No one is studying it. The most recent review article—which I quoted at your blog—recycles old information indicating that the ‘jury is still out’ on whether turf13 works by ‘addition of function’ or ‘loss of function’. More likely, it is through ‘loss of function’. That appears to be the current state of things, and no one seems interested in finding out more. If turf13 represented a definite ‘addition of function’, and we had some sense as to how that happened, then that would be of interest here. Since neither of the above happen to be the case, I think I’ve probably said my last about it.

They cannot even provide a working/ testable hypothesis based on their proposed mechanisms of accumulating genetic accidents.

Art must be real proud of that…

“Progress through degradation” is a fact of life (in every sense of the phrase). That this fact confounds ID tenets is just another nail in the lid of ID’s coffin. That ID proponents choose to pretend that this process doesn’t exist and cannot possibly contribute anything adds more to the disconnect between ID and biological reality.

Dr Spetner covered that in 1997, Art.

IOW once again you display ignorance of your opponents and think that ignorance is meaningful discourse.

Also BEFORE you can start degrading to get progress you FIRST have to build to that point.

PaV, I rather suspect that you don’t have a clue here about the interesting molecular mechanisms (including degradation) that work to build up complexity in living things. Digging in your heels and responding with nervous laughter and rank incredulity is no way to “win” a discussion, let alone learn something.

Nor is this sort of speculation about how another commenter feels. Did you hear nervous laughter over the written words? Did you smell the incredulity to decide that it was rank? This is no way to comment here or you will not be commenting anymore. Yes, this is a warning.

“Progress through degradation” is a fact of life (in every sense of the phrase).

This is a very confused philosophical position. Degradation doesn’t progress unless you use the term “progress” to mean something like decomposition. But no one would say that decomposition is a progression of life, it is a digression. Degradation is a digression.

1. CMS is studied actively and with much earnest at the present. T-urf13 hasn’t been (very much) studied for years, mainly because its origins and modes of action have been worked out (your claims the contrary notwithstanding).

2. CMS is a naturally-occurring characteristic in plants, and plays roles in the evolution of different sexual reproductive strategies (in the wild as well as in breeding programs). A useful google term – gynoecious.

Now, I rather suspect that you will claim that two “genders” – hermaphrodites and females – is less than one gender, but this is but another way that antievolutionists fail math.

3. Characteristics in living things that are controlled by degradation (a very tiny fraction of the complete list, but …): circadian rhythms, brains, the cell cycle, flowering, sexual reproduction, asexual reproduction, mitosis, meiosis, etc., etc., etc.

“Progress through degradation” is a fact of life (in every sense of the phrase). That this fact confounds ID tenets is just another nail in the lid of ID’s coffin. That ID proponents choose to pretend that this process doesn’t exist and cannot possibly contribute anything adds more to the disconnect between ID and biological reality.

PaV, I rather suspect that you don’t have a clue here about the interesting molecular mechanisms (including degradation) that work to build up complexity in living things. Digging in your heels and responding with nervous laughter and rank incredulity is no way to “win” a discussion, let alone learn something.

That point notwithstanding, when it comes to the status and stature of ID, we’re really accomplishing a lot with this discussion.

Art, I suspect that cms has been studied because of its commercial applications. It has not been well-studied. It was studied mostly in the 90’s. Not much interest has been shown since. If you look at the following quotes, it is apparent that URF13 is problematic for plant cells—as well as insect, worm and E. coli cells. The final sentence below says: “This male sterility gene is T-maize anther-specific and its origin is a genetic enigma.” So, here we have a gene that produces a protein that causes cell death, basically, and whose origin is enigmatic—-and, of course, is non-nuclear and thus non-Mendelian.

The Mendelian equivalent to all of this seems to me to be balanced polymorphisms, such as sickle-cell anemia. Now, when you compare a sickle cell to a normal cell, would you say that it is better or worse? Functionally we know the answer is that its “fitness” is lower. In the case of cms, it would seem that in nature this kind of deformation which T-urf13 causes is very likely lethal, though there might be some unknown advantage. Nevertheless, it is only because commercial companies can provide a seed that is heterotic and nonetheless does not need crossing that the issue of cms of any importance whatsoever. However, now we’re dealing with artificial selection, and not natural selection.

