One of the densest Creationist tropes has to be ‘Common Design’. It is proposed as a direct competitor to Common Descent – template mediated copying of DNA – as an explanation for the high sequence similarity of two DNA segments. But what is actually held in common? If we look at a particular transposon sequence, and find it is in A and B but not C, and another that is in A but not B, etc, we can generally organise a set of such markers into a ‘tree’ structure, much as would be predicted by Common Descent. But no, we are assured that these apparent markers are in fact part of the ‘design’. If A is a whale, B a pig and C a deer, there is something that is vital for the function of both whale and pig but is definitely not required in deer. Instead, a sequence which, in whale and pig, sits either side of the insertion, runs uninterrupted in the deer. That, too, is functional, supposedly, even though the insert would give a product which was the A/B one with a gap and possibly a frameshift, if it were transcribed.
But this is held to be the case even if the sequence, with and without transposon, is never transcribed. A sequence that does nothing, and organises hierarchically exactly as would be expected of common descent, is nonetheless functional … because?
On observation, there must be some genome pairs that are highly similar because they are commonly descended. We can see it happening. But there are, on this notion, supposed to be identically-patterened runs of similarity that are not due to common descent, but instead result from a completely different cause – some entity bolting together genomes, or parts thereof, from scratch, I guess, and choosing to repeat a known pattern – up to a point – in a manner that fools our most adept molecular taxonomists into seeing descent.
There must be a line in a taxonomy where the one shades into the other – on one side, sequence commonality is all Common Descent; on the other, Common Design. Where does this discontinuity reside? Species, genus, family, order? Is it a gradual transition, gene by gene, or all at once? How could you tell? Why does it not show up in computer analyses of blind datasets?
If I were to provide 3 genomes shorn of all differences, it would be impossible to tell which were commonly descended and which commonly designed from the data. But there must logically be a transition of causes, were I to take the genomes from sufficiently distant species and this idea were true. What persuades us to adopt this causal explanation in preference to that which explains the pattern better: Common Descent?
Could be. But it could be your lack of clarity. Nor did I say you made no sense. I said you weren’t comprehensible. You then made no attempt to explain yourself. At one point you cited a paper, which I read and attempted to summarize. You made no comment on my summary. I think confusion is one of your main techniques of argumentation, and I’m beginning to suspect it’s intentional.
In some cases that may be correct. Again, it’s work in progress. ERVs? It’s hard to make a case there for functionality rather than “selfishness”.
FWIW, I used to be heavily on the junkDNA side of the argument, but lab evidence changed my mind, and now I’m in the mode of wait and see.
I believed because of Adam’s sin, the genome got badly trashed, so most of it was junk. I had no problem with the junkDNA argument. The same trashing in man happened in the same spots in monkeys. Common malevolent design in mammals and primates…..
But now it seems we’re all just arguing in a vacuum till more data comes in. 2 decades ago, I would have had zero ammunition to argue for the function of transposons and other repetitive elements. How things can change and turn totally around when the right experimental results come to light!
There is some junk in the genome, but I think it’s an unhelpful policy to assume something can’t be functional. Biology is full of surprises.
How many times have you been told that it’s not just assumed to be non-functional? Geez
I hate that anti-complexity crowd. A bunch of simpletons, each and every one.
If he didn’t publish his model the whole thing is nonsense.
Sounds to me like Theobald has created a straw-man to defeat.
http://www.evolutionnews.org/2010/11/douglas_theobald_tests_univers041021.html
That’s simply untrue. Recently here at TSZ Allan Miller claimed that it’s more probable that life will appear on a sterile planet/earth than it is that life would appear on a planet/earth that already has life present. He appeared to think it quite unfair of me when I asked for his probability calculations.
Probability claims exist on both sides.
Obscure, obsolete, and just plain anti-complexity. Makes me want to take him out back and spank him with a modern biochemistry textbook.
I’m pretty sure Allan was using “probably” in a general sense of “more likely”. Surely you can see the opportunities for any life-form are less perilous in a “green-field” environment.
I think of a roulette wheel. Well-designed, the probability is that the ball will fall into a slot is 1. You can divide the wheel into equal or unequal slots or a slot so small there is zero probability of the ball ending up there. It’s not a matter of sides.
