There was a time when people believed the moon craters were the product of intelligent design because they were so perfectly round “they must have been made by intelligent creatures living on the moon”. That idea was falsified. If hypothetically someone had said back then, “The Flying Spaghetti Monster (FSM) made the moon craters”, the claim would have been falsifiable, but it really doesn’t make a positive case for the FSM, doesn’t make the FSM directly testable, doesn’t make the FSM science. Substitute the word “ID” instead for “FSM”, and one will see why I think even though ID is falsifiable, I don’t think ID has a positive case, and I don’t think ID is directly testable, and I don’t think ID is science at least for things like biology.
I accept stonehenge was intelligently designed because I’ve seen humans make similar artifacts. The case of design in life is a different matter because we have not seen a designer of such qualifications directly. If we saw God or some UFO sending flames down from the sky with a great voice and turning a rock into a living human, then I would consider ID a positive case at that point. For now there is no positive case, but a case based on some level of belief. One might redefine science to allow ID to be defined as science, but I prefer not to promote ID as science. I’m OK with calling ID science for man-made things, but not for God-made things, unless God shows up and gives us a visual demonstration.
NOTES:
Johannes Kepler
The invention of the telescope led scientists to ponder alien civilization. In the early 1600s, astronomer Johannes Kepler believed that because the moon’s craters were perfectly round, they must have been made by intelligent creatures.
Is Anybody Out There?
Sure I made an attempt. The underlying cause in my view is God did it through an act of miraculous special creation which has common designs but also TRFs that prevent a Universal Common Ancestry interpretation despite some similarities.
A falsifiable prediction is that attempts at phylogenies will keep having TRFs that sort of just poof out of nowhere no matter how one constructs the phylogeny.
As far as maximum likelihood, what is the likelihood a bacteria’s descendants will retain the basic features of a prokaryote N generations from now, where N is a large number? Close to 100%, for all practical purposes, 100%.
So why do you believe in Macro Evolution? You must be counting on an unlikely even or set of events that are waaay far from 100% certainty, maybe close to zero. At some point invoking exceptional, low probability events becomes indistinguishable from invoking miracles.
Perhaps, “we don’t know” is the most fair answer.
I’d don’t for sure, but I believe, and I’m not ashamed to say I believe, that is not a scientific belief, that is a faith statement.
As far as hypothesizing that macro-evolution came about via Darwinian selection vs. any other naturalistic or supernaturalistic scenario, I point out my response to the Wind Turbine Evolution:
We see and expect in the lab and field a prokaryote is going to stay a prokaryote. That’s why I don’t believe in prokaryote/eukaryote macro evolution.
The other macro steps, I’m not familiar with, but if one hypothesizes one POOF, one can hypothesize more. 🙂
I just don’t find evolutionary theory more believable than “God did it.” The monarch butterfly strikes me as the product of a mind beyond human imagination.
Where will you be publishing this?
What about eye-worms?
Personally, if I had to choose between a world populated only by humans, and a world that includes such wonders as eye worms, I’d go with the worms. 🙂
I’ll stop you right there. I have several problems with this.
1. The magnitude, or whatever else it is, needed for a TRF is unclear. Of the features mentioned, we have quite a good idea of where mitochondria, chloroplasts, multicellularity, and tissues come from. And of course the last three aren’t even features of eukaryotes but of various clades within them. I don’t personally know much about the other mentioned features, but I have no reason to suppose that poofing would be required. Who says that only minor differences can be due to evolution?
2. The number and size of what you think are “kinds” is likewise unclear. “Macroevolutionary phylogenies covers a lot of ground, from individual genera to all life. That makes discussion very difficult. Are, to pick an example not at random, all birds one kind? How would we tell?
3. The existence of features that couldn’t evolve through known, or even natural, processes has nothing to do with whether there are phylogenies. Behe, for example, agrees with universal common descent.
