your subconscious mind is a better decision maker than you are
I think that our conscious mind is more like a floating point processor than a cpu. It's very good at certain specialized problems, and very weak at most other things. Anybody who has tried to learn any kind of athletic skill knows that the conscious mind is simply lousy at controlling the body.
I also think that most of the time, our conscious mind is like the little kids you sometimes see in an arcade happily jerking the joystick around playing a video game--except that he never put in a quarter, and he's really "playing" the attract mode. I suspect that very often, what we perceive as our motivation is little more than an educated guess, made by a neural subsystem that has very little access to the ancient parts of our brain that actually motivate most of our actions.
Wegner makes the case that the conscious mind does not really make decisions, and that the experience of conscious decision making is an illusion, a kind of event tagging by which our brain distinguishes between those events that we are (probably) responsible for and those that are outside our control.
So... wild speculation (that such mechanisms could come from a Darwinian process) trumps experimental data (that such non-Darwinian mechanisms are the observable beneficial change agents) every time? At what point do speculations have to cash out for real evidence?
"Wild speculation" seems to be your term for the application of Occam's Razor--or as MD's put it, "when you hear hoofbeats, think horses before you think zebras." I find it particularly amusing that you reject known Darwinian mechanisms as "wild speculation," yet somehow do not regard it as speculative to hypothesize some sort of "mutational precognition" that cannot be explained by any known physical process.
Dvorak is the Rush Limbaugh of the computer industry. He has made a career out of being controversial, and it doesn't really matter that he is almost always wrong, because he is an entertainer, not a pundit.
But even a stopped clock is on time once in a while. And in this case, he may be close. Of course, there is zero chance that Apple is actually switching to Windows. On the other hand, Apple could do almost the same thing by supporting Windows applications under OS X. At one stroke, the major advantage of Windows--its large software library would be eliminated.
Not only would it be a great strategic move for Apple, but it is hard to see how they could pass up developing such a product, if only because they could give it such a great name.
After all, who could resist a product called AppleWINE?
Apple doesn't need to "win" a DRM battle--just introduce a bit of inconvenience to discourage the use of hacked versions for serious applications.
Officially opening up the Mac OS to cheap Windows machines would be a disaster for Apple. They'd be giving up the advantage of a small, known hardware base, which is a big part of OS X's reliability. They'd never be able to charge enough in the face of competition from Microsoft to make up for the costs of supporting the Mac OS X on all kinds of different PC hardware. And they'd still have to deal with competition from pirated copies.
A better direction for Apple is to support Windows applications under OS X using something like WINE.
It seems Apple just can't win this eternal struggle with the hackers
Of course not. And they probably don't expect to. Taking iTunes as an example, it is quite possible to strip off Apple's DRM, paying a small price in convenience in quality. Similarly, it will probably always be possible to get hold of cracked versions of the OS X, paying a small price in quality (lower reliability, lack of support).
Apple's DRM is little more than a "No trespassing" sign, less intended to actually keep people out than to put people on notice that they aren't welcome. In practice, a few hackers running OS X on non-Apple software is going to make little difference to Apple's business; hardly anybody with anything serious to do is going to be relying on an illicit copy of an OS. And some of those hackers will probably end up getting real Macs once they do have something serious to do.
The problem with Darwinism is that it is based around the idea that mutation cannot be directed. As Dembski has pointed out, the existance of mechanisms (or, as you say, constraints) that reliably produce beneficial mutations is evidence of design.
Actually, that is not true. There is no reason that evolution cannot favor a propensity for certain types of mutations over others, or mutations in particular regions. Even if the mechanisms that give rise to mutation are random, the outcome need not be. A particular codon mutates more easily to represent some amino acids than others. Repair mechanisms may be better at repairing some kinds of mutations than others. Transcription machinery may make some mistakes more often than others. Remember that modern organisms are those that have successfully evolved. So, for example, an organism that evolves a very effective means of getting rid of transposons may fail to evolve further, and be ultimately displaced by more mutable competitors when the environment changes.
A testable hypothesis put forth by Todd Wood (a YEC) is that transposons will be found to be activators of specific genes in response to specific stresses.
This is certainly a reasonable prediction from Darwinian theory. If a mechanism is available, it is almost inevitable that natural selection will find a use for it.
Aside, I don't see why heat must be an aggregate of unordered motion, because the case in which all the particles move in the same direction is still within the subset of possible aggregate motions called 'random motion.'
However, such cases occupy such a negligible volume of the state space that in practice they do not happen. This is the principle that underlies statistical thermodynamics. There is a finite probability that all of the molecules of air in your room will randomly collect under your desk, leaving you gasping for breath...but I wouldn't hold my breath waiting for it to happen.
