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Extra Characters to the Biological Code

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Even if compressed I’ve always thought that the known informational content was not enough data. This makes sense because from an engineering point of view because there doesn’t seem to be enough data storage space in a few billion base pairs of nuclear DNA to specify all the detail in a mammal or similarly complex animal. It’s enough room to store a component library of the nuts and bolts required to build individual cells of different types but not the whole animal.

Obviously no one can argue against the assertion that we do not fully comprehend the biological code. Unlike with computer code we cannot simply determine at a glance which informational content defines what biological function. The title of geneticist Sermonti’s book is “Why a Fly is not a Horse”. In it he writes the only thing we know for certain about why a horse is a horse and not a fly is because its mother was a horse.

Thus, based on our current level of knowledge, any calculations that quantify biological informational content are going to be rough estimates. Personally, when measuring the functional sequence complexity of code encoding proteins I’ve long biased any calculations I do by rounding up to several extra informational bits. And this action seems justified by this recent news:

“Anyone who studied a little genetics in high school has heard of adenine, thymine, guanine and cytosine–the A, T, G and C that make up the DNA code. But those are not the whole story. The rise of epigenetics in the past decade has drawn attention to a fifth nucleotide, 5-methylcytosine (5-mC), that sometimes replaces cytosine in the famous DNA double helix to regulate which genes are expressed. And now there’s a sixth: 5-hydroxymethylcytosine.

In experiments to be published online April 16 by Science, researchers reveal an additional character in the mammalian DNA code, opening an entirely new front in epigenetic research.

The work, conducted in Nathaniel Heintz’s Laboratory of Molecular Biology at The Rockefeller University, suggests that a new layer of complexity exists between our basic genetic blueprints and the creatures that grow out of them. “This is another mechanism for regulation of gene expression and nuclear structure that no one has had any insight into,” says Heintz, who is also a Howard Hughes Medical Institute investigator. “The results are discrete and crystalline and clear; there is no uncertainty. I think this finding will electrify the field of epigenetics.”

Genes alone cannot explain the vast differences in complexity among worms, mice, monkeys and humans, all of which have roughly the same amount of genetic material. Scientists have found that these differences arise in part from the dynamic regulation of gene expression rather than the genes themselves. Epigenetics, a relatively young and very hot field in biology, is the study of nongenetic factors that manage this regulation.”

Go to Science Daily for more.