I’m pretty sure that the sequence that isn’t present in deer is doing nothing at all for those deer. What do you think Allan?
Can you link to some articles at UD where you championed the cause of Junk DNA?
You’re so good at logic that it looks the same as probability to you. Great job.
What a maroon. If I define something a “CAEK” before hand it remains a cake even if I make it with bricks and poop.
Mung,
No. As I went to great pains to explain then, one can assert one outcome to be more probable than another without knowing the actual probabilities. It is more probable that you are six feet tall than that you are two foot six, for example. It is more probable that you can live in an unoccupied cave than one that is full of lions.
stcordova,
So I’ll ask the question again, for the third time before cock-crow: are you taking the position that there is no such thing as a non-functional bit anywhere in any genome?
This is where ‘you never know’ takes one.
stcordova,
It’s curious that you can make so much out of a hypothetical sequence! You really are saying there is no such thing as a non-functional sequence, then. There is NOTHING which could, even in principle, fit the bill of my non-functional sequences.
AND you are also saying that there is no such thing as a variation in functional sequence that makes no functional difference. Every last scratch and spot is essential for organismal function.
Mung,
In the hope that might be a serious question, in the matter of a SINE insert, the deer would have flanking sequence alone, the other species flanking sequence with the SINE inserted. The flanking sequence is different for each insert, and there isn’t just one.
One would have to suppose that deer relied upon “flanking sequence” to regulate some function, where pigs, hippos and whales relied on “flaSINEnking sequence”, at that particular site
Not forgetting that there are many thousands of these things, all capable of apparently resolving phylogeny down to a pretty low level, for anyone foolish enough to think this might be a reasonable inference: commonality arising through copying. Including genealogy, paternity tests and forensics. As if!
I don’t see how it’s even possible to live in an unoccupied cave.
Mung,
Who needs a biochemistry textbook when there are Sal’s pretty pictures to convince? Biochemistry was SOOOO simple in my day. There were just ‘humours’, and that was about it … oh, and glucose.
I’d be interested to know where in a modern biochemistry text we get to hear that there is no such thing as non-functional sequence, and nor are there functional variants that make no difference.
Mung,
Still on the yellow belt, Mung-san.
Just to be clear, here is the statement that seems to be causing such a fuss:
I agree there is a possibility that not being transcribed does not mean that it is non-functional. One can always hope for a function to be discovered in the future.
Does that change the expectation on common descent one iota? Nope. The only crumb of comfort derived from it is that a Design reason might be salvaged.
Some people seem mistakenly to think that molecular phylogeny is only done on non-functional sequence. That would be in error. For branches beyond a few tens of millions of years ago, non-functional sequence is no use, because it loses its signal. So if there is cryptic function for a single SINE insert, and the same for another, this does not invalidate their use in phylogenetic studies. What is useful about them is their binary nature, not their lack of function.
Further, there are variations within the SINE, and within the flanking sequence – SNPs. Its not just a question of pristine flanking sequence plus pristine SINE. Those differences nest as well. They are informative.
They are all functional? Really? Well, you never know …
It’s a disguise, hoping the lions won’t notice.
As a pause for thought, one might consider how SINEs useful in phylogeny are identified. Do you start with flanking sequence, or with a known SINE? How do you identify what’s a SINE in the first place and distinguish it from the rest of a genome? You certainly don’t sit there on the alert and wait for one to jump, like a flea …
The miracle, on Common Design alone, would be that flanking sequence primers can be made, based on what is held within them in certain species, and they then locate the same sequences anywhere else at all, with nothing inside. What on earth would lead us to expect to find uninterrupted versions of such flanking sequences in other organisms, if they did not commonly descend?
I guess this is what cause people to say ‘circular reasoning’. If one assumes common descent, and generates primers for sequences on that expectation, it is circular if one then actually finds them!
We are not observing the originally designed organisms. What we have now is the result of generations worth of changes.
Look, if Common Descent can only explain the similarities we already had Common Design to do that. If Common Descent cannot explain the anatomical and physiological differences observed then it is useless and should be discarded. We already have something that explains the similarities.
Real science doesn’t move beyond demonstrating that A Cause is responsible.
