Naked Science Forum
Life Sciences => Plant Sciences, Zoology & Evolution => Topic started by: Martin J Sallberg on 05/05/2013 17:09:55
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The ENCODE project shows that most of the human genome is active. This contradicts the predictions of neo-Darwinism, that most DNA must be junk or else there would be too many lethal mutations to be manageable by natural selection. The attempts to explain it away as "noise" ignores the fact that reading DNA takes energy (the moving proteins on chromosomes, opening and closing the DNA spiral), which rules out large amounts of "noise" genome activity. There is also the missing inheritance, twin studies show far more heredity than can be accounted for by the part of the genome that neo-Darwinism accepts as functional (its official numbers is about 1% protein coding and 4% regulatory, giving a total of 5% functional). Remember that mutations involved in, say, alternative splicing could be fatal just as easily as those in protein coding.
This means that it is mathematically proven that there are too many fatal mutations for natural selection to clean up. According to conventional medicine, we should all be dead. This shows that there must be mechanisms for correcting genetic defects that are far more efficient than natural selection by death or sterility of whole individuals. Interestingly, the immune system picks the antibodies that gets the job done, and mass-replicates them. In other words, function sensitivity guiding molecular change. See also "Amoebas anticipate climate change". The study "Aneuploid neurons are functionally active and integrated into brain circuitry" shows genetic diversity between neurons in the same brain. Other studies show similar diversity among immune system cells. There is also evidence for exosomes transporting DNA between different cells in the body. So the correction may work by cells function-sensitively borrowing the genetics they need from other cells in the body. And there are enzymes that build and decompose DNA. DNA cannot even replicate itself independently (nor can RNA).
As for the question "where is the evidence for such corrections of known genetic diseases", consider that belief in genetic determinism may create a nocebo (destructive placebo) effect paralyzing the correction, and that only people who believe in some form of genetic determinism bother screen their own genomes for defects. This skews the statistics and may hide lots of cases. Also, since tissues and organs differ in what genes are expressed, actual corrections are most likely to produce genetic chimeras. Some modified cells would leak into other organs, of course, but to a lesser extent than in the relevant organ itself.
Furthermore, although natural selection theory can explain the evolution of proteins with new functions across neutral gaps by "sometimes something useful just happens", that theory is lacking in ability to explain compatibility as transmittors and receptors of independently evolved proteins. It is just like how the neo-Darwinists themselves dismiss the chances of extraterrestrials (if they exist) being able to interbreed with earthlings, and for the same reason: not expecting independent evolutions to produce compatible results.
So how can proteins act together as receptors and transmittors? It can be explained if mutations are synchronized to produce compatible results, and not random. This theory predicts that adaptation to things that disrupts the communication between receptors and transmittors (such as many poisons) should produce extremely rapid genetic change (synchronized transmittoreceptory saltations). This is supported by the fact that arsenic tolerant earthworms differ more genetically from ordinary earthworms than humans from mice, after just 170 years of arsenic pollution (reference: "DNA sequence variation and methylation in an arsenic tolerant earthworm population" by Mark Hodson).
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"This means that it is mathematically proven that there are too many fatal mutations for natural selection to clean up. "
In the same way that it can be mathematically proven that bumble bees can't fly.
There's obviously a flaw in the model.
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"This means that it is mathematically proven that there are too many fatal mutations for natural selection to clean up. "
In the same way that it can be mathematically proven that bumble bees can't fly.
There's obviously a flaw in the model.
No, it does not mean that there has to be a flaw in the model. Yes, the bumblebee example overlooked air vortexes, but bumblebee flight cannot be explained by simple above-and-below air pressure. There was something more efficient than traditional flight theory. Similarily, being alive must be due to genetic correction mechanisms more efficient than natural selection. I listed several candidates. Assuming that natural selection must be the only genetic correction mechanism is exactly as naive as assuming that above-and-below air pressure must be the only flight mechanism.
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The gene-centered theory of speciation has multiple flaws. If speciation happened by gradual accumulation of mutations, large populations with little genetic drift would spontaneously die out when their individual genetic diversity builds to levels that causes species barrier style sterility, and that does not pan out. Also, it is not possible to predict such barriers from the quantitative amount of genetic sequence difference. The theory of single key mutations causing incompatibility instead has the problem of how the first mutant should find a mate. So gene-centered theory cannot explain speciation. There must be factors that change genetics from outside the genome, factors that synchronizes mutations.
Also, a first sexually reproducing individual would only have its own clones to mate with, and that would give no advantage at all. It would, according to gene-centered randomness theory, take many generations to get any advantage out of it, so the origin and initial survival of sex remains unexplained.
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There is error correction in DNA replication that can repair most "errors". Having two chromosomes, many of the more important genes will have two copies, in which a mutation would be required in both gene copies to be fatal. The probability of receiving two spontaneous mutations in the same gene.
Both the haploid egg and the haploid sperm must be viable for fertilization to occur, and at least with the sperm, "survival of the fittest" begins early. Even though the sperm may not have a brain, at least the metabolic functions must be reasonably intact for it to be viable. Then the developing blastocyst and embryo also must be viable otherwise they will be spontaneously aborted.