This is an ID or Creationist view of evolution, not a neo-Darwinistic one.
Not particularly. All it suggests is that there is some additional constraint on the sequence of those genes. For example, in-frame function may depend upon a particular sequence of amino acids that is incompatible with the presence of an out-of-frame stop codon. Or the DNA sequence might be a binding site for some regulatory factor. Or there may be circumstances in which those genes are in fact transcribed out of frame and the gene product thus produced is advantageous.
What distinguishes the Darwinian interpretations from a Creationist or ID one is that they immediately suggests additional testable hypotheses.
can be found in the study of Gouldian Finches, which were selected for bigger beaks (more access to food) during times of hardship, but that selection relaxed again when the hardship eased. This is not theory, competent people watched it happen.
You are making the unlikely assumption that there is no selective advantage to smaller beakes that offsets the large beak advantage depending upon diet. It is easy to imagine how some food sources can be more accessible with a small beak and some can be more accessible with a large beak.
There is no mechanism in Darwinian theory to select against features that are merely useless, although in small populations they are at greater risk of being lost by genetic drift.
...since I already covered parallelism, and parallelism doesn't cure all -- there are many definitely sequential dependencies -- and parallelism doesn't necessarily help as much as one might hope, considering that natural selection operates against the development of useless features (towards homeostasis unless there's a clear and present benefit in the difference).
No it doesn't. There is no selection against useless features.
The example you chose also left out a serious number of necessary supporting changes. A fish eye would be an encumbrance (ie selected against) if not well attached, and not appropriately connected to a suitably-adapted brain.
Yes, one would expect that an eye would most likely arise from neuronal tissue. There are many ways this can happen, as fortuitous photosensitivity seems to be a relatively common phenomenon in neurotransmitter receptors. Depending upon the nature of that neuronal input, it is easy to see how beneficial behavioral patterns might occur. For example, a neuronal pathway previously associated with fleeing from predators could trigger this behavior patter, while a neuronal pathway associated with feeding behavior might trigger approach behavior. Even something as simple as increased or decreased locomotor activity could be beneficial in certain context. And once you have some kind of benefit, there is strong selection pressure to improve that function.
There's also that word "can"; even useless large morphological changes are very much in the minority, which of course leaves to facing the prospect of choosing way-more-than-2000 correct mutations this way from a field of squillions of wrong (useless or damaging) ones.
But in fact, the probability of each of those beneficial mutations is completely independent of the number of other mutations that might occur elsewhere. It's not like drawing one card out of a deck--each genetic locus mutates independently of the others. At any given genetic locus, there is a fairly limited number of mutations that might occur. After all, there are only 20 amino acids.
Actually, in both cases, it is suggested that the activity arose by mutation of an existing enzyme. If the parent enzyme was the same in both cases, as seems most likely, sequence similarity would be expected, reflecting a common evolutionary origin of that parent enzyme. This seems particularly likely, if as the second paper hypothesizes, all that is required is a frame shift mutation--which could occur at multiple places in the enzyme.
You miss the point. The search space is so large and the targets so few, that, if the mutations were non-directional (and non-directional mutation is the fundamental teaching of neo-Darwinism) then beneficial mutations would be so rare that there would hardly even be one in the history of the universe.
It sounds like you've never actually made mutations. What you discover when you do is that a large fraction of mutations turn out to be fairly benign and to make only subtle alterations in function, and it is not that hard to stumble onto mutations that enhance function in one way or another. In other words, far from their being only a few mutational paths whereby one protein can be altered to another while retaining essential function, there are often many--i.e. many regions of the search space are fairly smooth rather than chaotic. This is, of course, just what people like Stuart Kauffman predicted, based simply on the reasoning that since organisms evolved by natural selection, the search space has to be organized in such a way that natural selection constitutes an efficient optimization algorithm.
Theoretically, the search space for beneficial changes is so large, that without direction there would be no possibility of it occurring.
A more scientifically useful way of expressing this (because it offers testable hypotheses) is that for organisms to evolve, the interdependencies between genes have to be such that natural selection constitutes an efficient search strategy. This has been addressed by Stuart Kauffman, who has explored what the characteristics of organisms have to be for evolution to be possible--which seem to match pretty well with the characteristics of actual organisms.
I'm not sure what you are saying. I'm not saying that any specific mutation is _prevented_.
If nothing prevents them, then beneficial changes have to occur, pretty much demolishing the "mutations are degenerative" argument.
Is it possible that some species may have stored diversity, in the form of systems that have been evolutionarily selected such that particular genes are primed to mutate under stress in particular directions that have been evolutionarily productive in the past? This is certainly a possibility. Something along these lines happens within the body in the development of the immune system.