ID doesn’t do any science based on discovering the Fact of Design, after all.
How could evolutionary theory do so? Especially since it’s False, because ID is True?
Glen Davidson
Frankie,
Even in that (wrong) statement, it does a crap job of that ‘explanation’. After all, in the extreme, identical twins would be the most commonly designed of all, if that’s its job: to explain similarities.
Reality is, it’s the pattern of similarities and differences that makes molecular phylogeny so powerful. Common Design is a mind-numbingly useless explanation for these patterns. Its proponents seem hugely confiused as to whether it’s similarities or differences they are talking about, as witness Sarfati’s dozy piece.
Frankie,
And then common design found tiktaalic. Oh, wait…
Yes, I actually agree with you. If I ever use the common design explanation please slap me. I just don’t see what’s gained by it.
Walter ReMine has an interesting thesis in his book The Biotic Message that life is designed to resist evolutionary explanations and to point to a single designer of life. It’s probably the best argument I’ve seen for what might be called a common design argument.
I just googled it and came across a presentation in youtube. 7 minutes in and I can already affirm: what a huge pile of pure, unadulterated bullshit this is
The statement is correct and Common Design does a great job of that explanation.
It explains similarities across the species, not just within one species.
Except given the complex nature of evolution we wouldn’t expect simplistic patterns as portrayed by phylogenetic analysis. And seeing tat you cannot account for the aforementioned differences you don’t have anything.
If you don’t have a mechanism capable of explaining the anatomical and physiological differences observed then you don’t have anything but wishful thinking. And you don’t have such a mechanism
And you don’t know if any cause can produce Common Descent
We do have such a mechanism. Evolutionary processes have been observed to successfully work in the lab, in the field, and is computer simulations. ID-Creationism is the claim that can offer zero mechanisms for the physical manufacture of life. Just lots of hot gas and hand waving.
There’s tons of empirical evidence that evolutionary processes produce common descent. Most ID-Creationists like you are unaware of them because they’ve never studied anything in the biological sciences.
Adapa, you can’t even find the alleged scientific theory of evolution. Natural selection and drift are impotent with respect to Common Descent but great for humans giving rise to humans. You don’t even have a mechanism to get beyond populations of prokaryotes and you have to be given starting populations of prokaryotes. You cannot bluff and equivocate your way through this so I don’t know why you even try.
Voles- A lot of micro but no macro
Yup after all this “evolution” a vole is still a vole. The evolutionary excuse- “they didn’t get the right mutations.”
That pattern does not exist. 🙂
The Independent Evolution of Eyes. What are the odds?
I’m saying, it’s not helpful to assume it has no function. 30% of the human genome that was assumed to be useless 20 years ago can’t be assumed to be now because of lab experiments. This figure could be revised upward in the next 100 years. I see no benefit in a rush to judgement, probably some damage for doing so.
I’ll give you one example that really gets under my skin personally. For the one week that I was a substitute for Denyse O’Leary, I wrote this article about some guys wanting to sweep 1,177 orphan genes out of the list of genes for humans merely because it disagreed with evolutionary theory:
So these guys just want to delete prospective genes from the databases because it doesn’t agree with their ideology? Wouldn’t it be better to just wait and see until the proteomes are sequenced for most cell types at various developmental stages at least? I was personally disgusted to learn of this.
It’s relatively easy to sequence mRNAs compared to actual proteins, at least in terms of expense. There isn’t any easy way to apply mass spectrometry to an entire cell and get all the alternative splices of every protein there is in that cell. We really don’t know if something is orphan or not, but evolutionary biologists again like Ayala and Graur and Ken Miller are throwing their opinions into realms that are none of their business, but rather the business of molecular biologists actually sequencing orphans proteins and enzymes!
The situation is summarized here.
We may have sequenced the genome, we’re no where near that with the proteome, the transcriptome, the epigenome, the epitranscriptome, the epiproteome.
Imho, it really is too premature to declare stuff non functional.
I’m saying it’s premature. We could be more confident making declarations of non-function if we knew more, but we know squat next to what could be known. As we know more, then we can be a little more forthright in our assertions as to non-function. Till then, it’s premature.
That brings back memories, lol.