Survival of the fittest in adults may also help select against harmful mutations.
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As far as how did sexual reproduction begin? Meiosis is a complex concept. It certainly did not just suddenly evolve overnight. Even bacteria have provisions for sharing genes through the use of plasmids and sampling environmental DNA. As multicellular organisms evolved, they would have needed a more stable method for swapping genes than just picking up environmental DNA.
Sexual reproduction may be little more than an extension of the plasmid concept. But, rather than just a small amount of plasmid DNA, essentially the entire genome becomes a type of plasmid (although, in this case, no longer circular). Anyway, it wouldn't be just one plant that suddenly invented sexual reproduction, but a long pathway eventually leading to a very precise gene sharing protocol between like organisms.
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There is error correction in DNA replication that can repair most "errors". Having two chromosomes, many of the more important genes will have two copies, in which a mutation would be required in both gene copies to be fatal. The probability of receiving two spontaneous mutations in the same gene.
If that was the case, then mainstream geneticists would not be claiming that most DNA must be junk to avoid too many lethal mutations. They are obviously referring to a too great risk of fatal dominant mutations spontaneously arising, making at least several per individual mathematically inevitable.
And why did you ignore both the examples of correction mechanisms vastly more efficient than natural selection, and the speciation problems?
And if sexual reproduction really is little more than an extension of the plasmid concept, that just supports what I said about eukaryotes adaptively doing horizontal gene transfer when they need it, just like bacteria (as if the empirical evidence was not enough, which it is).
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Some functions of non-protein coding DNA include physical separation of active genes (to protect them from shift mutations when there is an insertion and deletion) genetic switches, regulators of gene expression, operators, enhansers, silencers, promoters, teleomeres, etc. Noncoding DNA may also serve as the raw material for evolution, sometimes referred to as protogenes - in other words, organisms hang on to old, silenced genetic material "just in case."
Here are two interesting articles from Science Daily about recent discoveries of functions of non coding DNA:
http://www.sciencedaily.com/releases/2012/09/120905134912.htm
http://www.sciencedaily.com/releases/2012/09/120905135010.htm
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Some functions of non-protein coding DNA include physical separation of active genes (to protect them from shift mutations when there is an insertion and deletion) genetic switches, regulators of gene expression, operators, enhansers, silencers, promoters, teleomeres, etc. Noncoding DNA may also serve as the raw material for evolution, sometimes referred to as protogenes - in other words, organisms hang on to old, silenced genetic material "just in case."
Here are two interesting articles from Science Daily about recent discoveries of functions of non coding DNA:
http://www.sciencedaily.com/releases/2012/09/120905134912.htm
http://www.sciencedaily.com/releases/2012/09/120905135010.htm
Interesting possibilities. But nothing of it contradicts the principle that it must be kept healthy by something far more efficient than natural selection. For instance, protogenes could mutate into something coding for poison, among other possibilities.
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Okay, so what is more efficient than natural selection and how does it work?
Just so you know, I'm not being sarcastic or belittling when I say stuff like that. I'm just skeptical at times. And I just come here to learn new things, not convince anyone to believe what I believe. And I'm fine if someone corrects me if my facts are wrong or questions my conclusions. I'm cool with that.
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Okay, so what is more efficient than natural selection and how does it work?
Just so you know, I'm not being sarcastic or belittling when I say stuff like that. I'm just skeptical at times. And I just come here to learn new things, not convince anyone to believe what I believe. And I'm fine if someone corrects me if my facts are wrong or questions my conclusions. I'm cool with that.
I wrote about lots of things that are more efficient than natural selection in my original post. Genetic diversity between cells in the same body, horizontal gene transfer, function sensitivity feedbacks, enzymes building and decomposing DNA which cannot even replicate itself independently. And even if there was no known mechanism that was efficient enough, the math proving the inefficiency of anything known would still be valid. It would just have meant that "we do not yet know". Why always pretend to know it all?
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It might be more useful to take one of those items like horizontal gene transfer or function sensitivity feedbacks and discuss it in more detail.
I don't know if conventional genetics does claim to know it all. It has been successful in explaining or predicting many things, which is why researchers keep heading in that direction. When or if they hit a wall, they may need to take another direction.
The geneticist Ohno made the comment “It seems as though ‘junk DNA’ has become a legitimate jargon in a glossary of molecular biology. Considering the violent reactions this phrase provoked when it was first proposed in 1972, the aura of legitimacy it now enjoys is amusing, indeed.” A concept that was first opposed has become difficult to get rid of, now that some findings indicate that at least some of that junk is functional.
Mathematical models can be useful, but as you and several posters pointed out, it depends on what variables you throw into them and what you leave out, and what are known or unknown. You can end up with a bee that can't fly or one that can. Looking specifically at empirical evidence for individual biological mechanisms seems like a better bet to me in understanding how things in biology work. Theories are essentially models and also have limitations. But Koch's postulates of infectious disease, for example, didn't become "invalid" just because some diseases are not caused by microorganisms. They still work.