The generative mechanism is cell-directed transcription (as shown in the paper linked above). Mobile elements also seem to be involved, although the exact mechanism triggering and placing them is not known. But, contrary to the neo-Darwinian view of "parasitic elements", mobile elements are highly adaptive in helping organisms cope with stress in specific ways, and can even help restructure genomes.
Actually, while a Darwinian view allows for the existence of mobile elements that are parasitic, it also leads one to expect that there will be mobile elements that bear a more symbiotic relationship to the organism as a whole.
There is, however, a stupendous amount of ground to cover between a photosensitive patch and anything remotely resembling the eye (of an octopus, cat or person) and the very weakest of unintelligent forces working, hah, blindly along that path. Given a generational time of (reaches down, pulls out figure) one week, you only have about twenty (american) trillion generations to get the transition done in.
There are a few fundamental misunderstanding here. First, you are almost certainly greatly overestimating the number of changes required for evolution of the eye. Certain types of mutations, typically in developmental genes, can produce relatively large morphological changes. One somewhat simplistic model of eye evolution, simply assuming that mutations alter existing traits by 1%, within the range of variation, came up with 1829 mutations. Another error is imagining that these mutations have to occur in series. In fact, they occur in parallel across the population. The notion that the mutational distance between homologous genes is much larger than is consistent with rates of mutational change is an old objection that has pretty much collapsed now that the genomes are available and it is trivial to measure the actual mutational distances. The arguments that evolution of such features requires massive numbers of mutations turns out to be clearly wrong.
Oh, and you are also wrong in imagining that octopus eyes share the "unintelligent" backwards design of our retinas.
Even today, there are plenty of organisms that get along fine with just eyespots. And there are many ways in which small mutational changes can improve the function of an eyespot. For example, an eyespot in a pit will have directionality. Pit vipers make use of infrared-sensitive eyespots that work in this manner and supplement their regular eyes.
Yes and no. Heterozygous fractionation can cause phenotypic variation.
I am referring to genomic variation.
The idea that these differences are the results of accumulation of small changes is a presumption, not a result.
No, this is a result. All of the difference between species observed to date are the result of multiple changes of the sort that arise by mutation.
The changes that result from random mutations are degenerative, while adaptive mutations are beneficial.
This is nonsensical. A change is neither degenerative nor beneficial. It is just a change. Whether it is disadvantageous or beneficial depends upon environmental context, and the same alteration may be disadvantageous in one context and advantageous in another. Moreover, it would be impossible for all random changes to be disadvantageous, because random changes will necessarily produce some beneficial alterations. The only way to avoid this would be for mutation to be nonrandom. There is no known or imaginable mechanism to prevent mutations from producing the kinds of genomic changes from occurring that have been shown to underlie all species differences--and indeed, these genomic differences are of exactly the same kind that occur by mutation.
Actually, they assumed that, simply because the sequences were similar. However, that is a presumption, not the result of analysis. I think others disagree, as it has been shown to have come into both populations independently.
Do you have a reference? In any case, that is not inconsistent with horizontal gene transfer, because both could have received it from a 3rd source.
_Most_ of the variation that takes place is the result of Mendellian inheritance, which, by the way, was discovered by a creationist (who used it to argue _against_ transformism).
Mendelian inheritance is incapable of generating variation, it merely reshuffles the variation that already exists. Variation arises by mutation. Darwin recognized that for his theory to work, some method of generating new variation had to exist. This prediction was subsequently confirmed by the discovery of mutation, one of the most dramatic confirmations of a theory in the history of science. Although Darwin also knew nothing of Mendelian genetics, he predicted (because his theory required it) that there had to be some mechanism of passing traits down undiluted from generation to generation, so the discovery of genes is another remarkable confirmation of the predictions of evolutionary theory.
Please tell me what the evidence is that (a) everything shares a common ancestor, and that (b) random mutation + natural selection is sufficient for creating the diversity that exists today from that common ancestor.
Many species genomes have been sequenced, confirming the prediction of evolutionary theory that all differences between species are due to an accumulation of small changes at the genetic level--changes identical to those that have been demonstrated to arise by random mutation. This is another striking confirmation. The fact that predictions of a theory that predated knowledge of DNA are still being confirmed by molecular biology is a major reason why evolutionary theory is accepted by virtually all biological researchers.
The eyeballs halfway between man and fly must have been a wonder to behold.
Now that is pretty foolish, considering that the eyes of flies and man are thought to have evolved independently. So the closest common ancestor almost certainly didn't have anything resembling an eyeball--perhaps just a photosensitive patch of skin.
You can find the same kind of homologies in 6-aminohexanoate-cyclic-dimer hydrolase [pubmedcentral.gov] in Flavobacterium and Psedomonas, despite the fact that we have _observed_ their appearance as separate occurrences.
