1,177 human orphan genes removed by evolutionists from databases

_{Salvador Cordova

April 13, 2014

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Here is a case of evolutionary bias causing misrecognition of orphan genes in humans. Orphan genes are presumed protein coding genes that exist in only one species and have such non-similarity to anything in any other species they are called orphans (a play on words of the ORF acroym for Open Reading Frame).

This came up in the Nelson-Velasco debate where Velasco said there are 0 orphan genes, and Nelson pointed out the reason some say they are zero is because of their biases.

Nelson has been vindicated as I pointed out in New Mechanism of Evouion — POOF

Here’s is the proof of this cover up Distinguishing protein-coding and noncoding genes in the human genome:

1. “The remaining 1,177 cases were declared to be orphans, because they lack orthology, paralogy, or homology to known genes and are not obvious artifacts… If the orphans represent valid human protein-coding genes, we would have to conclude that the vast majority of the orphans were born after the divergence from chimpanzee. Such a model would require a prodigious rate of gene birth in mammalian lineages and a ferocious rate of gene death erasing the huge number of genes born before the divergence from chimpanzee. We reject such a model as wholly implausible. We thus conclude that the vast majority of orphans are simply randomly occurring ORFs that do not represent protein-coding genes… We found… 12 reported cases of orphans with experimental evidence for an encoded protein”

The problem with these authors is in 2007 they didn’t invoke the POOF mechanism of evolution which other evolutionists happily embrace now in 2013:

However, with the advent of sequencing of full genomes, it became clear that approximately 20–40% of the identified genes could not be associated with a gene family that was known before. Such genes were originally called ‘orphan’ genes

Evolutionary Origin of Orphan Genes

20-40% of the genes discovered cannot be explained by common ancestry or common descent. So what mechanism is left to explain it? Special creation? But evolutionists can’t accept special creation, so they just pretend they’ve made a discovery of a new mechanism of evolution that can work just as well.

They haven’t given it a name yet, so let us call it POOF. What is POOF? POOF is the mechanism by which proteins can easily arise out random nucleotide sequences like a poem can emerge out of randomly tossed scrabble letters. I bold one of their euphemisms for the POOF mechanism in the following paragraph:

Orphan genes may have played key roles in generating lineage specific adaptations and could be a continuous source of evolutionary novelties. Their existence suggests that functional ribonucleic acids (RNAs) and proteins can relatively easily arise out of random nucleotide sequences, although these processes still need to be experimentally explored.

😯

The reasoning they use goes like this, “we have all these genes that can’t be explained by slight successive modifications, so they must have arisen spontaneously out of nowhere. Because evolution is fact, this implies evolution can just take random material and create functional systems in a flash. We’ve made a fabulous discovery about the miracles of evolution even though we can’t demonstrate it experimentally.”