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It might be more useful to take one of those items like horizontal gene transfer or function sensitivity feedbacks and discuss it in more detail.
I don't know if conventional genetics does claim to know it all. It has been successful in explaining or predicting many things, which is why researchers keep heading in that direction. When or if they hit a wall, they may need to take another direction.
The geneticist Ohno made the comment “It seems as though ‘junk DNA’ has become a legitimate jargon in a glossary of molecular biology. Considering the violent reactions this phrase provoked when it was first proposed in 1972, the aura of legitimacy it now enjoys is amusing, indeed.” A concept that was first opposed has become difficult to get rid of, now that some findings indicate that at least some of that junk is functional.
Mathematical models can be useful, but as you and several posters pointed out, it depends on what variables you throw into them and what you leave out, and what are known or unknown. You can end up with a bee that can't fly or one that can. Looking specifically at empirical evidence for individual biological mechanisms seems like a better bet to me in understanding how things in biology work. Theories are essentially models and also have limitations. But Koch's postulates of infectious disease, for example, didn't become "invalid" just because some diseases are not caused by microorganisms. They still work.
Well, you can read "Amoebas Anticipate Climate Change" and some immunology to understand function-sensitive feedbacks. For horizontal gene transfer, it is all over the Internet. And for genetic diversity within the body, there is "Aneuploid neurons are functionally active and integrated into brain circuitry".
The idea that natural selection should be the primary corrector of genetic defects have undeniably hit a wall, at least if natural selection is defined as "purging of the gene pool through the death, sterility or other faliure of reproduction of whole individuals". The math shows that such is not efficient enough. And when it was shown that bumble bees can fly, it was by throwing in air vortexes, which is outside traditional flight theory. Likewise, survival with all that fallable DNA is only explainable by throwing in something outside natural selection. And lots of possibilities are there.
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Part of the definition of a living thing, whether it is a cell or an animal, is the ability to respond to stimuli, to adapt to environmental change to maintain internal homeostasis. Some of the things you describe are physiological events of this nature. I do not see how they contradict natural selection. It's almost like you're comparing apples and oranges.
I have taken some immunology courses. There is a tendency to anthropomorphize in discussing immunology, like when we talk about the immune system "learning" to recognize a microorganism and "remembering" it later. That's really just a metaphor for something that is much more mechanistic, involving antigens and antibodies that fit together like a lock and key. When a B lymphocyte receptor fits the antigen on a bacteria, it is stimulated to divide, making more, identical B lymphocytes with that same receptor. Some of the B lymphocytes remain in the body for months or even decades, and the immune response is faster and more intense the next time that bacteria appears.
Slime molds can do some pretty impressive things, like navigate mazes. I don't know how they can "anticipate", but Saigusa, (the author of the study you mention) "speculates that it instead depends on an internal mechanism of some kind, perhaps involving the perpetually pulsating gelatinous contents of its one cell, known as cytoplasm. The slime mold's membrane rhythmically constricts and relaxes, keeping the cytoplasm within flowing. When the amoeba's membrane encounters food, it pulsates more quickly and expands, allowing more cytoplasm to flow into that region; when it stumbles onto something aversive—such as bright light—its palpitations slow down and cytoplasm moves elsewhere. Somehow, the slime mold may be keeping track of its own rhythmic pulsing, creating a kind of simple clock that would allow it to anticipate future events" (from Scientific American Nov 2012)
I'm not sure what point you are using the Aneuploid study to support or refute. The study says that some brain cells have extra or missing copies of chromosomes. This sometimes happens in cell division, and is usually bad, and the researchers comment: "However, an unanswered question is whether these neurons represent functional rather than dying cells, with death being a common fate for aneuploid cells in other systems." But I guess, it does raise question of whether it could possibly serve any useful purpose if extra chromosome copies cranked up the transcription of certain proteins.
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Part of the definition of a living thing, whether it is a cell or an animal, is the ability to respond to stimuli, to adapt to environmental change to maintain internal homeostasis. Some of the things you describe are physiological events of this nature. I do not see how they contradict natural selection. It's almost like you're comparing apples and oranges.
I have taken some immunology courses. There is a tendency to anthropomorphize in discussing immunology, like when we talk about the immune system "learning" to recognize a microorganism and "remembering" it later. That's really just a metaphor for something that is much more mechanistic, involving antigens and antibodies that fit together like a lock and key. When a B lymphocyte receptor fits the antigen on a bacteria, it is stimulated to divide, making more, identical B lymphocytes with that same receptor. Some of the B lymphocytes remain in the body for months or even decades, and the immune response is faster and more intense the next time that bacteria appears.