That's not what the article you cite says--in fact, it says the opposite, that the similarity of sequences reflects a relatively recent common ancestral sequence, more recent than other genes of the bacteria in question, consistent with horizontal gene transfer, which is established to be relatively common in bacteria.
That absolutely has everything to do with embryonic development which is known to mirror vertebrate evolution, at least to those who follow science
Uh, no. This is an old notion that was long ago abandoned. See Gould's "Ontogeny & Phylogeny" for a cogent account of the history of this idea and its modern status. To summarize, the modern view is that embryonic development does not mirror vertebrate evolution (nor is their any reason why it should), but does preserve some aspects of the embryonic development of our common ancestors with other vertebrates. This is a somewhat subtle but important distinction. It is worth noting that many aspect of embryonic development do not make any sense at all other than in light of a common ancestry for all vertebrates.
If I were asked to guess what embryonic tissue shark's electroreceptors came from, my first guess would be neural crest. After all, this is the tissue that gives rise to electrically active tissues like nerve and muscle, which have receptors that do indeed "sense" electrical fields. This is not to allow the animal to sense electrical fields in its environment, but simply the way nerve conduction and muscle contraction work--a change in electrical field (typically produced by a chemically activated ion gate in a membrane) is "sensed" by a voltage-gated ion channel that responds by opening up additional channels, further altering the electric field, which stimulates other voltage-gated ion channels, and so forth. It is easy to see how such a process could be evolutionarily adapted for sensory purposes, just as fish that generate strong electric fields, such as Torpedo (the electric ray) do so with tissues that are evolutionarily derived from muscle.
So basically, all this is saying is that we and sharks have a common ancestor and as a result share similarities in the development of nervous tissue (which we knew already), and that sharks' electro receptors develop from the tissue that any biologist would identify as the "usual suspect."
Somehow, tens of millions of other customers seem to handle these allegedly defective cups without incident.
And doubtless tens of millions of people drive intoxicated each year without incident. So does that mean that you shouldn't be liable if you hurt somebody while driving drunk? Nobody really knows the incidence of burns from styrofoam cups, but considering that I have seen it happen multiple times, I don't believe that it is all that rare (although injuries this severe are doubtless uncommon). I've never known anybody to complain about it, much less sue, so the 700 complaints that McDonalds had received were doubtless a small fraction of the total.
From the point of view of liability, it was a predictable hazard that McDonalds was aware of, and that could have been avoided by a number of measures, such as cooler coffee, cups better suited to serving very hot liquids, or putting cream and sugar in before serving. It is hardly surprising that the jury found that McDonalds was at fault.
The cup didn't fail. She took the top off the cup, and spilled the contents. If the cup had melted or something, you'd have a point, but it didn't, so you don't.
What happens is that the styrofoam cup gets soft, but it holds its shape because it is stabilized by the stiff plastic cover. The cover is tight, so you need to hold the cup firmly to get it off. It is easy to squeeze a bit too hard, but you don't realize it because of the cover stabilizing the cup. When the cover comes off, that stabilization is suddenly lost, the sides of the softened styrofoam cup collapse from the pressure, and the liquid spills out. I've seen this happen to people dozens of times. It's annoying and sometimes painful when it happens to somebody seated at a table, but it usually doesn't do any real damage because the liquid quickly runs off their hand on to the table. But if you are sitting in a car, the scalding coffee ends up in your lap.
Basically, styrofoam cups are not suitable for serving coffee at the "proper" temperature. And serving it that way to somebody in an automobile is grossly irresponsible.
Since you are interested in context, you do realize that the plaintiff was 81 years old, don't you? You do realize that a coffee spill might affect an 81-year-old much more harshly than a healthy 30-year-old male. You do realize that placing a hot cup of coffee between you legs in a moving car might be contrued as a much more risky behavior for an elderly lady than a young person.
Now you are perpetuating a myth. The spill did not happen in a moving car. The accident occurred when the car was parked. I've seen how easily this can happen with styrofoam cups and hot liquids. The cup becomes very soft but this is not obvious because it is stabilized by the plastic lid. Often the lid is tight, and it is difficult to get the lid off. It is easy to squeeze the softened cup a bit too hard, and when the lid pops off the cup basically collapses. To make it worse, the insulating properties of the styrofoam maintain the coffee at a scalding temperature much longer than would be the case with a ceramic or cardboard cup. If a cup collapses at a table, you get a painful but not too damaging burn to your hand, because the scalding liquid runs right off--a little ice right away and it might not even blister. If it happens in a car, moving or not, you are likely to end up with a bad groin burn. Mcdonalds could have avoided the hazard either by reducing the temperature of the coffee or by using a more suitable cup, such as cardboard with an insulating sleeve.