HT JoeCoder
www.reddit.com/r/creation

Comments

BA at #90: I don't want to be fastidious, but I want to clarify well my position. You say:
Well if you say homology is best explained by common descent then it might be wise to considered if body plans might be reducible to sequence homologies. Just saying you are addressing the problem of ‘form’ from the wrong conceptual level!
So, I can only state again thyat I am not addressing the problem of "form" at all! I say that homology is best explained by common descent. That means exactly what it means, and nothing else. Can you find any reference to the problem of form or body plans in that statement? IOWs, what I say is: If a (a non coding sequence) in species A presents strong homology to b, an ORF in species B, common descent is the best explanation. That only means that the sequence b in B derives from the pre-existing sequence a in A, through some form of physical continuity. Obviously, it is the designer who modifies the sequence a so that it becomes b. Similarly, it is the designer who prepares the sequence a, so that in a second time it may become b. Nothing of that happens by chance. It is top down design all the way. Am I saying that the homology between a and b explains the new form or body plan in B? No, not at all. We simply don't know what determines a new form or body plan. I am sure that whatever it is, it will be shown to be the product of design, but I must say that IMO at present we don't know for sure how a body form or body plan is controlled. So, I am not affirming anything about what generates the new body plan. It could be a gradual process, or something more similar to a miracle. I just don't know. When I say that I accept common descent, I mean something very simple: whatever is the process that generates a new species, that process works, at least in some measure, on the species that already exists. And the reasons why I think so are many, and all of them are at the molecular level. The facts in favor of a derivation of new genes from existing non coding genes are among them. I am well aware that not all molecular observations are in favor of CD, and that some of them cast serious doubts on the idea of an universal CD. I am very interested in all the facts that will be discovered that can bring new light to the issue. But, for the moment, I remain of the idea that CD is the best explanation. And I state, again, that this implies nothing about the origin of new forms and body plans. I hope that is clear.gpuccio_{April 17, 2014
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No one knows to look for such a thing because no one thinks it exists. Well except for a few of us.
Meyer talks about the sugar codes in his book. They will look for it big time when it becomes obvious that it is controlling major events in development. Some may be doing that already. Maybe it will be digital in form, maybe not and if that is so then it may lead programmers to a new type of computing programming approach, one that is not digital.jerry_{April 17, 2014
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One of the points I made elsewhere is that many have said that the conservation of a DNA sequence means that it must have a function. Otherwise it would just mutate away over time.
But a lot of the so called junk DNA is extremely long sequences of repeating elements called LINES and SINES (Long Interspersed Elements and Short Interspersed Elements) The biologist looking at this once said it obviously cannot code for anything, it is just repetitive nonsense and by implication proof of a non-designer. I believe there were Darwinist on this site who made this point. But if these sequences had no function, they would disappear over time because mutations would make them into non-repetitive nonsense fairly quickly. But the fact that they are conserved means they are subject to natural selection which is preventing these regions from mutating. It must mean they have an important function and it appears that regulation is it.jerry_{April 17, 2014
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jerry, what if there is actual software that determines the final form? IOW even given all of the chemicals in a cell, including the membrane and cytoskeleton- just the hardware, nothing would happen without the controlling information that is none of the above. To me THAT is the problem with biology. No one knows to look for such a thing because no one thinks it exists. Well except for a few of us. It isn't enough to arrange all of the parts of a computer in a the correct configuration. Without n OS and application programs it ain't going to do much more than hold open doors and hold down papers.Joe_{April 17, 2014
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Behe’s argument in “Edge” is that unguided evolution cannot produce two new protein folds. The two mutations in the article just referred to a binding site with what, 10 bases?
Thank you. My comment at the end was then the correct assessment, that they really did not make much of a dent in Behe's argument. It is typical that the naturalist when presented with the incredible improbability of what they espouse will resort to the trivial to defend their position. In a very recent Teaching Company course on science, the lecturer resorts to the tree moths as an example to support Darwin. Either they are uninformed or just have no shame.jerry_{April 17, 2014
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I’m sure I’ve missed other criticisms that could be leveled, but I think the point is clear that the gradual ‘bottom up’ transition, envisioned by you, and Dr. Torley, is not nearly so easy as you might believe.
The most interesting thing about the Meyer book was his emphasis in the latter part of the book on this non-genomic control of development. There may be a hunt for structure of the information for this as there was for DNA 60 years ago. And when they find it, the form may be so strange that it will be hard to interpret. When they found DNA they already had primitive digital codes to relate it to. Who knows what the structure will be that controls development and how it varies from species to species. John Garvey has on his site a discussion about what makes human unique. It primarily references a paper by a population geneticist David Wilcox. Here is the Wilcox paper http://www.asa3.org/ASA/meetings/belmont2013/papers/ASA2013Wilcox.pdf One of the things it says is that the regulatory nature in the human genome is extremely more complex than the next species. Here is a quote:
What shall we say about the genes which make us human? We and chimps share 96% to 99% of our protein coding sequences. Why are we different? Not the 1.5% of our genome that codes for proteins but the 98.5% that controls their production. Literally, no other primate lineage has evolved as fast as our lineage has during the last 1.5 million years, and it’s all due to unique changes in our control genome. At least 80% probably more of our “non-coding” genome is also transcribed, starting from multiple start points, transcribed in both directions, with overlapping reading frames of many sizes and a whole spectrum of alterations, producing a whole zoo of ‘new’ types of RNA control elements – piRNA,siRNA, miRNA,sdRNA, xiRNA, moRNA, snoRNA, MYS-RNA, crasiRNA, TEL-sRNA, PARs, and lncRNA. Most of these unique RNA transcripts - and there are thousands, if not millions of them - are uniquely active in developing human neural tissue – uniquely active compared to their activity in chimpanzees, much less other primates or mammals. It is the new epigenetic world
We are only a short way there to understanding what is happening. And all this appeared by chance?jerry_{April 17, 2014
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jerry, Behe's argument in "Edge" is that unguided evolution cannot produce two new protein folds. The two mutations in the article just referred to a binding site with what, 10 bases? BTW Behe and the others did have a back-n-forth which is most likely on his UD siteJoe_{April 17, 2014
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"I said nothing about form and body plans. I just said that (sequence) homology is best explai ed by common descent." Well if you say homology is best explained by common descent then it might be wise to considered if body plans might be reducible to sequence homologies. Just saying you are addressing the problem of 'form' from the wrong conceptual level! “Humans and chimpanzees also differ significantly in many other anatomical respects, to the extent that nearly every bone in the body of a chimpanzee is readily distinguishable in shape or size from its human counterpart (38). Associated with these anatomical differences there are, of course, major differences in posture (see cover picture), mode of locomotion, methods of procuring food, and means of communication. Because of these major differences in anatomy and way of life, biologists place the two species not just in separate genera but in separate families (39). So it appears that molecular and organismal methods of evaluating the chimpanzee human difference yield quite different conclusions (40).” King and Wilson went on to suggest that the morphological and behavioral between humans and apes,, must be due to variations in their genomic regulatory systems. David Berlinski – The Devil’s Delusion – Page 162&163 Evolution at Two Levels in Humans and Chimpanzees Mary-Claire King; A. C. Wilson – 1975 http://academic.reed.edu/biology/professors/srenn/pages/teaching/BIO431S05_2008/431S05_readings/431s05_examples/king_wilson_1975(classic) K´necting The Dots: Modeling Functional Integration In Biological Systems – June 11, 2010 Excerpt: “If an engineer modifies the length of the piston rods in an internal combustion engine, but does not modify the crankshaft accordingly, the engine won’t start. Similarly, processes of development are so tightly integrated temporally and spatially that one change early in development will require a host of other coordinated changes in separate but functionally interrelated developmental processes downstream” (1) https://uncommondescent.com/intelligent-design/k%C2%B4necting-the-dots-modeling-functional-integration-in-biological-systems/bornagain77_{April 17, 2014