Comments
...Rybczynski is either a more common name than I thought...
I wonder whether Hazel is distantly related. Thanks for the link. Interesting stuff!Alan Fox
April 24, 2009
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gpuccio, Thank you for your informative #48. Out of courtesy I will defer comment pending the outcome of your discussion with Mr Nakajima concerning FCSI. Nakajima [42]:
Yes, I must have missed those detailed and quantitative discussion of calculating FCSI and or calculating FSCI.If you can provide links I will try to catch up.
To which gpuccio replied [44]:
And I will try to give you the links, as soon as I have time to find them.
I also would appreciate perusing your links. (I apologize for jumping in with my recollection about the FCSI of oxytocin. Please carry on.)Adel DiBagno
April 24, 2009
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Hi, Sorry for the off topic comment, but I just wanted to bring your attention to this site about the new fossil seal. It looks like Rybczynski is either a more common name than I thought it was, or being banned from UD leaves you copious free time to roam the high arctic in search of fossils. Congratulations Natalia!Nakashima
April 23, 2009
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Nakashima, Adel: Oxitocyn is a small peptide. Again, please look at the numbers in the Durston paper, you will find much more interesting facts. And the UPB is not, IMO, a good threshold to infer design. Personally, I would accept 1:10^30, or if you want up (or down) to 1:10^50 as much more useful thresholds for the biological context. But there is another approach which gives us a more realistic idea of where we are with darwinian explanations. Behe in TEOE has suggested that, in natural models like malaria, random mutations can, at best, provide two coordinated necessary mutations under a very strong selective pressure. Behe's arguments have been disputed (IMO, without any reasonable confutation). But that's not the point. The point is, let's say that Behe is partially wrong, and that in natural contexts like malaria (big populations, very strong and specific selective pressure, and very high reproductive rate) 3, or even 4 coordinated necessary mutations may, sometimes, happen. Where are we with darwinian theory, then? We are completely nowhere. 3 or 4 coordinated mutations cannot build anything of importance. I will be generous. Try to build a path from one protein to another one (different proteins, different superfamilies, different domains) by any sequence of 4 coordinated mutations, where each step is definitely selectable. That would be a model. Adel, you "have been following this site since Kitzmiller et al. in 2005". Well, I have been following scientific literature for even longer, and I am still waiting for such a model to be presented. Please, remember that all the models of microevolution we know of with some credibility are of 1, or at best 2 coordinated mutations. That is your explanatory power. That is your model. Those are your "testable hypotheses. You have nothing. The research I think of is already coming out everywhere. All biological research is ID research, because, you see, ID is not "another" theory which should change biology. ID is the only way to make sense of biology as it is. We only have to get rid of the pseudo-scientific interpretations which have corrupted the theory of origins of biological information, not biology itself. It's a shift of perspective, but the facts remain the same facts. But our interpretations will change, and will change much faster as our accumulation of facts increases. I don't understand what you expect from ID. Personally, I expect nothing from darwinian theory, and very much from biological research. That is a fundamental difference, I believe, between us. For me, research is research: it is not done to defend darwinism or to defend ID. It is done to understand reality. The more we know, the more we can understand, even if we don't spend all our time and resources to demonstrate that we are politically correct and that we strictly obey Popper, or Kuhn, or Feyerabend, or the next maitre à penser of the year. So, biological research is biological research, and it is for all, and it is owned by nobody. The more we know, the more we can understand. If ID is correct in its assumptions, the more we know the more ID will be obviously the best explanation. The opposite should be true if darwinian theory is correct. That's the only prediction which really counts. So, you can ask: "How is that research coming along?". But my simple answer is: it has been coming along for decades, and still it is coming along day by day. In the papers you quote, and in all the others you and myself don't even know of. You believe that ID is in the gaps. I believe the opposite: ID is in the details, in the numbers, in the defined paths, in the accurate description of how intelligently designed things work. That is and will be the strength of ID. In the meantime, let's see how the darwinists of the gaps try to cross the 2 (or, if you want, the 4) aminoacids boundary...gpuccio
April 23, 2009
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Mr Nakashima, Regarding FSCI of proteins, I remember a thread a couple of months back in which gpuccio calculated the FSCI of oxytocin. As I recall, the number was small enough to fit well within the universal probability bound, but that did not resolve the question of whether it was designed.Adel DiBagno
April 23, 2009
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gpuccio [40]: I enjoy your good humor, especially when you disarm my crankiness.
Explanation 1...Research will show who is right. Explanation 2...There are, certainly, many things we don’t know: who is the designer, how does he implement the information, and so on. But those are not gaps. They are only things to research.
How is that research coming along? I have been following this site since Kitzmiller et al. in 2005. So far, I have seen no progress in the arguments, nor any testable (or tested) hypotheses. Compare Astrology, which led to Astronomy, and Alchemy, which led to Chemistry. But I have hopes, and I'll keep on eye out.Adel DiBagno