One can get an idea of how many posts of mine Salvador deleted by looking at how many times I had to repeat myself. 🙂
And they turned out to be right. It would be preposterious to suggest amino acid sequences could change so much in so little time, for a few genes, and have them result in new protein coding genes with no homology to any previous genes.
The genetic sequences that encode these proteins have homologous DNA sequences in close relatives, so they didn’t evolve by one protein changing into another, and they also didn’t evolve by (as you deceptively try to suggest) just spontaneously arising out of nothing (which, ironically, is what YOU believe). Rather, the genetic material was already there, and relatively few mutations changed the non coding region so it became recognizable by transcription factors, leading to their eventual transcription and translation.
In other words, they aren’t really true orphans (making it a bit of a misnomer), since the DNA sequence they arise from is found in closely related species.
stcordova,
When will it ever be mature?
For all the smokescreen you pour into your posts, you seem to be pushing a very eccentric line: that there are no differences between individual sequences that make no difference. It is not merely ‘premature’ to find that debateable, it is at odds with principles both of biology and of ‘Design’.
It does seem odd, for a proponent of genetic entropy, to consider it likely that all differences are functional differences – that both of alleles A and B have their structure because it matters that they do – that both have been optimised by Design for the organism they are in. You argue two contradictory positions. You are by no means the first Creationist to do so.
One of the places SINEs tend to end up is within other SINEs, for reasons one could work out with some consideration of mechanism rather than need. So, you get “flanking sequence”, “flanSINEking sequence” and “flanSINsineEking sequence”. You ALSO get “flakSINEing seequence”, and “”flanSINsixeEking sequedce” , and so on and so on (guess how I generated those variants? It wasn’t Common Design!).
You would argue that it is ‘premature’ to say that ANY of those variants lacks functional significance. I’d say that’s pretty unreasonable. One would only make that argument to try to head off the Common Descent argument on non-functional difference, on the rather feeble grounds that ‘you never know’. Molecular phylogeny doesn’t depend solely upon on this genomic fraction anyway, so it would be a hollow victory even if conceded.
If anyone wants to find a function for this bit or that bit, they are perfectly free to do so. There is not some evolutionist-imposed cap on what percentage they are allowed to find. It’s funny when Creationists argue as if they are the True Defenders of Science.
stcordova,
I don’t know where you get that figure from, but in any case when I was at university no-one would have bat an eyelid at the claim 100% of the genome was functional. That is still pretty close to true for many species. Does this affect molecular phylogeny in those species?
Scientific progress led to a revision of this notion – for some species. If further progress discovers it was close to the mark after all, there will be some explaining to do on the ‘genetic meltdown’ argument, but it won’t have a massive effect on molecular phylogeny.
What are you talking about, sir? Rarely have I read such a confused mess.
Doing mass-spectometry to elucidate amino-acid sequence wont tell you whether it’s an orphan protein. It’ll just give you an amino acid sequence.
The only thing that can tell you if it’s an orphan is comparative genetics. Meaning you have to have whole genome sequences from multiple closely related species and look for a corresponding homologous coding region. If there’s a homologous DNA sequence in a related taxon, it’s not a true orphan.
And why are you blathering about alternative splicing, that has zero to do with whether it’s an orphan gene or not.
Are you just brainlessly sprinkling words from molecular biology into your posts now?
Sal, doesn’t it bother you that you have to engage in this kind of obscurantism? Do you even care?
Frankie,
The most ‘commonly designed’ sister species are therefore something along the lines of Common and Spotted Sandpipers. Slightly less Commonly Designed, perhaps, rats and mice. Even less Commonly Designed, we have mice and frogs. Less Commonly Designed still, mice and dandelions.
It still remains the case that, if you want Common Design to be the direct alternative to Common Descent, it must be most prevalent where it is least needed – ie most in evidence among related organisms. Common and Spotted Sandpipers must have more Design in common than any more distant taxonomic pair. Which is kind of the opposite of what you want.