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Therefore, a naturalist who refutes design a priori is the very sad situation of believing that chance alone originated all the genes that originated that way, maybe most of the functional genes we know, if that is to be considered a general mechanism. That explanation makes no sense. I wish them good luck, because they will really need it.
They will say it does make sense. All naturalist believe the process is gradual but not all of them believe the only thing working is a natural selection of coding regions. Which is why I said that focusing all this attention on the neutral theory is a red herring. There is a second process, they say that is also working very gradually, and it not subject to natural selection till at some time it gets transcribed into some meaningful piece of RNA which either produces a new protein or some RNA sequence that has function. Natural selection only affects coding regions that produce some transcribed sequence that then affects a survival characteristic of the organism. So for millions of years or more a DNA sequence is changing and is not subject to natural selection. This ends up appearing to be a sudden event but actually will take millions of years. It is a long road to this functional sequence and and as I have just said during that time it was not subject to natural selection. The Brosius article was published in a tribute to Stephen Gould and it meant to establish why some aspects of evolution are sudden and others are not. He is giving a rationale for punctuated equilibrium. I think it is futile to say the process does not exist when it obviously does. I also think it is futile to claim it is design when it is apparently the end result of some process that appears randomly. (this process may in fact be the result of a very intricately designed process to effect exactly what they say happens) I believe the process that they describe will fall under its own weight because it is not robust enough to produce all the functional variation we see in biological species over the planet. So it here that the research should concentrate. Arbitrarily saying it is design or didn't happen is not going to get ID anywhere. I believe the best approach is to say it is interesting but extremely inadequate. I proposed very testable hypotheses to look at this issue which I believe would bury not only the Darwinian version of evolution but this form of punctuated equilibrium. I have not read any of the other recent comments so don't know if I am just repeating what others have said.jerry_{April 17, 2014
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There just isn’t enough time for unguided evolution to produce a protein coding gene from non-coding DNA sequences.
The referenced article undermines Behe's conclusions in the Edge of Evolution about 2 mutations. I have no idea of the mathematics used to justify this but they say they refute Behe. Now I don't see just how much they refute him. Do they just reduce the time for these mutations to occur so the time required is still out of reach for anything meaningful to happen or do they reduce it to small amounts of time. The condemnation is not as strong as one would expect if the second scenario took place.jerry_{April 17, 2014
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BA: Again, I don't understand. I said nothing about form and body plans. I just said that homology is best explai ed by common descent.gpuccio_{April 17, 2014
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Stephen Meyer - Functional Proteins And Information For Body Plans - video https://vimeo.com/91322260 Dr. Stephen Meyer comments at the end of the preceding video,,, ‘Now one more problem as far as the generation of information. It turns out that you don’t only need information to build genes and proteins, it turns out to build Body-Plans you need higher levels of information; Higher order assembly instructions. DNA codes for the building of proteins, but proteins must be arranged into distinctive circuitry to form distinctive cell types. Cell types have to be arranged into tissues. Tissues have to be arranged into organs. Organs and tissues must be specifically arranged to generate whole new Body-Plans, distinctive arrangements of those body parts. We now know that DNA alone is not responsible for those higher orders of organization. DNA codes for proteins, but by itself it does not insure that proteins, cell types, tissues, organs, will all be arranged in the body. And what that means is that the Body-Plan morphogenesis, as it is called, depends upon information that is not encoded on DNA. Which means you can mutate DNA indefinitely. 80 million years, 100 million years, til the cows come home. It doesn’t matter, because in the best case you are just going to find a new protein some place out there in that vast combinatorial sequence space. You are not, by mutating DNA alone, going to generate higher order structures that are necessary to building a body plan. So what we can conclude from that is that the neo-Darwinian mechanism is grossly inadequate to explain the origin of information necessary to build new genes and proteins, and it is also grossly inadequate to explain the origination of novel biological form.’ Stephen Meyer - (excerpt taken from Meyer/Sternberg vs. Shermer/Prothero debate - 2009) Darwin's Doubt narrated by Paul Giem - The Origin of Body Plans - video http://www.youtube.com/watch?list=PLHDSWJBW3DNUaMy2xdaup5ROw3u0_mK8t&v=rLl6wrqd1e0&feature=player_detailpage#t=290bornagain77_{April 17, 2014
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That comment from Dr. Walker reminds me of this comment from Dr. Hameroff:
“Now the world appears to be divided into two realms, described by two different sets of physical laws. The quantum (world),, which is immaterial, coexisting possibilities, non-local, unified, connected, has some ultimate truth although we don’t know what it is yet, deeper levels of reality, and in many senses ‘spirit-like’. The classical world, the (illusory) billiard ball universe that we (appear to) live in right now, but not so, is material, Newtonian, definite, macroscopic, local, predictable, disconnected, post-modern, and somewhat boring actually. Now, what is life? If you approach life from classical physics, you see that biology is a set of self-organizing functions. There is no secret to life. Brain activities are equivalent to computers, consciousness is a epi-phenomenal illusion with no causal power. That’s the party line in standard neuroscience and philosophy. Accordingly, Thomas Huxley said years ago, ‘We are merely conscious automaton,’ helpless spectators., That’s the story we get from classical physics approach to the brain. Now,, applying quantum physics to biology, first by Erwin Schrodinger,,, quantum features (of biology include), non-local entanglement, super-position, unity, quantum coherence, quantum information. A kind of quantum vitalism, may play key roles in biological function.,,,” Stuart Hameroff – Does Quantum Biology Support A Quantum Soul? – video https://vimeo.com/29895068
Moreover,,,
Quantum Information/Entanglement In DNA - Elisabeth Rieper - short video http://www.metacafe.com/watch/5936605/ Quantum entanglement between the electron clouds of nucleic acids in DNA - Elisabeth Rieper, Janet Anders and Vlatko Vedral - February 2011 http://arxiv.org/PS_cache/arxiv/pdf/1006/1006.4053v2.pdf
,,,Encoded ‘classical’ information such as what Dembski and Marks demonstrated the conservation of, and such as what we find encoded in computer programs, and yes, as we find encoded in DNA, is found to be a subset of ‘transcendent’ (beyond space and time) quantum entanglement/information by the following method:,,,
Quantum knowledge cools computers: New understanding of entropy – June 2011 Excerpt: No heat, even a cooling effect; In the case of perfect classical knowledge of a computer memory (zero entropy), deletion of the data requires in theory no energy at all. The researchers prove that “more than complete knowledge” from quantum entanglement with the memory (negative entropy) leads to deletion of the data being accompanied by removal of heat from the computer and its release as usable energy. This is the physical meaning of negative entropy. Renner emphasizes, however, “This doesn’t mean that we can develop a perpetual motion machine.” The data can only be deleted once, so there is no possibility to continue to generate energy. The process also destroys the entanglement, and it would take an input of energy to reset the system to its starting state. The equations are consistent with what’s known as the second law of thermodynamics: the idea that the entropy of the universe can never decrease. Vedral says “We’re working on the edge of the second law. If you go any further, you will break it.” http://www.sciencedaily.com/releases/2011/06/110601134300.htm
,,,This preceding research also provides solid falsification for the late Rolf Landauer’s decades old contention that the information encoded in a computer is merely physical (merely ‘emergent’ from a material basis) since he believed it always required energy to erase it; It is very interesting to note that quantum entanglement, which conclusively demonstrates that ‘information’ in its pure 'quantum form' is completely transcendent of any time and space constraints, should be found in molecular biology on such a massive scale, for how can the quantum entanglement 'effect' in biology possibly be explained by a material (matter/energy) 'cause' when the quantum entanglement 'effect' falsified material particles as its own 'causation' in the first place? (J. Bell, A. Aspect. A. Zeilinger) Appealing to the probability of various configurations of material particles, as Darwinism does, simply will not help since a timeless/spaceless cause must be supplied which is beyond the capacity of the material particles themselves to supply! To give a coherent explanation for an effect that is shown to be completely independent of any time and space constraints one is forced to appeal to a cause that is itself not limited to time and space! i.e. Put more simply, you cannot explain a effect by a cause that has been falsified by the very same effect you are seeking to explain! Improbability arguments of various 'special' configurations of material particles, which have been a staple of the arguments against neo-Darwinism, simply do not apply since the cause is not within the material particles in the first place!