April 23, 2009
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womanatwell: ID can certainly approach the quantitative analysis of FSCI in different kinds of proteins. That's the easiest model to deal with. Regarding a cell state, I would say that its FSCI is certainly "at least" as great as the sum of its minimum necessary proteins. That's big enough, just to start. Obviously, there are higher levels of organization which are not so easy to analyze quantitatively. That's why for the moment nobody has really attempted to do that. But those level have almost certainly higher FSCI than the simple protein sequences, and moreover that FSCI is "in addition" to the simple FSCI of proteins and DNA genes. For the quantification of FSCI in proteins, I always recommend the Durston paper (and method) as an interesting start: "Measuring the functional sequence complexity of proteins". It's freely available on the web.gpuccio
April 23, 2009
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Nakashima:
But further, is it your position that every speciation event (under some non-tautological definition of species) is the result of intelligent intervention? That is how I understand your Explanation 2, above.
Yes, it is. And I will try to give you the links, as soon as I have time to find them.gpuccio
April 23, 2009
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gpuccio,
...in ID (and certainly in my posts) you will find so many arguments about protein complexity and the related probability resources, and much less, say, about the general rfegulation of transcriptomes in multicellular beings.
Would you consider an initial cell state as something ID can analyze. It seems a crucial question about viability of probionts is whether they can exist without the cell membrane regulation of pH, osmotic pressure, electrolytes, and other mechanisms of transport, which use specific membrane transport proteins along with a selectively permeable membrane. Perhaps you have a link for work already done in this area relating to FSCI and/or CSI.womanatwell
April 23, 2009
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Mr Gpuccio, Yes, I must have missed those detailed and quantitative discussion of calculating FCSI and or calculating FSCI.If you can provide links I will try to catch up. But further, is it your position that every speciation event (under some non-tautological definition of species) is the result of intelligent intervention? That is how I understand your Explanation 2, above.Nakashima
April 23, 2009
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Joseph,
The definition of “species” is ambiguous. IOW the two animals could be more closely related than we think.
true enough, but if the egg had as much control over development as you claim, you would expect the cloned gaur to have at least some cow-like features. but it did not.
Are sharks fish? And do shark fins have skeletal bones?
yes and yes. cartilaginous bones, but bones nonetheless. it's irrelevant anyway bc no one is suggesting that tiktaalik arose from shark-like ancestors. your claim of hand bones poofing into tiktaalik from nowhere is completely mistaken.Khan
April 23, 2009
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Adel: You are definitely more provoking when you give some argument or quote literature, but I can easily accept your more "emotional" expressions in the name of our old friendship :-) It's rater simple: the daily progress of biology is the greatest friend of ID because darwinism is based on lack of knowledge and on approximation, while research can give us the details that we need to understand and prove the simple concept that biological information can only be understood as the product of design. It's darwinism which thrives in the lack of understanding, because its "just so stories" have no explanatory power, and could stand no quantitative analysis. The poor and imaginary power of random variation and NS is only a myth, and like all myths it will not stand long in the face of facts. And I am afraid you are a little mistaken about gaps: ID does not need any gap. ID only needs that what is designed be recognized as designed, and that all the false explanations given up to now to deny that simple fact be recognized for what they are: false. In the design process there is no gap: the conception of the designer is implemented through a continuity of thought and information. In darwinian theory, there is no continuity of process, other than in the deluded hopes of darwinists: that's why darwinian theory is full of gaps, while ID isn't. o be more clear: fact1: a species is present fact2: after some time, a new species arises, more or less similar Explanation 1: RV+NS transform species 1 into species 2: as we cannot find any reasonable model and quantitative verification of that model, explanation 1 is full of gaps. You will say that those gaps are due to our poor knowledge of the details. I don't agree. I say that they are due to the poor quality of the explanatory model. Research will show who is right. Explanation 2: species 1 is transformed into secies 2 because a designer inputs the necessary information to implement the change. You can say that there are gaps in this theory, but that's not true. There are, certainly, many things we don't know: who is the designer, how does he implement the information, and so on. But those are not gaps. They are only things to research. Because we "know" that a designer can implemen information and obtain those results. We do that daily, even in biology. So, the model is consistent (which does not mean it is true, but it's a good start).gpuccio
April 23, 2009
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Nakashima: I suppose we had been doing a lot of quantitative argumentations about FSCI in proteins. Maybe you have not read them. On the contrary, I am still waiting for a quantitative model of macroevolution...gpuccio
April 23, 2009
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gpuccio:
As you know, I strongly believe that the daily progress of biology is the greatest friend of ID.