Slashdot Mirror
your subconscious mind is a better decision maker than you are
I think that our conscious mind is more like a floating point processor than a cpu. It's very good at certain specialized problems, and very weak at most other things. Anybody who has tried to learn any kind of athletic skill knows that the conscious mind is simply lousy at controlling the body.
I also think that most of the time, our conscious mind is like the little kids you sometimes see in an arcade happily jerking the joystick around playing a video game--except that he never put in a quarter, and he's really "playing" the attract mode. I suspect that very often, what we perceive as our motivation is little more than an educated guess, made by a neural subsystem that has very little access to the ancient parts of our brain that actually motivate most of our actions.
Wegner makes the case that the conscious mind does not really make decisions, and that the experience of conscious decision making is an illusion, a kind of event tagging by which our brain distinguishes between those events that we are (probably) responsible for and those that are outside our control.
So... wild speculation (that such mechanisms could come from a Darwinian process) trumps experimental data (that such non-Darwinian mechanisms are the observable beneficial change agents) every time? At what point do speculations have to cash out for real evidence?
"Wild speculation" seems to be your term for the application of Occam's Razor--or as MD's put it, "when you hear hoofbeats, think horses before you think zebras." I find it particularly amusing that you reject known Darwinian mechanisms as "wild speculation," yet somehow do not regard it as speculative to hypothesize some sort of "mutational precognition" that cannot be explained by any known physical process.
Dvorak is the Rush Limbaugh of the computer industry. He has made a career out of being controversial, and it doesn't really matter that he is almost always wrong, because he is an entertainer, not a pundit.
But even a stopped clock is on time once in a while. And in this case, he may be close. Of course, there is zero chance that Apple is actually switching to Windows. On the other hand, Apple could do almost the same thing by supporting Windows applications under OS X. At one stroke, the major advantage of Windows--its large software library would be eliminated.
Not only would it be a great strategic move for Apple, but it is hard to see how they could pass up developing such a product, if only because they could give it such a great name.
After all, who could resist a product called AppleWINE?
Apple doesn't need to "win" a DRM battle--just introduce a bit of inconvenience to discourage the use of hacked versions for serious applications.
Officially opening up the Mac OS to cheap Windows machines would be a disaster for Apple. They'd be giving up the advantage of a small, known hardware base, which is a big part of OS X's reliability. They'd never be able to charge enough in the face of competition from Microsoft to make up for the costs of supporting the Mac OS X on all kinds of different PC hardware. And they'd still have to deal with competition from pirated copies.
A better direction for Apple is to support Windows applications under OS X using something like WINE.
It seems Apple just can't win this eternal struggle with the hackers
Of course not. And they probably don't expect to. Taking iTunes as an example, it is quite possible to strip off Apple's DRM, paying a small price in convenience in quality. Similarly, it will probably always be possible to get hold of cracked versions of the OS X, paying a small price in quality (lower reliability, lack of support).
Apple's DRM is little more than a "No trespassing" sign, less intended to actually keep people out than to put people on notice that they aren't welcome. In practice, a few hackers running OS X on non-Apple software is going to make little difference to Apple's business; hardly anybody with anything serious to do is going to be relying on an illicit copy of an OS. And some of those hackers will probably end up getting real Macs once they do have something serious to do.
The problem with Darwinism is that it is based around the idea that mutation cannot be directed. As Dembski has pointed out, the existance of mechanisms (or, as you say, constraints) that reliably produce beneficial mutations is evidence of design.
Actually, that is not true. There is no reason that evolution cannot favor a propensity for certain types of mutations over others, or mutations in particular regions. Even if the mechanisms that give rise to mutation are random, the outcome need not be. A particular codon mutates more easily to represent some amino acids than others. Repair mechanisms may be better at repairing some kinds of mutations than others. Transcription machinery may make some mistakes more often than others. Remember that modern organisms are those that have successfully evolved. So, for example, an organism that evolves a very effective means of getting rid of transposons may fail to evolve further, and be ultimately displaced by more mutable competitors when the environment changes.
A testable hypothesis put forth by Todd Wood (a YEC) is that transposons will be found to be activators of specific genes in response to specific stresses.
This is certainly a reasonable prediction from Darwinian theory. If a mechanism is available, it is almost inevitable that natural selection will find a use for it.
Aside, I don't see why heat must be an aggregate of unordered motion, because the case in which all the particles move in the same direction is still within the subset of possible aggregate motions called 'random motion.'
However, such cases occupy such a negligible volume of the state space that in practice they do not happen. This is the principle that underlies statistical thermodynamics. There is a finite probability that all of the molecules of air in your room will randomly collect under your desk, leaving you gasping for breath...but I wouldn't hold my breath waiting for it to happen.