Information and entropy – top-down or bottom-up development in living systems? A.C. McINTOSH - Dr Andy C. McIntosh is the Professor of Thermodynamics (the highest teaching/research rank in U.K. university hierarchy) Combustion Theory at the University of Leeds. Excerpt: This paper highlights the distinctive and non-material nature of information and its relationship with matter, energy and natural forces. It is proposed in conclusion that it is the non-material information (transcendent to the matter and energy) that is actually itself constraining the local thermodynamics to be in ordered disequilibrium and with specified raised free energy levels necessary for the molecular and cellular machinery to operate. http://journals.witpress.com/paperinfo.asp?pid=420
bornagain77_{April 17, 2014
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gpuccio, all I was pointing out is that your 'sequential' evidence for common descent is much weaker than you seem to realize. Here are a few more notes on the fact that 'form' is not reducible to sequential information as you seem to presuppose:
Extreme Genome Repair - 2009 Excerpt: If its naming had followed, rather than preceded, molecular analyses of its DNA, the extremophile bacterium Deinococcus radiodurans might have been called Lazarus. After shattering of its 3.2 Mb genome into 20–30 kb pieces by desiccation or a high dose of ionizing radiation, D. radiodurans miraculously reassembles its genome such that only 3 hr later fully reconstituted nonrearranged chromosomes are present, and the cells carry on, alive as normal.,,, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3319128/ An Electric Face: A Rendering Worth a Thousand Falsifications - September 2011 Excerpt: The video suggests that bioelectric signals presage the morphological development of the face. It also, in an instant, gives a peak at the phenomenal processes at work in biology. As the lead researcher said, “It’s a jaw dropper.” http://darwins-god.blogspot.com/2011/09/electric-face-rendering-worth-thousand.html Not in the Genes: Embryonic Electric Fields - Jonathan Wells - December 2011 Excerpt: although the molecular components of individual sodium-potassium channels may be encoded in DNA sequences, the three-dimensional arrangement of those channels -- which determines the form of the endogenous electric field -- constitutes an independent source of information in the developing embryo. http://www.evolutionnews.org/2011/12/not_in_the_gene054071.html Body Plans Are Not Mapped-Out by the DNA Jonathan Wells - video http://www.youtube.com/watch?v=meR8Hk5q_EM What Do Organisms Mean? Stephen L. Talbott - Winter 2011 Excerpt: Harvard biologist Richard Lewontin once described how you can excise the developing limb bud from an amphibian embryo, shake the cells loose from each other, allow them to reaggregate into a random lump, and then replace the lump in the embryo. A normal leg develops. Somehow the form of the limb as a whole is the ruling factor, redefining the parts according to the larger pattern. Lewontin went on to remark: "Unlike a machine whose totality is created by the juxtaposition of bits and pieces with different functions and properties, the bits and pieces of a developing organism seem to come into existence as a consequence of their spatial position at critical moments in the embryo’s development. Such an object is less like a machine than it is like a language whose elements... take unique meaning from their context.[3]",,, http://www.thenewatlantis.com/publications/what-do-organisms-mean If DNA really rules (morphology), why did THIS happen? - April 2014 Excerpt: Researchers implanted human embryonic neuronal cells into a mouse embryo. Mouse and human neurons have distinct morphologies (shapes). Because the human neurons feature human DNA, they should be easy to identify. Which raises a question: Would the human neurons implanted in developing mouse brain have a mouse or a human morphology? Well, the answer is, the human neurons had a mouse morphology. They could be distinguished from the mouse ones only by their human genetic markers. If DNA really ruled, we would expect a human morphology. https://uncommondescent.com/intelligent-design/if-dna-really-rules-why-did-this-happen/ Epigenetics and neuroplasticity: The case of the rewired ferrets - April 3, 2014 Excerpt: Like inventive electricians rewiring a house, scientists at the Massachusetts Institute of Technology have reconfigured newborn ferret brains so that the animals’ eyes are hooked up to brain regions where hearing normally develops. The surprising result is that the ferrets develop fully functioning visual pathways in the auditory portions of their brains. In other words, they see the world with brain tissue that was only thought capable of hearing sounds. https://uncommondescent.com/neuroscience/epigenetics-and-neuroplasticity-the-case-of-the-rewired-ferrets/ DNA doesn’t even tell teeth what they should look like - April 3, 2014 Excerpt: A friend writes to mention a mouse experiment where developing tooth buds were moved so that the incisors and the molars were switched. The tooth buds became the tooth appropriate to the switched location, not the original one, in direct contrast to what we would expect from a gene’centric view. https://uncommondescent.com/intelligent-design/dna-doesnt-even-tell-teeth-what-they-should-look-like/ “It was long believed that a protein molecule’s three-dimensional shape, on which its function depends, is uniquely determined by its amino acid sequence. But we now know that this is not always true – the rate at which a protein is synthesized, which depends on factors internal and external to the cell, affects the order in which its different portions fold. So even with the same sequence a given protein can have different shapes and functions. Furthermore, many proteins have no intrinsic shape, taking on different roles in different molecular contexts. So even though genes specify protein sequences they have only a tenuous (very weak or slight) influence over their functions. ,,,,So, to reiterate, the genes do not uniquely determine what is in the cell, but what is in the cell determines how the genes get used. Only if the pie were to rise up, take hold of the recipe book and rewrite the instructions for its own production, would this popular analogy for the role of genes be pertinent." Stuart A. Newman, Ph.D. – Professor of Cell Biology and Anatomy Origin of life: A problem in the origin of information - April 2014 Excerpt: A hallmark of life is the way information flows between different levels of organization. In non-living systems, information flows from the bottom up–the properties of the individual parts determine the fate of the system. But with living systems, that flow goes both ways. Not only genes dictate the nature of proteins which in turn affect the functioning of cells, tissues and organisms, but the behavior of proteins, cells, and organisms also control gene expression. This is what Walker calls “top-down control” or “top-down causation.” And to Walker, this transition–from information seeping upward only to information flowing both up and down–is the key to understanding life’s origins. Put differently, the blueprint for building an organism isn’t stored in its DNA only, but it’s distributed in the state of the entire system. Dr. Sara Walker https://uncommondescent.com/intelligent-design/origin-of-life-a-problem-in-the-origin-of-information/
bornagain77_{April 17, 2014
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gpuccio, all I was pointing out is that your 'sequential' evidence for common descent is much weaker than you seem to realize. Here are a few more notes on the fact that 'form' is not reducible to sequential information as you seem to presuppose:
Extreme Genome Repair - 2009 Excerpt: If its naming had followed, rather than preceded, molecular analyses of its DNA, the extremophile bacterium Deinococcus radiodurans might have been called Lazarus. After shattering of its 3.2 Mb genome into 20–30 kb pieces by desiccation or a high dose of ionizing radiation, D. radiodurans miraculously reassembles its genome such that only 3 hr later fully reconstituted nonrearranged chromosomes are present, and the cells carry on, alive as normal.,,, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3319128/ An Electric Face: A Rendering Worth a Thousand Falsifications - September 2011 Excerpt: The video suggests that bioelectric signals presage the morphological development of the face. It also, in an instant, gives a peak at the phenomenal processes at work in biology. As the lead researcher said, “It’s a jaw dropper.” https://www.youtube.com/watch?v=0VULjzX__OM http://darwins-god.blogspot.com/2011/09/electric-face-rendering-worth-thousand.html Not in the Genes: Embryonic Electric Fields - Jonathan Wells - December 2011 Excerpt: although the molecular components of individual sodium-potassium channels may be encoded in DNA sequences, the three-dimensional arrangement of those channels -- which determines the form of the endogenous electric field -- constitutes an independent source of information in the developing embryo. http://www.evolutionnews.org/2011/12/not_in_the_gene054071.html Body Plans Are Not Mapped-Out by the DNA Jonathan Wells - video http://www.youtube.com/watch?v=meR8Hk5q_EM What Do Organisms Mean? Stephen L. Talbott - Winter 2011 Excerpt: Harvard biologist Richard Lewontin once described how you can excise the developing limb bud from an amphibian embryo, shake the cells loose from each other, allow them to reaggregate into a random lump, and then replace the lump in the embryo. A normal leg develops. Somehow the form of the limb as a whole is the ruling factor, redefining the parts according to the larger pattern. Lewontin went on to remark: "Unlike a machine whose totality is created by the juxtaposition of bits and pieces with different functions and properties, the bits and pieces of a developing organism seem to come into existence as a consequence of their spatial position at critical moments in the embryo’s development. Such an object is less like a machine than it is like a language whose elements... take unique meaning from their context.