Don’t confuse your unwillingness to try to understand what I said with obscurantism. For example you said:
What I said is hardly obscure:
Well gee, if you have sequenced a protein and it corresponds to an orphan gene, then that protein is taxonomically restricted (you can call it orphan if you like) to that species. That corresponds to this statement by the evolutionary researchers who are advocating real obscurantism by deleting potential genes from the database merely because of research conducted so far, but excluding research yet-to-be done (like relevant mass spectrometry experiments):
That means they want to delete 1177 genes from the database only because only 12 reports of proteins that match those genes have come in SO FAR. That’s real obscurantism. What if we had deleted those 1177 genes before those 12 proteins were discovered. That’s 12 proteins from orphan genes suppressed from discovery by evolutionary theory.
What if, after we sequence the entire proteome of hundreds of cell types in thousands of developmental contexts and discover 100 proteins that are from those 1177 orphan genes? That’s more suppression of science by evolutionary theory. We won’t know till we look will we. Guys like this should just butt out. It’s none of their business. It’s the business of proteomic researchers in real laboratories, not evolutionary biologists doing arm-chair molecular biology.
NO! Not if we are talking protein coding genes that code for real proteins. If we’re talking RNA genes (like say RNAs like Xist, HOTAIR, etc.) that’s another story (can we say ENCODE!).
So the question of protein sequencing is important as alluded to in the paper I cited with these words:
What they mean is 12 cases SO FAR, but not necessarily in the future after more sequencing is actually done, and not just for one isolated cell, but hundreds of cell types in thousands, maybe tens of thousands of developmental contexts.
This is an example of evolutionary biologists being totally unhelpful, probably even harmful to scientific progress.
If you get a list of all the alternative splices of every protein in a cell, that is the most comprehensive list of proteins in the cell, therefore you’re not going to miss any proteins in the cell, therefore you’re not going to miss any orphans in the cell. But one cell of one cell type is not enough. It has to be tens of thousands, maybe hundreds of thousands. Who knows. But that sort of research is too expensive and prohibitive at this time.
If that’s the case, it’s way too early for evolutionary biologists to start advocating deletion of genes from databases merely because it disagrees with their sorry theories. That’s none of their business to be meddling with lab researcher’s databases as to what these lab researchers can and cannot discover.
That goes back to this presumptuous remark in the OP:
It’s too early to make such pronouncements.
We don’t Sal. You’re well known for your meaningless verbosity in trying to impress people. It may work for some fellow IDiots but it just makes you look foolish to those who understand the science.
Correct me if I’m wrong but wasn’t one of your earlier goals in life to be a professional Creationists conman like Meyer or Wells? Didn’t you start several now defunct web sites (Young Cosmos, Creation Evolution University) to hone your bafflegab and bullshit rhetoric so you’d sound more convincing to the science illiterati?
As far as alternative splicing (mRNA), there is trans splicing of mRNAs and then protein splicing of the protein!
https://en.wikipedia.org/wiki/Protein_splicing
Now regarding Rumraket’s comment:
Depends on how you define orphan. If a protein, or splice variant is unique to a species and is functionally significant, does that count as an orphan?
Now it could get hard to actually map proteins to genes since it’s evident the 1-to-1 correspondence is only approximate.
We can have:
1 Orphan DNA transcripts
2 Orphan RNA transcripts
3 Orphan proteins and enzymes
NOTE:
the word “orphan enzyme” unfortunately has two meanings. The meaning of “orphan enzyme” sometimes refers to enzymes not yet mapped to a gene, but there is a potential such proteins(enzymes) may not be 1-to-1 mappable to a gene as pointed out by the issue of protein splicing.
We really know too little to be making pronouncements of non-function.
But we do know enough to say that life is evidently the result of miracles.
Consistency is not your strong point.
Glen Davidson
You can say life is a miracle without knowing all its function. Knowing every thing could be a sufficient but not necessary condition to assert a miracle.
Don’t equate your mischaracterization of my position with inconsistency.
But just for your remedial training, here are some pointers in logic:
http://mathworld.wolfram.com/Sufficient.html
In analogous manner, life can be a miracle without us establishing every DNA sequence is functional.
Your accusation of my lack of consistency is based on your illogic.
Since its been a long time since I’ve gotten anything of value from you. You’re now on my ignore list.
I haven’t even responded to your tripe in ages.
So you just lie and accuse, like usual, trying to smear with your typical lack of substance and knowledge.
Good to be ignored by someone so devoid of intelligent responses.
Glen Davidson