This is an ID or Creationist view of evolution, not a neo-Darwinistic one.
Not particularly. All it suggests is that there is some additional constraint on the sequence of those genes. For example, in-frame function may depend upon a particular sequence of amino acids that is incompatible with the presence of an out-of-frame stop codon. Or the DNA sequence might be a binding site for some regulatory factor. Or there may be circumstances in which those genes are in fact transcribed out of frame and the gene product thus produced is advantageous.
What distinguishes the Darwinian interpretations from a Creationist or ID one is that they immediately suggests additional testable hypotheses.
can be found in the study of Gouldian Finches, which were selected for bigger beaks (more access to food) during times of hardship, but that selection relaxed again when the hardship eased. This is not theory, competent people watched it happen.
You are making the unlikely assumption that there is no selective advantage to smaller beakes that offsets the large beak advantage depending upon diet. It is easy to imagine how some food sources can be more accessible with a small beak and some can be more accessible with a large beak.
There is no mechanism in Darwinian theory to select against features that are merely useless, although in small populations they are at greater risk of being lost by genetic drift.
...since I already covered parallelism, and parallelism doesn't cure all -- there are many definitely sequential dependencies -- and parallelism doesn't necessarily help as much as one might hope, considering that natural selection operates against the development of useless features (towards homeostasis unless there's a clear and present benefit in the difference).
No it doesn't. There is no selection against useless features.
The example you chose also left out a serious number of necessary supporting changes. A fish eye would be an encumbrance (ie selected against) if not well attached, and not appropriately connected to a suitably-adapted brain.
Yes, one would expect that an eye would most likely arise from neuronal tissue. There are many ways this can happen, as fortuitous photosensitivity seems to be a relatively common phenomenon in neurotransmitter receptors. Depending upon the nature of that neuronal input, it is easy to see how beneficial behavioral patterns might occur. For example, a neuronal pathway previously associated with fleeing from predators could trigger this behavior patter, while a neuronal pathway associated with feeding behavior might trigger approach behavior. Even something as simple as increased or decreased locomotor activity could be beneficial in certain context. And once you have some kind of benefit, there is strong selection pressure to improve that function.
There's also that word "can"; even useless large morphological changes are very much in the minority, which of course leaves to facing the prospect of choosing way-more-than-2000 correct mutations this way from a field of squillions of wrong (useless or damaging) ones.
But in fact, the probability of each of those beneficial mutations is completely independent of the number of other mutations that might occur elsewhere. It's not like drawing one card out of a deck--each genetic locus mutates independently of the others. At any given genetic locus, there is a fairly limited number of mutations that might occur. After all, there are only 20 amino acids.
Actually, in both cases, it is suggested that the activity arose by mutation of an existing enzyme. If the parent enzyme was the same in both cases, as seems most likely, sequence similarity would be expected, reflecting a common evolutionary origin of that parent enzyme. This seems particularly likely, if as the second paper hypothesizes, all that is required is a frame shift mutation--which could occur at multiple places in the enzyme.
You miss the point. The search space is so large and the targets so few, that, if the mutations were non-directional (and non-directional mutation is the fundamental teaching of neo-Darwinism) then beneficial mutations would be so rare that there would hardly even be one in the history of the universe.
It sounds like you've never actually made mutations. What you discover when you do is that a large fraction of mutations turn out to be fairly benign and to make only subtle alterations in function, and it is not that hard to stumble onto mutations that enhance function in one way or another. In other words, far from their being only a few mutational paths whereby one protein can be altered to another while retaining essential function, there are often many--i.e. many regions of the search space are fairly smooth rather than chaotic. This is, of course, just what people like Stuart Kauffman predicted, based simply on the reasoning that since organisms evolved by natural selection, the search space has to be organized in such a way that natural selection constitutes an efficient optimization algorithm.
Theoretically, the search space for beneficial changes is so large, that without direction there would be no possibility of it occurring.
A more scientifically useful way of expressing this (because it offers testable hypotheses) is that for organisms to evolve, the interdependencies between genes have to be such that natural selection constitutes an efficient search strategy. This has been addressed by Stuart Kauffman, who has explored what the characteristics of organisms have to be for evolution to be possible--which seem to match pretty well with the characteristics of actual organisms.
I'm not sure what you are saying. I'm not saying that any specific mutation is _prevented_.
If nothing prevents them, then beneficial changes have to occur, pretty much demolishing the "mutations are degenerative" argument.
Is it possible that some species may have stored diversity, in the form of systems that have been evolutionarily selected such that particular genes are primed to mutate under stress in particular directions that have been evolutionarily productive in the past? This is certainly a possibility. Something along these lines happens within the body in the development of the immune system.