[3]",,, http://www.thenewatlantis.com/publications/what-do-organisms-mean If DNA really rules (morphology), why did THIS happen? - April 2014 Excerpt: Researchers implanted human embryonic neuronal cells into a mouse embryo. Mouse and human neurons have distinct morphologies (shapes). Because the human neurons feature human DNA, they should be easy to identify. Which raises a question: Would the human neurons implanted in developing mouse brain have a mouse or a human morphology? Well, the answer is, the human neurons had a mouse morphology. They could be distinguished from the mouse ones only by their human genetic markers. If DNA really ruled, we would expect a human morphology. https://uncommondescent.com/intelligent-design/if-dna-really-rules-why-did-this-happen/ Epigenetics and neuroplasticity: The case of the rewired ferrets - April 3, 2014 Excerpt: Like inventive electricians rewiring a house, scientists at the Massachusetts Institute of Technology have reconfigured newborn ferret brains so that the animals’ eyes are hooked up to brain regions where hearing normally develops. The surprising result is that the ferrets develop fully functioning visual pathways in the auditory portions of their brains. In other words, they see the world with brain tissue that was only thought capable of hearing sounds. https://uncommondescent.com/neuroscience/epigenetics-and-neuroplasticity-the-case-of-the-rewired-ferrets/ DNA doesn’t even tell teeth what they should look like - April 3, 2014 Excerpt: A friend writes to mention a mouse experiment where developing tooth buds were moved so that the incisors and the molars were switched. The tooth buds became the tooth appropriate to the switched location, not the original one, in direct contrast to what we would expect from a gene’centric view. https://uncommondescent.com/intelligent-design/dna-doesnt-even-tell-teeth-what-they-should-look-like/ “It was long believed that a protein molecule’s three-dimensional shape, on which its function depends, is uniquely determined by its amino acid sequence. But we now know that this is not always true – the rate at which a protein is synthesized, which depends on factors internal and external to the cell, affects the order in which its different portions fold. So even with the same sequence a given protein can have different shapes and functions. Furthermore, many proteins have no intrinsic shape, taking on different roles in different molecular contexts. So even though genes specify protein sequences they have only a tenuous (very weak or slight) influence over their functions. ,,,,So, to reiterate, the genes do not uniquely determine what is in the cell, but what is in the cell determines how the genes get used. Only if the pie were to rise up, take hold of the recipe book and rewrite the instructions for its own production, would this popular analogy for the role of genes be pertinent." Stuart A. Newman, Ph.D. – Professor of Cell Biology and Anatomy Origin of life: A problem in the origin of information - April 2014 Excerpt: A hallmark of life is the way information flows between different levels of organization. In non-living systems, information flows from the bottom up–the properties of the individual parts determine the fate of the system. But with living systems, that flow goes both ways. Not only genes dictate the nature of proteins which in turn affect the functioning of cells, tissues and organisms, but the behavior of proteins, cells, and organisms also control gene expression. This is what Walker calls “top-down control” or “top-down causation.” And to Walker, this transition–from information seeping upward only to information flowing both up and down–is the key to understanding life’s origins. Put differently, the blueprint for building an organism isn’t stored in its DNA only, but it’s distributed in the state of the entire system. Dr. Sara Walker https://uncommondescent.com/intelligent-design/origin-of-life-a-problem-in-the-origin-of-information/
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There just isn't enough time for unguided evolution to produce a protein coding gene from non-coding DNA sequences. (see waiting for two mutations)Joe_{April 17, 2014
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BA: Ah, you say: "gradual ‘bottom up’ transition". I don't understand. The scenario I suggested is certainly "gradual", but why "bottom up"? A protein engineering through guided mutations, which is the only way a non coding sequence could be modeled to give a functional ORF, can be more or less gradual, but it is certainly "top down", and not "bottom up". Could you please explain your point?gpuccio_{April 17, 2014
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BA: I don't understand your problems. I just commented that the recent evidence for the derivation of some genes from non coding genes is, if it is confirmed, a strong argument for design. I remain of this idea. In that case, the design would be gradual, guiding the transformation of the sequence until it is ready to be used in the right context. I have never said: a) That this is the only way new genes are designed. In other contexts, the realization of the new gene could be realized in shorter times, for example through guided transposon activity. However, all these theories can be evaluated according to facts, as we gather more understanding of molecular data. For example, a "quicker" appearance of new protein coding genes would give us orphan genes without any homology with non coding sequences in previous species. b) That new orphan protein coding genes, however generated, can explain speciation. I absolutely agree with you that the most important part of new information in new species must be regulatory. Many times I have argued in that sense. That's why the study of transcriptomes and of various RNA regulatory forms is of primary importance. I believe that we have at present very scarce understanding of the regulatory procedures, least of all of how they could "evolve", or simply be generated. c) If your problem is simply that you don't accept common descent, that's fine for me. I respect your opinion, but I am afraid that we have to disagree on that point, at least until I change my mind because of new facts, or of some different interpretation of known facts that convinces me (which is perfectly possible, but has not yet happened) Finally, the ideas I have expressed here are mine and mine only. I am not sure what is VJ's position on these issues, but he can certainly speak for himself.gpuccio_{April 17, 2014
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"Where (chimps and humans) really differ, and they differ by orders of magnitude, is in the genomic architecture outside the protein coding regions. They are vastly, vastly, different.,, The structural, the organization, the regulatory sequences, the hierarchy for how things are organized and used are vastly different between a chimpanzee and a human being in their genomes." Raymond Bohlin (per Richard Sternberg) - 9:29 minute mark of video http://www.metacafe.com/watch/8593991/
Yet altering such regulatory sequences, involved in embryonic development, is found to be 'always catastrophically bad':
A Listener's Guide to the Meyer-Marshall Debate: Focus on the Origin of Information Question -Casey Luskin - December 4, 2013 Excerpt: "There is always an observable consequence if a dGRN (developmental gene regulatory network) subcircuit is interrupted. Since these consequences are always catastrophically bad, flexibility is minimal, and since the subcircuits are all interconnected, the whole network partakes of the quality that there is only one way for things to work. And indeed the embryos of each species develop in only one way." - Eric Davidson http://www.evolutionnews.org/2013/12/a_listeners_gui079811.html Darwin or Design? - Paul Nelson at Saddleback Church - Nov. 2012 - ontogenetic depth (excellent update) - video Text from one of the Saddleback slides: 1. Animal body plans are built in each generation by a stepwise process, from the fertilized egg to the many cells of the adult. The earliest stages in this process determine what follows. 2. Thus, to change -- that is, to evolve -- any body plan, mutations expressed early in development must occur, be viable, and be stably transmitted to offspring. 3. But such early-acting mutations of global effect are those least likely to be tolerated by the embryo. Losses of structures are the only exception to this otherwise universal generalization about animal development and evolution. Many species will tolerate phenotypic losses if their local (environmental) circumstances are favorable. Hence island or cave fauna often lose (for instance) wings or eyes. http://www.saddleback.com/mc/m/7ece8/
Yet, despite such a 'catastrophically bad constraint' for 'bottom up' mechanisms, and completely contrary to evolutionary thought, 'new' ORFan genes are found to be just as essential as 'old' genes in embryonic development:
Age doesn't matter: New genes are as essential as ancient ones - December 2010 Excerpt: "A new gene is as essential as any other gene; the importance of a gene is independent of its age," said Manyuan Long, PhD, Professor of Ecology & Evolution and senior author of the paper. "New genes are no longer just vinegar, they are now equally likely to be butter and bread. We were shocked." http://www.sciencedaily.com/releases/2010/12/101216142523.htm New genes in Drosophila quickly become essential. - December 2010 Excerpt: The proportion of genes that are essential is similar in every evolutionary age group that we examined. Under constitutive silencing of these young essential genes, lethality was high in the pupal (later) stage and (but was) also found in the larval (early) stages. http://www.sciencemag.org/content/330/6011/1682.abstract