What could be the basis of this strange belief, which other ID supporters here have expressed? I hypothesize that it is based on the fundamental premise of ID: where there are gaps in evidence, an Intelligent Designer must have intervened. Therefore, regular science assists ID pseudoscience by energetically creating more gaps! (Just as each transitional fossil discovery generates two more missing links.) Happy to be of service! On further reflection, I think it is unfair to characterize ID as pseudoscience, since real pseudosciences have historically had research programs, involving testable prediction and experimentation. It will be interesting to watch whether ID ever rises to the level of Astrology or Alchemy.Adel DiBagno
April 23, 2009
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Mr Gpuccio, You see, we in ID prefer to discuss things where we can go into details and be qunatitative, rather than give “just so stories”, even if about issues which would certainly be in favour of our position. "Can" is not "do". The last detailed and quantitative discussion on this site that I recall was about the performance metrics of a toy program written in 1986. The discussion didn't go very well for the design detection perspective, if I recall. What was the previous detailed and quantitative discussion before that? I suppose we shouldn't include any discussion of microevolution, population genetics, or common descent, since those are not areas of controversy. We should probably keep all software simulations off the table also, since Mr Scheesman informs me that they are irrelevant (pace Dr Dembski, Mr Kairosfocus, etc.).Nakashima
April 23, 2009
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Jerry, I read the book- evo in 4 dimensions. Good read and good stuff but to me the authors worshipped natural selection just a little too much. And yes real good stuff on epigenetics...Joseph
April 23, 2009
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The Common carp or European carp (Cyprinus carpio) is a widespread freshwater fish most closely related to the common goldfish (Carassius auratus), with which it is capable of interbreeding.
Joseph
April 23, 2009
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gpuccio,
You are an inexhaustible source of indications!
On the contrary, I am easily exhausted. But I think that a useful response to arguments from ignorance is to present evidence that may alleviate ignorance. Please resist the urge to randomly insult people. -- AdminAdel DiBagno
April 23, 2009
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I think the answers to a lot of these questions reside in the relation of structure to function, both in proteins and now, as epigenetics is finding, DNA. DNA sequences are one-dimensional. The structures actually involved are three dimensional. As gpuccio noted, time is also involved as these structures degrade and are replaced quickly. It could be considered four dimensional in that regard.tragic mishap
April 23, 2009
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Nakashima: I am not sure of what you exactly mean by "developmental programs", but if your point is that the nature of regulations and the development of body plans and the general coordination of multicellular organisms are a stronger argument for ID than mere protein sequence complexity, I may agree with you. But the problem is exactly that: those are levels of complexity about which we really do not understand much (unless Adel's issue of sciencemag may shed new light on them...). That's really the only reason why in ID (and certainly in my posts) you will find so many arguments about protein complexity and the related probability resources, and much less, say, about the general rfegulation of transcriptomes in multicellular beings. You see, we in ID prefer to discuss things where we can go into details and be qunatitative, rather than give "just so stories", even if about issues which would certainly be in favour of our position. We are not darwinists, after all... :-)gpuccio
April 22, 2009
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Adel: You are an inexhaustible source of indications! :-) OK, I will try to read as much as I can. As you know, I strongly believe that the daily progress of biology is the greatest friend of ID. And, beyond that, I am really curious, which is always the best motivation...gpuccio
April 22, 2009
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Ms Womanatwell, It would be even more amazing if a different system than concentrations of molecules were used. Bacterial signaling is based on concentrations. I do not know if it is possible to trace a homolgy in this case.Nakashima
April 22, 2009
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How do discoveries such as this affect the standard argument re design in natural environments? Is there an implication that developmental programs are too intricate to have developed without a designer? Since this would be a more specific claim than the general ID hypothesis, it would also be stronger.Nakashima
April 22, 2009
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Correction: That was Ingolia et al.: http://www.sciencemag.org/cgi/content/abstract/324/5924/218Adel DiBagno
April 22, 2009
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Hi, gpuccio, I'm here, and your post indicates that you are in fine fettle.
Where is the plan? Where are the details? Where are the procedures?
I have been catching up on my reading in Science magazine, to which I have a subscription. The details that are being developed are staggering. I don't have the intellectual capacity or the energy to do more than direct you to the Website: http://www.sciencemag.org/ Take a look at the 10 April issue, for example, especially the paper by Ignolia et al. And, of course, there are scores of other front-line scientific journals plowing the same ground. I you are really interested in finding answers, you must read the literature.Adel DiBagno
April 22, 2009