The generative mechanism is cell-directed transcription (as shown in the paper linked above). Mobile elements also seem to be involved, although the exact mechanism triggering and placing them is not known. But, contrary to the neo-Darwinian view of "parasitic elements", mobile elements are highly adaptive in helping organisms cope with stress in specific ways, and can even help restructure genomes.
Actually, while a Darwinian view allows for the existence of mobile elements that are parasitic, it also leads one to expect that there will be mobile elements that bear a more symbiotic relationship to the organism as a whole.
There is, however, a stupendous amount of ground to cover between a photosensitive patch and anything remotely resembling the eye (of an octopus, cat or person) and the very weakest of unintelligent forces working, hah, blindly along that path. Given a generational time of (reaches down, pulls out figure) one week, you only have about twenty (american) trillion generations to get the transition done in.
There are a few fundamental misunderstanding here. First, you are almost certainly greatly overestimating the number of changes required for evolution of the eye. Certain types of mutations, typically in developmental genes, can produce relatively large morphological changes. One somewhat simplistic model of eye evolution, simply assuming that mutations alter existing traits by 1%, within the range of variation, came up with 1829 mutations. Another error is imagining that these mutations have to occur in series. In fact, they occur in parallel across the population. The notion that the mutational distance between homologous genes is much larger than is consistent with rates of mutational change is an old objection that has pretty much collapsed now that the genomes are available and it is trivial to measure the actual mutational distances. The arguments that evolution of such features requires massive numbers of mutations turns out to be clearly wrong.
Oh, and you are also wrong in imagining that octopus eyes share the "unintelligent" backwards design of our retinas.
Even today, there are plenty of organisms that get along fine with just eyespots. And there are many ways in which small mutational changes can improve the function of an eyespot. For example, an eyespot in a pit will have directionality. Pit vipers make use of infrared-sensitive eyespots that work in this manner and supplement their regular eyes.
Yes and no. Heterozygous fractionation can cause phenotypic variation.
I am referring to genomic variation.
The idea that these differences are the results of accumulation of small changes is a presumption, not a result.
No, this is a result. All of the difference between species observed to date are the result of multiple changes of the sort that arise by mutation.
The changes that result from random mutations are degenerative, while adaptive mutations are beneficial.
This is nonsensical. A change is neither degenerative nor beneficial. It is just a change. Whether it is disadvantageous or beneficial depends upon environmental context, and the same alteration may be disadvantageous in one context and advantageous in another. Moreover, it would be impossible for all random changes to be disadvantageous, because random changes will necessarily produce some beneficial alterations. The only way to avoid this would be for mutation to be nonrandom. There is no known or imaginable mechanism to prevent mutations from producing the kinds of genomic changes from occurring that have been shown to underlie all species differences--and indeed, these genomic differences are of exactly the same kind that occur by mutation.
Actually, they assumed that, simply because the sequences were similar. However, that is a presumption, not the result of analysis. I think others disagree, as it has been shown to have come into both populations independently.
Do you have a reference? In any case, that is not inconsistent with horizontal gene transfer, because both could have received it from a 3rd source.
_Most_ of the variation that takes place is the result of Mendellian inheritance, which, by the way, was discovered by a creationist (who used it to argue _against_ transformism).
Mendelian inheritance is incapable of generating variation, it merely reshuffles the variation that already exists. Variation arises by mutation. Darwin recognized that for his theory to work, some method of generating new variation had to exist. This prediction was subsequently confirmed by the discovery of mutation, one of the most dramatic confirmations of a theory in the history of science. Although Darwin also knew nothing of Mendelian genetics, he predicted (because his theory required it) that there had to be some mechanism of passing traits down undiluted from generation to generation, so the discovery of genes is another remarkable confirmation of the predictions of evolutionary theory.
Please tell me what the evidence is that (a) everything shares a common ancestor, and that (b) random mutation + natural selection is sufficient for creating the diversity that exists today from that common ancestor.
Many species genomes have been sequenced, confirming the prediction of evolutionary theory that all differences between species are due to an accumulation of small changes at the genetic level--changes identical to those that have been demonstrated to arise by random mutation. This is another striking confirmation. The fact that predictions of a theory that predated knowledge of DNA are still being confirmed by molecular biology is a major reason why evolutionary theory is accepted by virtually all biological researchers.
The eyeballs halfway between man and fly must have been a wonder to behold.
Now that is pretty foolish, considering that the eyes of flies and man are thought to have evolved independently. So the closest common ancestor almost certainly didn't have anything resembling an eyeball--perhaps just a photosensitive patch of skin.
You can find the same kind of homologies in 6-aminohexanoate-cyclic-dimer hydrolase [pubmedcentral.gov] in Flavobacterium and Psedomonas, despite the fact that we have _observed_ their appearance as separate occurrences.