Why should TRFs be organized hierarchically? There seems no reason to suppose such a thing other than common descent.
Hard to say how to account for a TRF unless you mention some. Of the ones you imply by quoting Wikipedia, some have clear evolutionary explanations. And as I said before, even if poofs are needed, that doesn’t change the inference of phylogenetic relationships.
Your personal incredulity and Michael Lynch’s interest in neutral evolution are not arguments in favor of poofing. Citing other people’s opinions are not arguments either.
What sort of orchard model do you propose? We need to get specific about how many kinds there are. Being a chordate myself, I would be most interested in your ideas of how many separate trees there are within chordates. Your Orchard model has in fact been tested at the domain level; I presume you are familiar with Theobald’s paper in Nature on the subject.
I would like to see Sal put his awesome math fu to work building a creationist orchard model that fits the data.
And continues to fit as more genomes are sequenced.
Don’t need whole genomes, just characters, genetic or otherwise.
But how often would you expect such tranformations to occur? It would be an exceptional event or set of events.
I respect your data points are different than mine, but the spliceosomes and sliceosomal introns and histones are not minor things.
https://en.wikipedia.org/wiki/Spliceosome
http://theskepticalzone.com/wp/wp-content/uploads/2016/01/Spliceosome_ball_cycle_new2.jpg
When we make transgenic E. Coli with human DNA we have to strip out the sliceosomal introns and histones they wrap around. The prokaryotic and Eukarytoic machines are different.
Sure one can say a eukaryote evolved slowly from a prokaryote and we shouldn’t compare how they work today. OK, but the problem is still one of a mechanically feasible trajectory of evolution from prokaryote-like to eukaryte-like.
One could probably throw some human DNA for spliceosome parts into an E. coli (after stripping out the splicesomal introns!), and get the E. coli to express the some of the spliceosomal parts.
But why should we expect this new strain of E. coli to start evolving spliceosomal introns? Conversely we could throw DNAs with spliceosomal introns into E. Coli, and it likely will jam the reading frames, maybe kill or otherwise compromise the E. Coli. It seems both features must be in place simultaneously for the system to make functional sense.
Given that the papers linked earlier have shown the natural tendency is toward genome size reduction in microbes, why should a prokaryote-like ancestor expand it’s genome size for no good reason with spliceosomal introns (which would jam the reading frames no less) and then evolve spliceosomes to cope with this intrusion of so many spliceosomal introns?
The question of reductive evolution (which I raised several times and provided several papers) is relevant to the question of how likely a prokaryotic-like system will become a eukaryotic-like system.
If reductive evolution is the dominant mode of evolution (as Koonin asserts), then some poof (Koonin uses the word spurt IIRC), or some mode of evolution not consistent with modes of evolution we see in operation today must have been at work in the past.
Does anyone say that?
stcordova,
I don’t know squat about spliceosomes or spliceosomal evolution. Best talk about the other parts of my response.
Don’t feel bad, neither does any evolutionist on planet Earth! 🙂
We can grant them for the sake of argument, but then what about the TRFs like the one sjust mentioned?
That’s exactly my point. You can build a phylogeny with some features, but then we have others that sort of poof into existence with no plausible ancestor. The Splicesomes and splicesomal introns, the histones, Kozak instead of Shine Dalgarno sequences, different origin recogition complexes (ORCs).
The laundry list of just the Prokaryote/Eukaryote gaps are listed by a Ivy-League PhD cellular Biologist associate professor at Missouri, Change Tan:
https://assets.answersingenesis.org/doc/articles/pdf-versions/arj/v8/bacteria_eukarya_eukaryogenesis.pdf
and
https://cdn-assets.answersingenesis.org/doc/articles/pdf-versions/arj/v8/archaea_eukaraya_homologs_eukaryogenesis.pdf
I crawled through these papers and I realized they identified lots of TRFs.
And some eukaryotic genes have no homologs in E. Coli, not the least of which are the spliceosomal intron parts of Eukaryotic genes!