Slime molds can do some pretty impressive things, like navigate mazes. I don't know how they can "anticipate", but Saigusa, (the author of the study you mention) "speculates that it instead depends on an internal mechanism of some kind, perhaps involving the perpetually pulsating gelatinous contents of its one cell, known as cytoplasm. The slime mold's membrane rhythmically constricts and relaxes, keeping the cytoplasm within flowing. When the amoeba's membrane encounters food, it pulsates more quickly and expands, allowing more cytoplasm to flow into that region; when it stumbles onto something aversive—such as bright light—its palpitations slow down and cytoplasm moves elsewhere. Somehow, the slime mold may be keeping track of its own rhythmic pulsing, creating a kind of simple clock that would allow it to anticipate future events" (from Scientific American Nov 2012)
I'm not sure what point you are using the Aneuploid study to support or refute. The study says that some brain cells have extra or missing copies of chromosomes. This sometimes happens in cell division, and is usually bad, and the researchers comment: "However, an unanswered question is whether these neurons represent functional rather than dying cells, with death being a common fate for aneuploid cells in other systems." But I guess, it does raise question of whether it could possibly serve any useful purpose if extra chromosome copies cranked up the transcription of certain proteins.
I did not "compare apples to oranges". I showed mathematically that natural selection is not efficient enough to do even a major fraction of the necessary adaptive evolution work.
What does your distinction between "intelligence" and "mechanism" mean? Saying that "intelligence is just a metaphor" when talking about cells implies a belief that thinking should require some magical ingredient. It is, in other words, scepticism or "caution" against so-called "anthropomorphization" that is dualistic. If you were not dualistic but still cling to your claim about metaphors, you would say that the description of humans as "intelligent" is also just a metaphor. I have never ever heard a concrete definition of what should separate so-called "true" intelligence from so-called "metaphorical" intelligence. It is just the same empirically unsupported distinctional frenzy as in saying that chimps do not really understand how tools work, just with the goalposts moved a bit down. And no matter how definitions are quibbled, the existence of cellular function sensitivity is undeniable, and that is all it takes to make molecular change non-random with respect to its function.
In the original post, I did not use the "Aneuploid neurons are functionally active and integrated into brain circuitry" in isolation. I supplemented it with the fact that in "Got fetal DNA on the brain?", it is shown that neurons dominated by the mother's own DNA sometimes contain partial elements of foreign DNA, in other words horizontal gene transfer between cells. The point is the combination of cellular function sensitivity, genetic variation between cells in the same body, horizontal gene transfer between them, and enzymes processing DNA.
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No I was not implying anything dualistic or magical at all about intelligence - just the opposite. It's a level of complexity. For example, Toshiyuki Nakagaki, another one of the researchers in that amoeba study "cautions that amoebas do not have a brain and that this is not an example of classic “Pavlovian” conditioned response behavior. Nevertheless, it might represent more evidence for a primitive sensitivity or “intelligence” based on the dynamic behavior of the tubular structures deployed by the amoeba." (Saigusa et al., Physical Review Letters;11 January 2008)
I am fine with using the word intelligence that way provided there is some understanding how things work on a cellular or molecular level, or an attempt to investigate it. (Our own memories or experience of time probably also involve chemical cycles in cells as well.) But there is a big difference in your saying previously saying that a lymphocyte "picks the antibodies that gets the job done" and the mechanism by which specific antibodies are actually produced. Metaphors or analogies are a convenient, shorter way of explaining something, but they also create confusion.
I would argue that you did not "show mathematically" that natural selection is too inefficient to cause adaptive changes in evolution. You just said it was.
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No I was not implying anything dualistic or magical at all about intelligence - just the opposite. It's a level of complexity. For example, Toshiyuki Nakagaki, another one of the researchers in that amoeba study "cautions that amoebas do not have a brain and that this is not an example of classic “Pavlovian” conditioned response behavior. Nevertheless, it might represent more evidence for a primitive sensitivity or “intelligence” based on the dynamic behavior of the tubular structures deployed by the amoeba." (Saigusa et al., Physical Review Letters;11 January 2008)
I am fine with using the word intelligence that way provided there is some understanding how things work on a cellular or molecular level, or an attempt to investigate it. (Our own memories or experience of time probably also involve chemical cycles in cells as well.) But there is a big difference in your saying previously saying that a lymphocyte "picks the antibodies that gets the job done" and the mechanism by which specific antibodies are actually produced. Metaphors or analogies are a convenient, shorter way of explaining something, but they also create confusion.
You have still not provided any empirically testable definition of your distinction between so-called "true" intelligence and so-called "metaphorical" intelligence.
I would argue that you did not "show mathematically" that natural selection is too inefficient to cause adaptive changes in evolution. You just said it was.
I never claimed that natural selection was "too inefficient to cause adaptive change in evolution". I just showed that natural selection is too inefficient to keep the human genome and other complex genomes viable, and I showed that mathematically. I never denied that it would be theoretically possible for natural selection to keep a very simple organism (maybe some of the world's smallest bacteria) viable.
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You have still not provided any empirically testable definition of your distinction between so-called "true" intelligence and so-called "metaphorical" intelligence.