Then there is the little problem that poly-functionality presents in terms of limiting any potential variability within a species' body plan.
Multiple Overlapping Genetic Codes Profoundly Reduce the Probability of Beneficial Mutation George Montañez 1, Robert J. Marks II 2, Jorge Fernandez 3 and John C. Sanford 4 - May 2013 http://www.worldscientific.com/doi/pdf/10.1142/9789814508728_0006
Then there is the little problem that multiple simultaneous 'top down' morphological alterations would be needed to accomplish such a transition:
"Humans and chimpanzees also differ significantly in many other anatomical respects, to the extent that nearly every bone in the body of a chimpanzee is readily distinguishable in shape or size from its human counterpart (38). Associated with these anatomical differences there are, of course, major differences in posture (see cover picture), mode of locomotion, methods of procuring food, and means of communication. Because of these major differences in anatomy and way of life, biologists place the two species not just in separate genera but in separate families (39). So it appears that molecular and organismal methods of evaluating the chimpanzee human difference yield quite different conclusions (40).” King and Wilson went on to suggest that the morphological and behavioral between humans and apes,, must be due to variations in their genomic regulatory systems. David Berlinski - The Devil's Delusion - Page 162&163 Evolution at Two Levels in Humans and Chimpanzees Mary-Claire King; A. C. Wilson - 1975 http://academic.reed.edu/biology/professors/srenn/pages/teaching/BIO431S05_2008/431S05_readings/431s05_examples/king_wilson_1975(classic).pdf K´necting The Dots: Modeling Functional Integration In Biological Systems - June 11, 2010 Excerpt: “If an engineer modifies the length of the piston rods in an internal combustion engine, but does not modify the crankshaft accordingly, the engine won’t start. Similarly, processes of development are so tightly integrated temporally and spatially that one change early in development will require a host of other coordinated changes in separate but functionally interrelated developmental processes downstream” (1) https://uncommondescent.com/intelligent-design/k%C2%B4necting-the-dots-modeling-functional-integration-in-biological-systems/
I'm sure I've missed other criticisms that could be leveled, but I think the point is clear that the gradual 'bottom up' transition, envisioned by you, and Dr. Torley, is not nearly so easy as you might believe.bornagain77_{April 17, 2014
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gpuccio you state:
In all the cases quoted here, we know that because of a strong homology between the new ORF (which is found only in the final species, for example in humans) and non coding sequences that are found in the precursor species (for example primates). A strong homology is something that cannot be denies. It is a fact which cannot be explained as causal, and requires explanation. Simple derivation of the new sequence from the old one is the best explanation,
So, correct me if I'm wrong, do you think God gradually transformed an ape into a human by some gradual 'bottom up' mechanism as Dr. Torley does??? If it is, that is a mighty large intellectual leap, hurdling over many empirical problems, you, and he, are making there!
Did (ORFan) Proteins Evolve From Long Non Coding RNAs? - Cornelius Hunter - Dec. 2012 Excerpt: The review paper did not actually explain how orphans could have evolved. Rather, it assumed they evolved and explained that, given that orphans evolved, how fast they must have evolved,,, http://darwins-god.blogspot.com/2012/12/did-proteins-evolve-from-long-non.html Orphan Genes (And the peer reviewed 'non-answer' from Darwinists) - lifepsy video http://www.youtube.com/watch?v=1Zz6vio_LhY
I certainly don't think you, or Dr. Torley, have such a firm foundation that you guys think that you do if you are making such a gargantuan leap to such a tentative conclusion for gradualness. For instance there is the little problem that you guys overlooked that genotypes (sequences) and phenotypes (body plans) do not map to one another,,
Not Junk After All—Conclusion - August 29, 2013 Excerpt: Many scientists have pointed out that the relationship between the genome and the organism — the genotype-phenotype mapping — cannot be reduced to a genetic program encoded in DNA sequences. Atlan and Koppel wrote in 1990 that advances in artificial intelligence showed that cellular operations are not controlled by a linear sequence of instructions in DNA but by a “distributed multilayer network” [150]. According to Denton and his co-workers, protein folding appears to involve formal causes that transcend material mechanisms [151], and according to Sternberg this is even more evident at higher levels of the genotype-phenotype mapping [152]. https://uncommondescent.com/junk-dna/open-mike-cornell-obi-conference-chapter-11-not-junk-after-all-conclusion/ With a Startling Candor, Oxford Scientist Admits a Gaping Hole in Evolutionary Theory - November 2011 Excerpt: As of now, we have no good theory of how to read [genetic] networks, how to model them mathematically or how one network meshes with another; worse, we have no obvious experimental lines of investigation for studying these areas. There is a great deal for systems biology to do in order to produce a full explanation of how genotypes generate phenotypes,,, http://www.evolutionnews.org/2011/11/with_a_startling_candor_oxford052821.html “Live memory” of the cell, the other hereditary memory of living systems - 2005 Excerpt: To understand this notion of “live memory”, its role and interactions with DNA must be resituated; indeed, operational information belongs as much to the cell body and to its cytoplasmic regulatory protein components and other endogenous or exogenous ligands as it does to the DNA database. We will see in Section 2, using examples from recent experiments in biology, the principal roles of “live memory” in relation to the four aspects of cellular identity, memory of form, hereditary transmission and also working memory. http://www.ncbi.nlm.nih.gov/pubmed/15888340
That is NOT a minor consideration! Then there is the little problem that sequences can be highly similar in widely divergent species
Kangaroo genes close to humans Excerpt: Australia's kangaroos are genetically similar to humans,,, "There are a few differences, we have a few more of this, a few less of that, but they are the same genes and a lot of them are in the same order," ,,,"We thought they'd be completely scrambled, but they're not. There is great chunks of the human genome which is sitting right there in the kangaroo genome," http://www.reuters.com/article/science%20News/idUSTRE4AH1P020081118 First Decoded Marsupial Genome Reveals "Junk DNA" Surprise - 2007 Excerpt: In particular, the study highlights the genetic differences between marsupials such as opossums and kangaroos and placental mammals like humans, mice, and dogs. ,,, The researchers were surprised to find that placental and marsupial mammals have largely the same set of genes for making proteins. Instead, much of the difference lies in the controls that turn genes on and off. http://news.nationalgeographic.com/news/2007/05/070510-opossum-dna.html Shark and human proteins “stunningly similar”; shark closer to human than to zebrafish - December 9, 2013 Excerpt: “We were very surprised to find, that for many categories of proteins, sharks share more similarities with humans than zebrafish,” Stanhope said. “Although sharks and bony fishes are not closely related, they are nonetheless both fish … while mammals have very different anatomies and physiologies. https://uncommondescent.com/intelligent-design/shark-and-human-proteins-stunningly-similar-shark-closer-to-human-than-to-zebrafish/
Then there is the little problem of widely divergent genetic regulatory sequences,
Evolution by Splicing – Comparing gene transcripts from different species reveals surprising splicing diversity. – Ruth Williams – December 20, 2012 Excerpt: A major question in vertebrate evolutionary biology is “how do physical and behavioral differences arise if we have a very similar set of genes to that of the mouse, chicken, or frog?”,,, A commonly discussed mechanism was variable levels of gene expression, but both Blencowe and Chris Burge,,, found that gene expression is relatively conserved among species. On the other hand, the papers show that most alternative splicing events differ widely between even closely related species. “The alternative splicing patterns are very different even between humans and chimpanzees,” said Blencowe.,,, http://www.the-scientist.com/?articles.view%2FarticleNo%2F33782%2Ftitle%2FEvolution-by-Splicing%2F
bornagain77_{April 17, 2014
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Pav: Please, have a look at the 3 papers kindly provided by Evolve at post #49. In the first (mouse gene) the gene is proved functional by a knockout experiment, and is expressed in the testis. In the second one (drosophila) the abstract says: "Comparative genomic analyses have revealed that genes may arise from ancestrally nongenic sequence. However, the origin and spread of these de novo genes within populations remain obscure. We identified 142 segregating and 106 fixed testis-expressed de novo genes in a population sample of Drosophila melanogaster. These genes appear to derive primarily from ancestral intergenic, unexpressed open reading frames, with natural selection playing a significant role in their spread. These results reveal a heretofore unappreciated dynamism of gene content." Emphasis mine. Please, note that NS is supposed to intervene only at the end, when the functional genes are already there. The third link is again about further research in drosophila, but unfortunately it does not give any details (it is not a paper, but only a short news).gpuccio_{April 16, 2014