A mouse has 2000 more genes than E. Coli period! That’s lots of TRF barriers to breach if few of those are homologous.
and
I find some these TRFs really problematic for macro evolution (Eukaryogenesis).
This means you know the actual history in pathetic detail.
That, or you are pulling it out of your ass.
Looking back over the last 200 years, how’s that god of the gaps theme working out?
Heh. Remind us all how old that planet earth is?
Now you’re just descending to the sound bite level. It took me 30 seconds with google to find this:
http://www.ncbi.nlm.nih.gov/pubmed/25626174
I’m going to stop you right there again. Why the creationist trope of puffing up the qualifications of someone you use to support your claims? “Ivey-League PhD”? Seriously? It doesn’t make a naked opinion look more convincing. Now, you claim to accept everything I said for the sake of argument, but then you completely ignore it. I’m not even sure you read me past the first paragraph. None of this has anything to do with phylogeny; we don’t have to know how a feature arose to see that it arose on a tree of descent. And what about common descent within chordates?
Sal –
What’s the catalytic core of the spliceosome made of, what is it similar to, and where else do we find it? Extra credit – how does this tie into the origin of mitochondria?
stcordova,
Unless fossilisation captures the record in exquisite detail, there must be a rate of evolution too fast to be captured by fossilisation, but still within reach of ‘normal’ mechanism. That’s pretty much punctuated equilibrium too. The moment you notice a TRF, it has ‘suddenly’ appeared. Inevitably, a fossil record must show apparent leaps even in an underlying continuum.
Yes and it says:
But there is good evidence, normal is reductive, starting with Behe’s paper on loss of function in lab evolution which even Coyne had to respect as generally accurate. And then beyond that Lenski (with endosymbionts) and Koonin (and non endosymbionts) and the Sixth great extinction, etc.
It may well be “normal” is reductive as far as today. A fair statement is that evolution would have to work other than the way we actually see it in operation today with out own eyes.
stcordova,
It wouldn’t. I don’t see any reason to suppose that prokaryotes evolved big genomes prior to endosymbiosis.
The Last Eukaryote Common Ancestor had mitochondria, sex, a cytoskeleton, linear chromosomes, multiple origins of replication. These cause numerous changes to the mode of life which relax the selection on genome size and introduce modes of element transmission absent from prokaryotes. The LECA may or may not have had introns, but a eukaryote finds extra genetic material much more affordable than a prokaryote, and there are additional dynamics resulting from the 3 genomes in a diploid.
Koonin again
stcordova,
As I’ve already said, I don’t think accelerated mutagenesis is a realistic model of natural evolution. You can’t simulate a steady drip by turning on a hose. You can’t make pitch flow faster by hitting it with a hammer.
stcordova,
Endosymbionts are irrelevant!
He claims bimodal change. I’m actually dubious anyway, but it is still not net reduction.
That is irrelevant to historic evolution. Of course, no-one disputes the other 5 (or the many smaller ones). The geologic column is subdivided by them. But there is no evidence of a genetic component to mass extinction – that they all got genetically unlucky at once, then some few managed to get their act together. Anyway, I thought YECs tended to go for just one mass extinction, with no genetic component at all?
I had imagined you were better than that.
Prp8 with an RNase H1 domain found in some mitochondria.
I never said there was, and I’ve already corrected that mischaracterization of my position, earlier, and this is at least the second time.
Genetic deterioration isn’t the major cause of mass extinction, but mass extinction is a component of genetic extinction — 100% functional loss. Selection doesn’t arrest that, in fact it helps speed the elimination.
Genetic deterioration isn’t the major cause of mass extinction, but mass extinction is a component of genetic extinction — 100% functional loss. Selection doesn’t arrest that, in fact it helps speed the elimination. Said it again, 2nd time at least.
