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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.
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.
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 [nofollow]http://www.sciencedaily.com/releases/2012/09/120905135010.htm [nofollow]
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.
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.
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.
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.
You have still not provided any empirically testable definition of your distinction between so-called "true" intelligence and so-called "metaphorical" intelligence.
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.
Quote from: Martin J Sallberg on 13/05/2013 13:12:19I 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?
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.
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).
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.
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?
Quote from: cheryl j on 16/05/2013 03:23:19Physiology 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.
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....
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.
Quote from: Martin J Sallberg on 21/05/2013 09:11:34You 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.
Quote from: cheryl j on 22/05/2013 17:32:52Yes, 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?
Quote from: cheryl j on 22/05/2013 17:08:30Can 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").
Quote from: Martin J Sallberg on 23/05/2013 09:11:58Quote from: cheryl j on 22/05/2013 17:32:52Yes, 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."
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 [nofollow]
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.