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PaV: You ask: "Question: It is being repeated here that a portion of non-coding DNA somehow becomes a ‘gene.’ How do we know that?" In all the cases quoted here, we know that because of a strong homology between the new ORF (which is found only in the final species, for example in humans) and non coding sequences that are found in the precursor species (for example primates). A strong homology is something that cannot be denies. It is a fact which cannot be explained as causal, and requires explanation. Simple derivation of the new sequence from the old one is the best explanation, IMO (obviously, that tells nothing of the mechanism of variation which produced the non coding region and which transforms it into the final ORF by a few last mutations). For that, as I have argued, designed engineering is the best, indeed the only explanation available. In the paper we quoted about this scenario, such as this: http://genome.cshlp.org/content/19/10/1752.full.pdf and this: http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1002379#pgen-1002379-g002 (which was kindly provided by VJ on another thread) the general idea is that the new genes are probably coding and functional. And there is some good evidence of their expression. And, if you look at figure 2 of the second paper, you will see that they are preferentially expressed in the brain and in the testes, which is exactly what we would expect of new functional genes which contribute to speciation. I have not the references available now, but I think I remember a similar scenario is true on other species, probably drosophila, where new genes derived from non coding sequences have been found.gpuccio_{April 16, 2014
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jerry: Well, if you mean that naturalists will use that argument in their favor, then you are not wrong. I did not mean that. They will certainly do. They use anything they can in their favor. But, if you mean that there is any sense in the idea that the derivation of new genes from non coding regions already existing in other species is in favor of naturalism, then you are wrong. That's what I meant. So, it is up to you. You ask: "Common descent from what? Where did these coding sequences arise?" Well, it is simple. If a non coding region is in the chimp, and a (presumably) functional ORF arises from it in humans, usually with only a few mutations, that mean two things: 1) The human ORF derives from the non coding sequence in chimps. That is best explained if descent of humans from chimps is true. Therefore, it is evidence if favor of common descent. 2) The non coding sequence in chimps already had most of the sequence information that will enable it to be functional once it becomes an ORF in humans. Now, the simple point is that the non coding sequence in chimps (or any other precursor species) is not there from OOL. Whenever it originated, it originated by variation. And that variation is by definition "neutral", because it does not affect any function. Or, even if the non coding region were functional at other levels (for example, regulatory), and the variation that modifies it be negative, positive or neutral) that will be completely unrelated to the future ORF, which at present is not an ORF, is not translated and therefore is not visible to NS. So, what we have is variation which is neutral, or anyway unrelated to the "ORF to come", which builds in some way the correct sequence for the future functional protein, without any help from NS. Obviously, once the ORF is "completed", and in some lucky way it becomes translated, then NS can help fixing it. But that mean nothing. The role of NS in a classical darwinist scenario is to build gradually the sequence, not just to use it when it is ready. Now, the variation which builds the sequence before it becomes an ORF can only be: a) Random b) Designed There are no other alternatives, except maybe the "algorithmic adaptation" scenario, which is even more in favor of design, but is not very plausible as a general mechanism of new gene formation. Therefore, a naturalist who refutes design a priori is the very sad situation of believing that chance alone originated all the genes that originated that way, maybe most of the functional genes we know, if that is to be considered a general mechanism. That explanation makes no sense. I wish them good luck, because they will really need it.gpuccio_{April 16, 2014
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A question and a comment: Question: It is being repeated here that a portion of non-coding DNA somehow becomes a 'gene.' How do we know that? If the ORPHAN gene is NOT producing a protein---i.e., is not 'coding'---then how do we know it is NOW a 'gene'? Further, if we isolate such ORPHAN genes, then what is the mechanism of the isolation (I admit not having read the 2013 paper---I have absolutely NO time for this right now)? And, is it being said that the ORPHAN 'gene' comes from a "non-coding" portion of DNA because of sequence matching? I looked through the paper and saw no specific examples, but I'll presume that they do have such examples. ****************************** My comment is this: If there is a difference between humans and chimps, then it can't really be due to little, small differences in the genes that are basically shared between us. We've already shown that you're looking at probably a 1 amino acid difference between their genes and ours; and, this a.a. difference very likely is 'neutral.' So, if "de novo" genes are going to make the difference between being a chimp and being a human, then, logically, the genes should be expressed in the very earliest stages of development. If that is the case, then if we are examining chimps and humans that have already been born in determining what proteins are being produced, then these ORPHAN 'genes' will show that they have promoter regions and other regulatory regions, but will not produce anything. It seems logical that if you want to know something about these ORPHAN genes, then you're going to have to look to early development. And, of course, in the case of humans, this would be highly unethical. Nevertheless, if there are ORPHAN genes in other species, then the same logic should apply to them, and the activity of these ORPHAN genes can be studied in early embryological stages.PaV_{April 16, 2014
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you can maybe look at my posts #58, 72, 73 and 76 in VJ’s thread “When I am wrong”
Ok, I read them. I am not going to comment on your calculations. You do not seem to realize that you are preaching to the choir here. I as well aware of the mathematical improbability of generating a new protein. I would remove the word neutral from your discussions because by definition a non coding region is neither positive, negative or neutral. Only when it gets expressed will those characteristics be applicable. But what you are not explaining is where the various similar coding regions came from in the other primates. Rather then try to interpret your comments, I would ask you to try to explain it better. If you are going to appeal to common descent why do non-coding regions in precursor species suddenly become functional in humans. What is the origin of these precursor DNA sequences? People like Brosius will say it arose randomly through mutations and at some point a sub-population mutated further till it became functional. I have no idea what Allen MacNeill will say so you should ask him. I have asked him to comment but he comes here sporadically. I believe the debate will change when these testable hypothesis are researched. And every ORF is testable. It will take lots of time and money but each is getting more favorable each year.jerry_{April 16, 2014
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No, you are wrong.
Wrong about what? Based on lots of conversations/comments/writings in the past here and elsewhere, my statement is accurate.
That is simply the heart of a common descent scenario, which I fully accept.
Common descent from what? Where did these coding sequences arise?
No, you are wrong. That is not the heart of the naturalist theory.
I think you should ask Allen MacNeill about this. I have asked him to comment on this. It is how I read him and his past comments but I could be wrong. It is certainly how Brosius sounds and he was the lead author in the Vrba/Eldredge book highly recommended by MacNeill. There are many naturalist theories. Meyer covers most of them. So you will have to be specific about which one you are objecting to. I believe they all are deficient but I am just presenting what some would say. The example about human and primate coding regions supports their assertions.
The “non coding DNA” -> “functional ORF” scenario is wholly incompatible with NS.
They don't think so and I cannot see any reason why it would be so. NS just acts on variation and the theory in question is about new variation.
The only reasonable explanation for what we observe, and especially for functional proteins arising from non coding segments, is that they are engineered.
The naturalist certainly do not think so. I agree that design is the best explanation but have said they represent testable hypothesis that will solve the debate. I will read your other comments that you referenced on another thread later in the day when I have more time. But nothing that you said above here changes anything that I said. It seems to reinforce what I have said.jerry_{April 16, 2014
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jerry: Regarding the probabilistic powers of mere neutral variation, you can maybe look at my posts #58, 72, 73 and 76 in VJ’s thread “When I am wrong”, here: https://uncommondescent.com/intelligent-design/when-im-wrong/ I think they "address" in detail the idea you mention, ond of which, believe me, I, like many others, am fully aware.gpuccio_{April 16, 2014
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jerry: I am well aware that "the naturalist" and Allen ManNeill would not agree with me. Indeed, I don't agree with them. That's why I am a fully convinced IDist, and they are not. You say:
Maybe I read your post wrong but it said there was a coding region in humans which has similar but non-coding regions in other primates and this is heart of the naturalist theory.