Genetic deterioration isn’t the major cause of mass extinction, but mass extinction is a component of genetic extinction — 100% functional loss. Selection doesn’t arrest that, in fact it helps speed the elimination. Said it again, 3rd time at least.
Just making sure that the following argument isn’t attributed to me since I never made or at least never intended to make it:
“Elimination of Species by means of Natural selection or the preservation of favored races in the struggle for existence” the book Darwin should have written.
Net loss of function is the direction of evolution in the present day. Extinction by natural selection of the extinct species is net loss of function for that species line. It shows Gould to be wrong about life never getting simpler, it can die, it can’t get simpler than being dead, that’s the real wall (floor). Ergo, there is no inherent guarantee for more functionality evolving naturally.
If wrote a program ANNIHILATOR instead of WEASEL, it would allow for this mode of evolution whereby functional species become functionless. Then ANNIHILATOR would allow for reductive evolution on top of that. Then ANNIHILATOR would allow for accumulation of mutations way past genetic load limits (ala Muller) on top of that.
Which is closer to what is observed today in the real world? ANNIHILATOR or WEASEL?
It’s worth a more careful methodical look than the dismissals I’m seeing in this discussion. I’ve provided some starting points both theoretical and empirical.
Some of you all may not like the possibility of the ANNIHILATOR model being real. I can’t say I’m thrilled either. I’d be glad on some level to be wrong, but I think it is correct.
It is a worthy empirical question.
It’s already been answered, Sal. You don’t like the answer, but the world goes on.
OK Sal, let’s do that.
Before about 52 MYA there are zero bats in the fossil record.
Around 52 MYA we see the appearance of the first primitive bats like Onychonycteris
Later than 52 MYA up to today we have fully flight capable bats.
Where did the function of flight in the bats come from Sal? Did the bats lose the ability to not fly?
The earth is old, life is young. Do keep up.
How old is the Earth and how young is life Mung? How do you know?
Since I mentioned the spliceosome, I have to point out how glibly the phylogenetic narratives are so vehemently asserted when we even barely know the components and structure and function of spliceosomes.
It seems awfully hasty to be asserting evolutionary explanations for systems that aren’t even characterized!
We know a few things each year. Here is a 2003 essay:
http://onlinelibrary.wiley.com/doi/10.1002/bies.10394/pdf
HT Jonathan McLatchie
How many new species emerging each year? Here is what one evolutionary biologist said:
Faith in evolution, not actual facts.
Ok lets look at endangered plant species:
http://www.plants.usda.gov/java/threat
Lots eh?
How about documented modern extinctions:
https://en.wikipedia.org/wiki/List_of_extinct_plants#Modern_extinctions
and this:
http://www.theguardian.com/environment/2010/sep/29/plant-species-face-extinction
Looks like ANNIHILATOR is a better model than WEASEL.
Here Sal, since you seem to be having trouble with your facts.
Examples of incipient speciation
Still waiting for you to explain how extant bats lost the ability to not fly.
stcordova,
Reasonable inference, though. If you look at taxonomically distinct but only recently diverged species, you can measure the ratio of of divergence to commonality – the expected difference between a random member of each population vs any two from the subpopulations. That ratio is either on an upward, downward, or level trajectory, even if there is interbreeding at contact zones. If gene flow is diminishing or stopped, it is hard to see how divergence can be on anything but an upward curve. Especially since the more divergence there is, the more gene flow is pinched. For the statement to be universally false, separated populations must never diverge, which would violate known genetics. People place a certain amount of faith in the findings of genetics, I guess.
stcordova,
OK Sal, keep your hair on! You’re not the only one who gets misrepresented you know! 😉
Essentially, all the ‘sorting’ processes of evolution involve extinction at some level, and hence loss of variation. Fixation of an allele in a population is extinction of the rival. At a higher level, species competing equally for a resource will still result in the extinction of one or other – this is genetic drift at the species level. Or, there could be better use by one than the other. This, I guess, would be Natural Selection at the species level.