But maybe you would like to provide more information—because there surely is not much out there, and it’s old, and, quite frankly, I’m not really interested in looking further. I suspect you work with commercial grain companies and hence your interest in T-urf13; but this places you in a very small circle of people.

Quotes taken from: Hybrid Cultivar Development by Surinder S. Banga Springer-Verlag 1998

”An interesting feature of male sterile T-cytoplasm maize plants is that their mitochondrial genome produces a 13-kDa polypeptide (URF-13) which is unique to this cytoplasm and absent in other maize cytoplasms . . . Unlike the larger open reading frame, which hybridizes to transcripts from all maize cytoplasm, the smaller open reading frame hybridizes to the transcripts available only in the T-cytoplasm and not to those of other sterile or fertile maize cytoplasm. Thus the T-urf13 sequence (115 codons) is unique to the mt genome of male sterile T-cytoplasm plants and is composed of sequences sharing homoloyg to the 3’-flanking (88 codons) and the coding region (18 codons) of the 26S r RNA gene, together with nine codons of unknown origin. . . .

In order to ascertain if the 13 kDa protein (designated URF13) encoded by the T-urf gene is involved in this specific sensitivity of T-mitochnodria to T-toxin, the T-urf13 gene was cloned and transferred to E. coli by Dewey et al. (1988). This gene expressed in E. coli cells and caused inhibition of whole cell respiration and growth, massive ion leakage, and spheroplast swelling. . . . Thus, the interaction of T-toxin and URF13 results in sensitivity by permeabilizing the membranes of the bacterial cells and T-mitochondria. . .

These authors demonstrated that the expression of the universal code equivalent to the T-urf13 gene in the yeast nucleus mimics its effects in maize, viz. respiratory growth of yeast is inhibited, respiration deficient cytoplasmic mutants . . . accumulated and NADH oxidation of the isolated mitochondria is coupled. . . These observations provide direct evidence that URF13 is responsible for the susceptibility of T-mitonchondrial genomes to fungal toxin, and male sterility is due to anther mt dysfunction caused by the T-urf13 gene. . .

. . . After adding T-toxin or methomyl to the in vitro cultured fall army worm cells, permeabilization of the plasma membrane occurs. Furthermore, the gene URF13 is toxic to these in vitro cultured insect cells even without T-toxin or methomyl addition. . . .

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. . . Because mutations in or deletions of the T-urf13 gene are associated with both the loss of male sterility and disease susceptibility, URF13 appear to be directly responsible for both these traits in T-cytoplasm maize. . .

This male sterility gene is T-maize anther-specific and its origin is a genetic enigma.

Arthur also said:

And I’m impressed (in a sort of way) that you think digits are regressive compared with webbing. Would you like to look at a longer list of biological characters that are controlled by degradation? Are you seriously going to argue that this mechanism is always one that subtracts from an organism?

When I was seventeen, I ended up with a thyro-glossal duct cyst, which had to be operated on twice. The reason for this was that the cyst came about because the thyro-glossal duct did NOT degenerate in utero. So I’m all in favor of ‘nature’ degenerating things. But you are trying to place the same importance on the degeneration of the thyro-glossal duct as anyone would put on the formation of the thyroid, for which the thyro-glossal duct temporarily exists.

I just love Darwinists. How does natural selection work? Through species becoming more fit. How do species become more fit? Through natural selection. How does life come about? Through natural selection. How does natural selection work? Through selective death. Thus, life through death. Or progress through degradation. Is there any objectivity out there in Darwinland anywhere?

I would love to get my hands on a nice æ, but the radical Alphabetists have suppressed the evidence of the superiority of Olde English.

It was evolution by natural selection…

Perhaps you should go buy a vowel…

I would love to get my hands on a nice æ, but the radical Alphabetists have suppressed the evidence of the superiority of Olde English.

Perhaps you should go buy a vowel…

DNA Sequencer too expensive to add to your basement laboratory?