. No, you are wrong. That is not the heart of the naturalist theory. That is simply the heart of a common descent scenario, which I fully accept. The "heart of the naturalist theory" is that the non coding regions in the primates evolved by mere chance, and that by mere chance they become ORFs and are translated as soon as they are functional. That is faith in magic. It is not science. The only reasonable explanation for what we observe, and especially for functional proteins arising from non coding segments, is that they are engineered. The only reasonable explanation is design. The "non coding DNA" -> "functional ORF" scenario is wholly incompatible with NS. It can rely only on mere chance. A "naturalistic" (non design) explanation of that scenario is pure folly.gpuccio_{April 16, 2014
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Two of the links above to Allen MacNeill's blog were broken. The links to his discussions on variation are: http://evolutionlist.blogspot.com/2007/06/what-is-engine-of-evolution.html http://evolutionlist.blogspot.com/2007/10/rm-ns-creationist-and-id-strawman.htmljerry_{April 16, 2014
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The derivation of functional protein coding genes from non coding regions is, as I have stated many times, the best argument for design and for guided variation.
I am not sure the naturalist would agree with you. If you can get the Brosius article, read it. He certainly would not. It is in a journal titled, Paleobiology (Paleobiology 31(sp5):1-16. 2005 ). http://www.bioone.org/doi/abs/10.1666/0094-8373%282005%29031%5B0001%3ADAEBAC%5D2.0.CO%3B2 If I was a theist evolutionist, I could claim that this is the process by which evolution can proceed to greater complexity over millions of years. And in that sense was design since it was built into the original cell machinery. But this is not design in the sense that Stephen Meyer is using the term whereby he believes there were insertions of information over time to direct evolution. The examples you listed in your post are just what I am talking about, where non coding regions somehow turn into functional proteins.
The problem, with MacNeill’s “engines of variation”, is simply that either they are guided (and therefore they are tools of design) or they are random, and therefore add nothing to random mutations.
I am not sure Allen MacNeill would agree with you nor would I except to say they were designed into the basic cell in such a way to produce new functional information de novo. If only a couple of MacNeill's engines of variation produce non coding regions which then could over time turn into functional information then that would support the naturalist point of view. I have said that this a way to test Axe's thesis that functional proteins are so rare that such a process could not hope to produce more than a few. Your example of the human protein forming this way may be counter to Axe's thesis. We would have to get more information on just what happened but it seemed to follow the pattern that I said must exist if this process is viable. Maybe I read your post wrong but it said there was a coding region in humans which has similar but non-coding regions in other primates and this is heart of the naturalist theory.
Here we have documented particular DNA sequence changes in the evolution of three human-specific ORFs and have demonstrated in each case that at least one critical mutation that enables the ORF is human-specific because an identical disabled state is found in chimp, gorilla, gibbon, and macaque. We cannot, at present, determine whether the ORF originated before or after expression was acquired because EST coverage is so low for chimp. However, such an analysis would not be informative in any case because we are sure that chimp cannot produce any of these proteins; so, irrespective of RNA expression, the protein-coding gene can only be present in human.
I have asked Allen MacNeill to have a dialogue on this and he said he was not against it but it may have to wait till a time he is less busy, maybe at the end of the school year. MacNeill has discussed this briefly in the past on this site. Here is the link: https://uncommondescent.com/intelligent-design/microbe-evolution-virtually-finished-25by-ago/ Search for both my name and MacNeill and you will find the discussion on this theory, five years ago. There were several others that participated in the discussion and like most threads there are sub-threads that have nothing to do with this concept. Here are two sample quotes from the thread: https://uncommondescent.com/intelligent-design/microbe-evolution-virtually-finished-25by-ago/#comment-306698
According to Darwin (and virtually all evolutionary biologists), natural selection has three prerequisites: 1) Variety (generated by the “engines of variation” 2) Heredity (mediated by the transfer of genetic material, either vertically – from parents to offspring – or horizontally – via viral transduction, retrotranscription, etc.) 3) Fecundity (reproduction, usually at a rate that exceeds replacement). Given these three prerequisites, the following outcome obtains: 4) Demography: some individuals survive and reproduce more often than others. Ergo, the heritable variations of such individuals become more common over time in populations of those organisms. Natural selection is synonymous with #4; it is an outcome of the three processes listed first, not a “mechanism” in and of itself. Ergo, the real dispute here is not over natural selection per se, but rather the properties and capabilities of the “engines of variation”. I have written extensively about these here: http://evolutionlist.blogspot......ution.html and here: http://evolutionlist.blogspot......awman.html Yes, natural selection (i.e. #4, above) is conservative not creative. It produces no new genetic nor phenotypic information, which is why Darwin eventually came to prefer the term “natural preservation” rather than “natural selection”. However, it is also abundantly clear that the “engines of variation” – that is, the processes the produce phenotypic variation among the members of populations of living organisms – are both extraordinarily creative and extraordinarily fecund. The real problem in biology is not producing new variation, but rather limiting the production of new variation to the point that the “engines of variation” do not cause the rapid disintegration of living systems. As just one example of this problem, the genetic elements known as transposons generate a huge amount of new genetic variation, much of which is either phenotypically neutral or deleterious to the organism. There are biochemical mechanisms by which cells can monitor the incidence of transposition in themselves, and limit its consequences (up to and including the active self-destruction of the cell via apoptosis). At the same time, there is very good evidence in the genomes of many organisms that retrotransposition events mediated by transposons have produced genetic changes that have resulted in increased survival and reproduction of the organisms in which such events have taken place. There is a large and growing literature on this phenomenon, all of which points to the inference that retrotransposition via transposons both creates new genetic and phenotypic variation, and that in some cases such variation can provide the raw material for evolutionary adaptations, which are preserved via natural selection. So, if you really want to find out where the “intelligent designer” might create new variations, you should follow the lead of Darwin’s good friend, Asa Gray, and look for the telltale evidence for such intervention in the “engines of variation”. Of course, you will have to show pretty conclusively, using empirical investigations and statistical analysis, that such “creation events” are not the result of purely natural, unguided processes. If you can do this, you will undoubtedly win a Nobel Prize and a Crafoord Prize (plus a MacArthur or two). Notice that this will involve looking carefully into the mechanisms by which new variations are produced, rather than pointing to the outcomes of such processes (i.e. natural selection) and simply asserting that “you can’t get here from there”. Simply asserting (without empirical evidence) that something can’t happen isn’t “doing science” at all. In fact, it’s doing just the opposite…
https://uncommondescent.com/intelligent-design/microbe-evolution-virtually-finished-25by-ago/#comment-306750
“repeat after me: no random process can be expected to create information placing well-designed structures in the right place at the right time.” This is not what they say. There is no right place and right time. They say random processes are busily creating changes to genomic parts that are not functional, maybe thousands of places in any one organism and this multiplied by the number of organisms represents a very large number of places where changes are being made. If just one of these places somehow turns into something that causes a morphological difference then it may now be added to the gene pool. And if this morphological change affects reproduction then it may be selected for or not depending upon the environment. And presto we have a new protein or some other form of control in the genome. There is no right time, right place or right combination. But eventually there will be a change that will affect the organisms, maybe in small ways or maybe in a much bigger way as a result of these random processes. This is the theory. Whether it ever happened or not is the question. Of course it probably happened a few times but how many and were they big enough changes to cause the formation of new complex capabilities. I doubt it because it would leave a forensic trail in the genome to look for but we do not see the examples. But this is the theory.
It is these ideas which have to be addressed. That they have been around here several years ago and yet most are not aware of them is something that should be corrected. This is very long and I hope there are no inconsistencies but if there are they should be corrected.jerry_{April 15, 2014
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