An asteroid will result in stochastic losses of species.
Yes, all these processes lead to loss of variation. But there is another side to the picture of course: new variation, and its promotion via NS, drift, divergence and radiation. What you seem to be hoping for is that the known processes of generation of variation – recombination and mutation within species; speciation above – are never sufficient to cope with losses. If you focus on a narrow band where they are insufficient – during a mass extinction, for instance – you will indeed see a net reduction. But look elsewhere, it will go up – during adaptive radiation into cleaned-out niches for instance. The latter process is inevitably slower than the former, and so harder to see. But I don’t see any reason to suppose that the processes of ‘re-variation’ are insufficient to account for diversity at any particular level.
stcordova,
We can still look at what we know and hazard some reasonable guesses. Some 2% of the genome is exon, 25% is intron. If the reason for introns is simply alternative splicing, that would require 12 alternative transcripts per gene to make the space worthwhile. The cost of this method is that a mutation or misread could potentially affect 12 different proteins instead of just one, to say nothing of the potential for errors in editing. In reality, it is not certain that anything like that proportion of intron-containing genes produces functional alternative transcripts. Most seem to produce 1 – especially in unicellular eukaryotes, the reasonably assumed original type when introns first arose.
If alternative splicing is widespread, it would have interesting implications for Axe-style belief that sequence space is function poor. Being able to completely shuffle sequence and getting functional product several ways has implications for the capacity of evolution to uncover new function by a similar process of module shuffling – something many would prefer to deny.
It may be the case that introns originated to support alternative splicing and were originally much smaller. But creating a gap creates an opportunity for ‘selfish’ genetic elements to insert themselves, safe from damaging effect because they will be excised from the final transcript.
Agreed for alleles (diverging genes), but not emergence of new complex TRFs (new genes not alleles, but also non-genic features in the cytoplasm or wherever).
And that divergence can also be interpreted as genetic deterioration from a functional ideal. The Y-chromosomal divergence and deterioration is an example because the is no gene flow as a matter of principle.
🙂 Wish I could keep more of it by choice.
Agreed, and I like “Natural Selection at the species level. ” Well said.
Why is it not surprising that Sal ignores the evidence for incipient speciation and continues to preach his “genomes can only lose function” nonsense? Must be hard for him to argue in a venue where he can’t surreptitiously edit other people’s posts and change the words in their posts to his own fabrications.
I actually sympathize with you on this, the notion of function needs some reworking to get clarity. There are infinite ways to make keys and passwords, hence the functional space is infinite.
Axe would have a better argument in terms of sets of highly specific interacting parts.
There is an infinite space of functional lock-and-key combinations, the problem is showing that a certain infinite subspace of lock-and-key combinations is exceptional (improbable, but not because of an after-the-fact probability calculation) as a matter of principle. Behe’s binding site arguments are a little closer to what is needed.
Regarding intron, here is the best paper on function of introns. It suggests to me Larry Moran and Dan Graur’s views are quickly getting obsolete, and for that matter, if some IDists are still clinging to the Alternative Splicing as a primary reason for introns, they may be getting obsolete too.
I highlight there are 5 phases where the spliceosomal intron participates in Eukayotes:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3325483/
The intron provides function in each of the five phases.
The review is breath taking in its thoroughness of the intron function in each phases.
I feel the evolutionary angle of the paper however was unnecessary and gratuitous, but still an excellent paper.
PS
ERATA, the minimum number of proteins for introns has been revised from 300 to 150. 300 was the quoted figure from the 2003 paper quoted above:
http://onlinelibrary.wiley.com/doi/10.1002/bies.10394/pdf
err… not quite, but I can guess which paper you’re reading.