That's not what the article you cite says--in fact, it says the opposite, that the similarity of sequences reflects a relatively recent common ancestral sequence, more recent than other genes of the bacteria in question, consistent with horizontal gene transfer, which is established to be relatively common in bacteria.
That absolutely has everything to do with embryonic development which is known to mirror vertebrate evolution, at least to those who follow science
Uh, no. This is an old notion that was long ago abandoned. See Gould's "Ontogeny & Phylogeny" for a cogent account of the history of this idea and its modern status. To summarize, the modern view is that embryonic development does not mirror vertebrate evolution (nor is their any reason why it should), but does preserve some aspects of the embryonic development of our common ancestors with other vertebrates. This is a somewhat subtle but important distinction. It is worth noting that many aspect of embryonic development do not make any sense at all other than in light of a common ancestry for all vertebrates.
If I were asked to guess what embryonic tissue shark's electroreceptors came from, my first guess would be neural crest. After all, this is the tissue that gives rise to electrically active tissues like nerve and muscle, which have receptors that do indeed "sense" electrical fields. This is not to allow the animal to sense electrical fields in its environment, but simply the way nerve conduction and muscle contraction work--a change in electrical field (typically produced by a chemically activated ion gate in a membrane) is "sensed" by a voltage-gated ion channel that responds by opening up additional channels, further altering the electric field, which stimulates other voltage-gated ion channels, and so forth. It is easy to see how such a process could be evolutionarily adapted for sensory purposes, just as fish that generate strong electric fields, such as Torpedo (the electric ray) do so with tissues that are evolutionarily derived from muscle.
So basically, all this is saying is that we and sharks have a common ancestor and as a result share similarities in the development of nervous tissue (which we knew already), and that sharks' electro receptors develop from the tissue that any biologist would identify as the "usual suspect."
Somehow, tens of millions of other customers seem to handle these allegedly defective cups without incident.
And doubtless tens of millions of people drive intoxicated each year without incident. So does that mean that you shouldn't be liable if you hurt somebody while driving drunk? Nobody really knows the incidence of burns from styrofoam cups, but considering that I have seen it happen multiple times, I don't believe that it is all that rare (although injuries this severe are doubtless uncommon). I've never known anybody to complain about it, much less sue, so the 700 complaints that McDonalds had received were doubtless a small fraction of the total.
From the point of view of liability, it was a predictable hazard that McDonalds was aware of, and that could have been avoided by a number of measures, such as cooler coffee, cups better suited to serving very hot liquids, or putting cream and sugar in before serving. It is hardly surprising that the jury found that McDonalds was at fault.
The cup didn't fail. She took the top off the cup, and spilled the contents. If the cup had melted or something, you'd have a point, but it didn't, so you don't.
What happens is that the styrofoam cup gets soft, but it holds its shape because it is stabilized by the stiff plastic cover. The cover is tight, so you need to hold the cup firmly to get it off. It is easy to squeeze a bit too hard, but you don't realize it because of the cover stabilizing the cup. When the cover comes off, that stabilization is suddenly lost, the sides of the softened styrofoam cup collapse from the pressure, and the liquid spills out. I've seen this happen to people dozens of times. It's annoying and sometimes painful when it happens to somebody seated at a table, but it usually doesn't do any real damage because the liquid quickly runs off their hand on to the table. But if you are sitting in a car, the scalding coffee ends up in your lap.
Basically, styrofoam cups are not suitable for serving coffee at the "proper" temperature. And serving it that way to somebody in an automobile is grossly irresponsible.
Since you are interested in context, you do realize that the plaintiff was 81 years old, don't you? You do realize that a coffee spill might affect an 81-year-old much more harshly than a healthy 30-year-old male. You do realize that placing a hot cup of coffee between you legs in a moving car might be contrued as a much more risky behavior for an elderly lady than a young person.
Now you are perpetuating a myth. The spill did not happen in a moving car. The accident occurred when the car was parked. I've seen how easily this can happen with styrofoam cups and hot liquids. The cup becomes very soft but this is not obvious because it is stabilized by the plastic lid. Often the lid is tight, and it is difficult to get the lid off. It is easy to squeeze the softened cup a bit too hard, and when the lid pops off the cup basically collapses. To make it worse, the insulating properties of the styrofoam maintain the coffee at a scalding temperature much longer than would be the case with a ceramic or cardboard cup. If a cup collapses at a table, you get a painful but not too damaging burn to your hand, because the scalding liquid runs right off--a little ice right away and it might not even blister. If it happens in a car, moving or not, you are likely to end up with a bad groin burn. Mcdonalds could have avoided the hazard either by reducing the temperature of the coffee or by using a more suitable cup, such as cardboard with an insulating sleeve.