This is a distinction you are making, not me. I didn't use the word metaphor to describe a type of intelligence. I said metaphorical language can cause confusion when discussing biology. As I said in my last post, there is nothing wrong with using the word "intelligence" as in "information processing" to describe what a brain does, or what the amoeba in the study did, as long as we are clear about the cell processes involved and they are not assumed to be identical in complexity or share all of the same properties. And I think that was the point Nakagaki made as well when he said the amoeba's behavior should not be confused with classic Pavlovian conditioning. However, I think one of the reasons such studies are done, is to study information processing at the most basic level, as it may shed light on how cells work in more complex structures like brains.
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I never claimed that natural selection was "too inefficient to cause adaptive change in evolution". I just showed that natural selection is too inefficient to keep the human genome and other complex genomes viable, and I showed that mathematically. I never denied that it would be theoretically possible for natural selection to keep a very simple organism (maybe some of the world's smallest bacteria) viable.
Natural selection and its affect on traits in large and small organisms can be demonstrated in nature and the laboratory. Whether it is mathematically feasible or not according to your model, it happens anyway, as surely as a bee flies. But we may simply have to agree to disagree about that.
What I would like, is a clearer explanation of is your alternative theory, as I do not see how the information in the studies you cited, or "the combination of cellular function sensitivity, genetic variation between cells in the same body, horizontal gene transfer between them, and enzymes processing DNA" leads to evolution or speciation.
I can't follow the logic of many of your posts. For example, you mention a study in which fetal cells have been found in the organs of some women. Ok, I too have read this. So in terms of your theory, this finding means.... what exactly?
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I never claimed that natural selection was "too inefficient to cause adaptive change in evolution". I just showed that natural selection is too inefficient to keep the human genome and other complex genomes viable, and I showed that mathematically. I never denied that it would be theoretically possible for natural selection to keep a very simple organism (maybe some of the world's smallest bacteria) viable.
Natural selection and its affect on traits in large and small organisms can be demonstrated in nature and the laboratory. Whether it is mathematically feasible or not according to your model, it happens anyway, as surely as a bee flies. But we may simply have to agree to disagree about that.
What I would like, is a clearer explanation of is your alternative theory, as I do not see how the information in the studies you cited, or "the combination of cellular function sensitivity, genetic variation between cells in the same body, horizontal gene transfer between them, and enzymes processing DNA" leads to evolution or speciation.
I can't follow the logic of many of your posts. For example, you mention a study in which fetal cells have been found in the organs of some women. Ok, I too have read this. So in terms of your theory, this finding means.... what exactly?
In the case of too inefficient natural selection, I am using the exact same math as mainstream geneticists use to claim that most DNA must be irrelevant, "junk" or else there would be too many lethal mutations. I shown in my original post evidence that it isn't junk, so therefore there really is too many lethal mutations for natural selection to clean up.
It was not only fetal cells found in some women's organs. It was also cells dominated by the woman's own DNA but with partial elements of fetal DNA in them. The study "Got fetal DNA on the brain?" explicitly mentions such cases. It is empirical evidence that horizontal gene transfer between cells happens. If it can happen between fetal cells and the mother's own cells, it can sure happen to mutations occured in a single or a few cells in the body spreading to other cells too.
The function-sensitivity of cells means that they can notice when something does not work, and that includes noticing when their own DNA does not do its job properly. I propose that triggers selective accepting of horizontal gene transfer from other cells in the body, borrowing mutations that makes the DNA capable of getting its job done. This has a crucial advantage over natural selection: the organism is not stuck with any fixed genetic deal, but can instead correct it function-sensitively. I treat multicellular organisms as bacterial colonies containing many bacteria in this model. Thus, the genetic diversity between cells in the same body provides raw material, but the non-random part is provided by the function-sensitivity guiding the acceptance or rejection of horizontal gene transfer, as opposed to blunt natural selection that would simply have killed the cells with the wrong genes.
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The function-sensitivity of cells means that they can notice when something does not work, and that includes noticing when their own DNA does not do its job properly. I propose that triggers selective accepting of horizontal gene transfer from other cells in the body, borrowing mutations that makes the DNA capable of getting its job done. This has a crucial advantage over natural selection: the organism is not stuck with any fixed genetic deal, but can instead correct it function-sensitively. I treat multicellular organisms as bacterial colonies containing many bacteria in this model. Thus, the genetic diversity between cells in the same body provides raw material, but the non-random part is provided by the function-sensitivity guiding the acceptance or rejection of horizontal gene transfer, as opposed to blunt natural selection that would simply have killed the cells with the wrong genes.
Thank you. That is much clearer. It would, however, involve some pretty complex feed back loops than what is normally found in physiology. In the endocrine system, hormones are the chemical messengers between glands, and between glands and cells in organs. In the simplest endocrine feedback loop, the decrease of a substance causes the release of a hormone from a gland, which circulates in the blood system. The hormone binds with a receptor on a target cell which makes that target cell do something, such as increase transcription of the substance that has decreased.
So, in your case, you would also need a chemical messenger that somehow signals the cell to borrow genetic material from other cells, assuming they have different genes, and assuming that these genes can produce the new product needed. Those genetically different cells have to come into contact some way, or the genetic material has to be ferried between them. In addition, your cell would have be sensitive to the absence of a material that it may never have produced or needed in the past, in order to meet some new biological need. It is hard to imagine the mechanism for a feedback loop like this, in terms of biochemistry.