Here’s the thing – for someone claiming “evolutionists” don’t know anything about the origin of the spliceosome, you’re doing a pretty good job of ignoring or avoiding talking about the widely held theory for the spliceosome’s origin that’s supported by both structural and biochemical analysis. It’s been referred to directly by both papers you’ve specifically cited, and in the paper John cited (which you apparently read far enough to get to the one sentence that you agree with*). The origin isn’t some huge mystery, there are pretty big clues which suggest that the spliceosome’s origin ties in with the origin of the mitochondria, which itself is well supported.
* by the way, the one paper the authors cite in contradiction to the group II intron theory itself states “Although group-II introns provide a reasonable source for the original presence of spliceosomal introns and of the splicing machinery in the LECA, some aspects of the group-II introns origin hypothesis remain unclear” – if you read further, it’s clear they’re disputing the origin of most eukaryotic introns, not the spliceosomal machinery itself.
David,
Thank you for your criticism. In light of the complexity of both the spiceosomal intron (function in 5 phases) and the spliceosome itself, I just don’t find the mechanical feasibility arguments compelling.
Evolutionists place greater weight on similarity arguments (phylogenetic signals), but to the extent some splicesomal features are totally absent from the alleged Eukaryotic ancestor, it looks like those features just came from nowhere.
Some have said Prp8 has no homology outside of the RNase H1 domain.
If indeed the Spiceosome has a metal (non-amino acid) component, there has to be some post-translational modification helping put it there. We don’t even know where post-translational information resides in the cell. So I think it premature for anyone to say they KNOW how anything came about. All that can be asserted is what people believe in the absence of direct observation.
Sal’s idea of intellectual honesty – science can’t provide every last detail so all the millions of other things science does know about evolution and the age of the Earth are wrong.
Topped off with the Ken Ham stupidity “were you there??? Did you see it???
Never asked with regard to scripture.
Yeah, I know.
God I hate those guys.
The funny-sad thing is that faith is actually their highest virtue. Sal referred to it, obliquely, when he talks about the children who will have to accept christianity by faith alone, never seeing a miracle or direct evidence of god. And yet, if anyone has “faith” in the scientific worldview, in the overall accuracy of our theories about the universe (which work well enough to bring us GPS, golden rice, nuclear medicine, etc.) then suddenly that character is worthy of scorn.
Of course, it’s not true that “faith” in science is the same as “faith” in any religious sense, but if they were exactly equivalent, all it would mean is that the Sals and Kens of the world are unconsciously dissing themselves when they gabble “were you there, were you there”.
I guess, if we don’t know the precise function of spliceosomes and introns yet, we’d have to hang fire on any conclusion that they are designed.
stcordova,
Unreasonable extrapolation!
If two species are diverging with respect to their Y chromosomes, I’m not sure which is deteriorating. Both? Why? Obviously, there’s Muller’s Ratchet. But this is acting because it is a lengthy(ish) haplotype. That’s not applicable to anything but the Y, plus a few ‘boxed’ haplotypes while comparatively rare.
And the Y chromosome does ‘flow’, in fact, just as a rather larger lump than the average recombinant locus. It still integrates in genomes, but only via independent segregation as opposed to segregation and/or crossover. Segregation can be seen as coarse, position-invariant crossover.
Sal,
The catalytic core of the spliceosome is not just a metal (ion), nor does it involve post translational modifications. It doesn’t involve translation at all, for that matter. The spliceosome seems to be a lot more mysterious to you than to scientists. Also worth noting that as a general principle, proteins do not need post translational modifications to coordinate metal ions.
Great! We’re tired of hearing that ignorance is an excuse.
Hi, Barry!
This is a good time to explain to your fellow UDers that despite all your crowing, you actually believe that you’re losing the “war” — badly:
Thank you for your criticism, however:
One of the core elements is Prp8, and it has at least one class of Post Translational Modifcations:
So I think I’m correct to invoke PTMs on spliceosomal proteins, not just in their original formation but even during the operations associated with the spliceosme.
Thanks for the info.
That’s true, I have much to learn.
Yet despite this you know the origin of life (poof!) and that the earth is young.