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Interesting thread... I would be glad to admit that both genetic and epigenetic information is contributing to the final results, and maybe trans species cloning experiments (which are probably still too few) can clarify some of the influences. But the problem is IMO different. The problem is: where is the information, and how is it stored? I will be more clear. There is a part of the information which we know pretty well (but probably not as well as we think). That is the part in the protein coding genes. Well, we do not really understand everything. The very correct citations about alternative splicing, exon shuffling, and, I could add, post translational modifications and many other possible steps, clearly show that the genesis of the proteome is much more complex than a simple transcription and translation of a few nucleotide sequences. But that's not really the point. The point is that, for protein coding genes, we have at least some ideas of how the information in stored. We have the genetic code, a symbolic code which allows us to read the information, to understand at least in part its structure and function (building the right proteins). But what about the rest? Are we still believing that the only problem is having the right proteins? No, that is only a very "small" part of the problem (small in comparison with the rest, I mean). No. The true problem is: which proteins do we need, and when, and in what quantity? That is a dynamic problem. It changes at each moment and state. And, above all, it changes for each cell type, in multicellular beings. IOW, that is a problem of control. In a software, that would grossly correspond to the procedures. What is the program doing, and when? That is the real problem. In biological information, be it in DNA or in epigenetic structures, we have no idea of where and how the procedures are stored. It may be interesting to know if and how much they are in the nucleus, in the dNA, in the cytoplasm, or who knows where. But the true problem is: what kind of information is that? How is it written? How is it stored? So, I agree with magnan: nobody knows where the information is coded. But nobody know, how it is coded, too. Let's take non coding DNA. There is little doubt that some of the regulation information is there, but the good question is: how? Is it in introns? And is so, what kind of information is it? Why are so many and so long introns necessary? Why are genes so fragmented? Probably, to achieve different levels of control. But again, what controls? Where is the controlling scheme? And so for macroscopic schemes, too. We can agree that many of human functions are possible because of the ordered connections of our 10^11 neurons in 10^14 synapses. Well, I suppose that is a rather complex scheme of connections. I don't believe it can be realized without written code. We have 3x10^9 nucleotides in our genome. A long sequence, but is it long enough? And that, including everything. Protein coding DNA is only 1.5% of that. Nucleotides are grouped in codons in the genetic code. But that is only to code for proteins. But how does it work for all the rest? How are individual transcriptomes implemented, controlled, corrected? How is macroscopic form achieved? How is intercellular regulation regulated? If transcription factors control the transcriptome, what controls the sub-transcriptome of transcription factors? (Adel, are you there?) Where is the plan? Where are the details? Where are the procedures? As Sermonti says, why is a fly a fly?gpuccio
April 22, 2009
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What amazes me in embryonic development is that genetic receptors are sensitive to the CONCENTRATIONS of molecules which diffuse from the mother cells (as studied in Drosophila) to the embryo's DNA. This determines the differential development of head, thorax and tail. See: http://www.princeton.edu/~wbialek/our_papers/gregor+al_cell07b.pdfwomanatwell
April 22, 2009
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There is also a phenomena called overlapping gene instructions. Namely the same DNA sequence will code for more than one protein. Here is a link http://genome.cshlp.org/content/14/2/280.full.pdf There ie an example from Don Johnson's book on evolution. Here it is ATGTGTGATGCTACCCCCTAGTCCAAAAGGGCACCTTG Note the start codon, ATG, appears three times and each can represent an entirely different protein. So this is one way that a sequence can produce multiple proteins. And because this frequently represents a frame shift the amino acids can be quite different.jerry
April 22, 2009
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Development is still largely a mystery. I am sure that they know a lot more than they did 10 years ago and each period brings new knowledge. But how it all unfolds is still basically a mystery. Also development takes place long after birth as we all know about growth and changes that take place in different species after birth. Just look at your children and if you do not have any, look at what has happened to others over time. And then it all winds down and at different rates per species. Again a mystery. You would think that longevity would be a trait that would be number one for natural selection but it seems to have eluded it. If one wants to read an interesting but often convoluted book on epigenesis and other interesting topics, get Jablonka and Lamb's Evolution in Four Dimensions: Genetic, Epigenetic, Behavioral, and Symbolic Variation in the History of Life. These are far from pro ID people but there is nothing that undermines ID in the book. Also at one point they make the observation that there is no evidence for the origin of any species.jerry
April 22, 2009
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Basically, DNA in the cell has an incredibly complex shape. It's folded many different times and many different ways. http://www.youtube.com/watch?v=5UoKYGKxxMI I assume that epigenetics has something to do with how chromosomes are packed in the cell. Ultimately though, it must depend on DNA somewhere, since you can't just carry around proteins from your mother's egg for the rest of your life.tragic mishap
April 22, 2009
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