In addition, you also have to consider that genes that code for something are often separated from regulatory genes, and you may have to excise and transport both from another cell's DNA, and then correctly reincorporate it. And since you do not have the vast amount of time involved in natural selection, you have to get this right pretty much on the first try to keep your organism functioning well.
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Thank you. That is much clearer. It would, however, involve some pretty complex feed back loops than what is normally found in physiology. In the endocrine system, hormones are the chemical messengers between glands, and between glands and cells in organs. In the simplest endocrine feedback loop, the decrease of a substance causes the release of a hormone from a gland, which circulates in the blood system. The hormone binds with a receptor on a target cell which makes that target cell do something, such as increase transcription of the substance that has decreased.
So, in your case, you would also need a chemical messenger that somehow signals the cell to borrow genetic material from other cells, assuming they have different genes, and assuming that these genes can produce the new product needed. Those genetically different cells have to come into contact some way, or the genetic material has to be ferried between them.
There are plenty of exosomes ferrying genetic material between cells all the time. They do not necessarily have to signal to the cell that have the gene.
In addition, your cell would have be sensitive to the absence of a material that it may never have produced or needed in the past, in order to meet some new biological need. It is hard to imagine the mechanism for a feedback loop like this, in terms of biochemistry.
No problem. The cell just senses that it is not all right, or that it does not get its job done properly. That triggers a search for something that works. It starts with a general "something does not work, something must be done", not a specific mechanism for one thing. If repairing was about fixed specific mechanisms, repair enzymes would have been useless since they would not have solved the problem, only moved it (about the same risk of the enzyme treating correct DNA as flawed and sabotaging it as a DNA without repairing enzymes breaking).
In addition, you also have to consider that genes that code for something are often separated from regulatory genes, and you may have to excise and transport both from another cell's DNA, and then correctly reincorporate it. And since you do not have the vast amount of time involved in natural selection, you have to get this right pretty much on the first try to keep your organism functioning well.
It is possible that cells, when packing exosomes, form them according to function-sensitivity rather than oiginal position of the material, placing the coding and the regulatory material in the same exosome. Another possibility is that the cell may only need to borrow the coding part and can tweak its own regulatory DNA (if your "problem" with coding and regulatory was taken seriously, it would have prevented natural selection as well, in exactly the same way as it would have prevented this other form of evolution). And considering the fact that red blood cells survive for many weeks, even a few months, with no DNA at all, nobody knows what you mean with "pretty much on the first try".
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No problem. The cell just senses that it is not all right, or that it does not get its job done properly. That triggers a search for something that works. It starts with a general "something does not work, something must be done", not a specific mechanism for one thing. If repairing was about fixed specific mechanisms, repair enzymes would have been useless since they would not have solved the problem, only moved it (about the same risk of the enzyme treating correct DNA as flawed and sabotaging it as a DNA without repairing enzymes breaking).
That is where you are absolutely wrong. Physiology is specific. The cell cannot sense that "something is just not right" or the "job is not getting done." Cells only react to specific chemicals. Regardless of the cause of dysfunction, whether someone is squeezing your throat with their hands and cutting off your air supply to the lungs, or you are drowning in a lake, or having a heart attack, or you are hemorrhaging, it has biochemical results - a group of cells in the aorta, the carotid arteries, and the brain react to rising levels of CO2 and hydrogen ions (acid) and decreased oxygen. These cells stimulate nerves that send impulses to the brain, which send other nerve impulses back that increase heart rate, the force of contractions of heart muscle cells, and increase respiration, constrict blood vessels to raise blood pressure. All of this happens because of specific chemical reactions - too much or too little of a certain molecule, and messages propagated by charged ions flowing in and out of cell membranes of nerve cells.
Repair mechanisms can work somewhat non specifically. A Natural killer T lymphocyte, for example, does not target specific foreign microbes it has receptors for. It combines with normal receptors on cells, and if a cell doesn't have them, (because it has been infected with a virus or is a cancer cell), it destroys that cell. But this process is still specific in the sense that it involves molecules fitting together in certain ways. What you are suggesting is quite different - the cell just somehow "knows" that something is wrong, and randomly looks for, or receives, genes from other body cells that might code for some molecule that will fix the problem. As far as mathematical models go, what are the odds of that happening?
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Physiology is specific. The cell cannot sense that "something is just not right" or the "job is not getting done." Cells only react to specific chemicals.
Wrong. If some important key function is malfunctioning, the indirect effects are spreading throughout the organism, inevitably leading to a sense that something is wrong. If the "standard" solutions do not work, it may well trigger a generalized search for a solution that does work.
Repair mechanisms can work somewhat non specifically. A Natural killer T lymphocyte, for example, does not target specific foreign microbes it has receptors for. It combines with normal receptors on cells, and if a cell doesn't have them, (because it has been infected with a virus or is a cancer cell), it destroys that cell. But this process is still specific in the sense that it involves molecules fitting together in certain ways. What you are suggesting is quite different - the cell just somehow "knows" that something is wrong, and randomly looks for, or receives, genes from other body cells that might code for some molecule that will fix the problem. As far as mathematical models go, what are the odds of that happening?
If cells relied on a sum of specific mechanisms, as you are claiming, that would have taken impossible amounts of space for fitting into a microscopic cell. General solution search is necessary to fit into the space. Indirect effects explains how cells can know that something is wrong.
Furthermore, how should fitting together of specific molecules have evolved? Granted, the neo-Darwinian explanation of protein evolution passing neutral gaps because they do no harm and something useful something happens holds insofar it only claims that something useful sometimes happens. But fitting together of, say, a transmittor substance and a receptor, is a completely different level. Think of what the neo-Darwinists themselves say about that other idea of compatibility between independently evolved things, i.e. their refutation of earthling/extraterrestrial hybridization (I am referring to probability of compatibility, not to the questions of whether or not extraterrestrials exist and if they can travel here, which is irrelevant). It is self-contradicting to apply such double standards.
You completely ignored, say, the possibility that a cell successfully solving a problem, be it through its own mutation or a borrowing, tags copies of it as useful so that other cells recognizes it. If the useful proteins leaking from other cells are attached to pieces of DNA or RNA, the cell may, when "feeling" that the protein solves its problem, adopt the piece of DNA or reverse-transcript the piece of RNA into its own genome and activate it.
Furthermore, you still do not provide one scrap of evidence of any flaws in the mathematical necessity of function-sensitive self-correction.
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Physiology is specific. The cell cannot sense that "something is just not right" or the "job is not getting done." Cells only react to specific chemicals.
Wrong. If some important key function is malfunctioning, the indirect effects are spreading throughout the organism, inevitably leading to a sense that something is wrong. If the "standard" solutions do not work, it may well trigger a generalized search for a solution that does work.
Can you give me any known examples of this kind of process in biology, where a cell somehow senses that it is malfunctioning in some general way and then "searches" for a novel substance, or genes that code for a novel substance, that it has never required in the past? Is it just a process of trial and error? The success of this would seem pretty mathematically improbable in the time span of a single organism's life, and even more improbable if the organism had to rely on this process to meet many physiological or environmental challenges. What is so wrong with natural selection and differential gene expression within the same cell? It seems so much simpler than the process you are suggesting and a lot more likely. You constantly bring up mutational load and errors, but the potential for error in what you are proposing seems a lot greater. It's as if each cell has to reinvent the wheel all the time. And since these are somatic cells, the body has no efficient way to pass on these biological solutions or innovations to the next generation.
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You completely ignored, say, the possibility that a cell successfully solving a problem, be it through its own mutation or a borrowing, tags copies of it as useful so that other cells recognizes it.....
Furthermore, you still do not provide one scrap of evidence of any flaws in the mathematical necessity of function-sensitive self-correction....
Martin, you're asking people to debate the likelihood, or the effectiveness, of things that do not, as far as anyone knows, actually exist. Yes, there is "function sensitive self correction" - all sorts of physiological feedback loops that maintain homeostasis - just not the kind you are proposing.
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Can you give me any known examples of this kind of process in biology, where a cell somehow senses that it is malfunctioning in some general way and then "searches" for a novel substance, or genes that code for a novel substance, that it has never required in the past?
Yes. The "hypermuation" in certain immune system cells actually specifically targets the relevant genes, which is unexplainable by the standard definition of hypermutation as "stress lowering the cell's ability to repair errors". The only reason why it is not flat-out called directed mutation is because it is non-deterministic and produces diversity, as opposed to the strawman used rhetorically by neo-Darwinists when they false-dichotomistically claim that "either you believe that mutations are completely random with respect to their results or you believe that cells have an omniscient noetic ability that produces a deterministic outcome" (sounds a lot like "you are either with us or against us").
Also, a 2006 follow-up of John Cairns 1988 study "The origin of mutants" confirmed that the frequency of the necessary mutation was millions of times higher than explainable by random chance (although not billions as originally proposed by Cairns).
Is it just a process of trial and error? The success of this would seem pretty mathematically improbable in the time span of a single organism's life, and even more improbable if the organism had to rely on this process to meet many physiological or environmental challenges.
Now you are naively assuming a single try at a time. Why should a cell not be able to try multiple mutations at once? The mutation the cell tries at once may be treated as a mutation group. The mutation groups that does not solve the cell's problem may simply be expelled, while the mutation group that gets the job done may later be pruned to eliminate meaningless genes that just happened to coincide in time with the necessary mutation.
What is so wrong with natural selection and differential gene expression within the same cell? It seems so much simpler than the process you are suggesting and a lot more likely. You constantly bring up mutational load and errors, but the potential for error in what you are proposing seems a lot greater.
Natural selection is mathematically proven to be vastly insufficient in efficiency. And the versatility of general correction means that it does not simply move the problem, but actually solves it, so the "potential for error" objection does not hold up.
It's as if each cell has to reinvent the wheel all the time.
Not true. Consider horizontal gene transfer.
And since these are somatic cells, the body has no efficient way to pass on these biological solutions or innovations to the next generation.
Bollocks. Just consider exosomes, symbiotic retroviruses and micro-RNA.
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You completely ignored, say, the possibility that a cell successfully solving a problem, be it through its own mutation or a borrowing, tags copies of it as useful so that other cells recognizes it.....
Furthermore, you still do not provide one scrap of evidence of any flaws in the mathematical necessity of function-sensitive self-correction....
Martin, you're asking people to debate the likelihood, or the effectiveness, of things that do not, as far as anyone knows, actually exist.
Exosomes spreading from cell to cell in the body are known to contain both DNA and proteins.
Yes, there is "function sensitive self correction" - all sorts of physiological feedback loops that maintain homeostasis - just not the kind you are proposing.
What do you believe is the principial difference, if any?
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Yes, there is "function sensitive self correction" - all sorts of physiological feedback loops that maintain homeostasis - just not the kind you are proposing.
What do you believe is the principial difference, if any?
The principal difference is that in physiological feed back loops, cells respond to changes in concentrations of specific molecules, increases in CO2, H+ concentration, increases or decreases in energy containing molecules, hormones, neurotransmitters. In your theory, you still need to identify what it is the cell is sensing, when it is sensing that "something is wrong."
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Can you give me any known examples of this kind of process in biology, where a cell somehow senses that it is malfunctioning in some general way and then "searches" for a novel substance, or genes that code for a novel substance, that it has never required in the past?
Yes. The "hypermuation" in certain immune system cells actually specifically targets the relevant genes, which is unexplainable by the standard definition of hypermutation as "stress lowering the cell's ability to repair errors". The only reason why it is not flat-out called directed mutation is because it is non-deterministic and produces diversity, as opposed to the strawman used rhetorically by neo-Darwinists when they false-dichotomistically claim that "either you believe that mutations are completely random with respect to their results or you believe that cells have an omniscient noetic ability that produces a deterministic outcome" (sounds a lot like "you are either with us or against us").
That is actually a pretty good example that would support certain aspects your theory (see link) but it does not involve cell to cell transfer of genes. And as the article points out, hyper mutability of white blood cells has a down side - like lymphoma and autoimmune diseases.
http://en.wikipedia.org/wiki/Somatic_hypermutation
Processes like these, or epigenetics, don't contradict or disprove conventional genetic processes like genetic change through recombination of genes during meiosis, sex, and natural selection. They just add to them. I still feel you are throwing the baby out with the bath water.
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Yes, there is "function sensitive self correction" - all sorts of physiological feedback loops that maintain homeostasis - just not the kind you are proposing.
What do you believe is the principial difference, if any?
The principal difference is that in physiological feed back loops, cells respond to changes in concentrations of specific molecules, increases in CO2, H+ concentration, increases or decreases in energy containing molecules, hormones, neurotransmitters. In your theory, you still need to identify what it is the cell is sensing, when it is sensing that "something is wrong."
Since vital functions in the cell affect everything else in the cell, the cell will inevitably "feel ill" even if it has no specific sensor for that particular error.
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That is actually a pretty good example that would support certain aspects your theory (see link) but it does not involve cell to cell transfer of genes.
But the principle can be combined with gene transfer between cells. If many cells need to correct the same error (as in either a genetic defect or an environmental change requiring new adaptation) the gene transfer between cells becomes very useful. As for the mechanism, I can imagine that since exosomes contain both proteins and DNA, when an exosome containing the proteins that helps the cell get the job done comes, the cell adopts the DNA content in the exosomes that happen to be within it. While that particular cell also retains many exosome DNAs that just happened to be within it, other cells will be hit by the exosomes in a different order and therefore not promote the same "freeloaders", so only the actually useful mutations are fileshared en masse. The quantity of that means that it will start leaking into other tissues including reproductive cells. Furthermore, the vast amounts of micro-RNA released when getting the production up and running floods the body, and is reverse-transcripted into DNA in reproductive cells by the vast amounts of symbiotic retroviruses that are empirically proven to be present in the reproductive organs.
And as the article points out, hyper mutability of white blood cells has a down side - like lymphoma and autoimmune diseases.
http://en.wikipedia.org/wiki/Somatic_hypermutation
Any process can have downsides when used improperly. There is no reason to assume that a more proper use of the same process should not be able to solve those problems. See thread "Body's defences not immune to brain control".
Processes like these, or epigenetics, don't contradict or disprove conventional genetic processes like genetic change through recombination of genes during meiosis, sex, and natural selection. They just add to them. I still feel you are throwing the baby out with the bath water.
I never claimed that there was no natural selection. I just shown that it was far to inefficient, and provided a more efficient form of evolution to do the bulk of the job. I agree that it would be theoretically possible (in mutation load terms) for conventional evolution to do the job alone on very simple bacteria, although I do not believe even them to be "stupid" enough to not use anything more efficient anyway, considering the general advantages of more efficient evolution.