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Counting Dogs

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Recently, Mark Frank and I had a brief dialogue in the OP,“Didn’t everyone already know this about dogs?”
I’ve decided to clean it up a bit and re-post it because after my last question, I received no responses. At the outset, I would like to say that I place no blame about lack of responses on Mark Frank or anyone else in the last OP (as my post was rather quickly buried.)

Having said that, in this OP I would like somebody to address the question.

After one go around where I’d suggested that “success” should be counted as an increase in genetic information, Mark Frank corrected me, writing:

In biology success is breeding in the available environment. As a result there are about 400 million dogs in the world. There are about 200,000 wolves and they are extinct or endangered in many geographies. It is irrelevant how they would thrive without us. We are the dog’s environment and they have exploited that very effectively getting us to care for them by manipulating our parental instincts (and also providing some services).

and

I had in mind the biologist’s definition of the success of a species. This is purely and simply the species ability to reproduce in the world as it is . . . The genome is only relevant to the extent that it contributes to this. Any other definition of success leads to the odd result that a species could be highly “successful” but failing to survive.

In both cases, Mark Frank references “(I)n biology” and “the biologist’s” definition, so I will stipulate for the sake of this post that the convention in biology is that a species’ success is simply increase in number.

My response to Mark Frank:
According to your definition, evolutionary success has only to do with the genome (of the organism in question) so far as it informs the ability to reproduce “in the world as it is.” Is that about right?

In the case of domesticated dogs, I am informed that there is a loss of genetic information. And, you stated that dogs enjoy (numerical) success. Dogs, whether by breed or by number, are successful because of their responses to specific environmental nuances (e.g. we like dogs that chase sheep without eating them, so we feed them kibble and help them reproduce). This is easily measured by the increase in number of dogs (as compared to wolves, for example). One might even suggest that even if the narrative concerning sheep and kibble is just that, an unscientific narrative. Numbers don’t lie. Is that about right?

Onward:
Michael Behe in his controversial book, The Edge of Evolution, writes that such is generally the case for malaria-resistance — that the battle involves organisms “enjoying” loss of genomic info, to better get over on malaria so they can live to reproduce, (oh, and in turn, strains of plasmodium falciparum are doing likewise, sacrificing function, via loss of genetic information, to reproduce) –all of this only when necessary, or as Mark Frank suggested, “in the world as it is.”

Please, correct me if I am wrong, but don’t most (all?) scientists in the field agree with Behe’s assessment? That is, the “trench warfare” described by Behe is not actually that controversial, but an accepted finding.

It seems to me that an organism’s response to the environment (“in the world as it is”) involves dumping, if necessary, genomic information to succeed. Whether the selection is artificial or natural, the far, far, easier pathway for organisms is to lose genomic information. In fact, this is the dominant, almost universal, response according to scientific studies. . .

My question:

How could these more immediate pathways of losses of information possibly square with the evolutionary claim that natural selection (along with its numerical “success”) accounts for increased information in the genome, not only in a given organism, but for all organisms over the entire history of life on earth?

I thank you in advance for your considered responses.

Comments
Mark Frank:
1) information is a word with many meanings. If you take the kind of formal definition that ID proponents like to use then it is something like –log2(the probability of a given outcome assuming a uniform probability distribution over all outcomes). It is not clear how you apply that to canine genomes – what outcomes? what probability distribution?
It's not our fault that evolutionists fail at information science. They should drop all pretense of there being any such thing as "information" in the genome.Mung
November 4, 2014
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phoodoo @103:
First, I assume that all you can really test in a lab is bacteria, so you really aren’t testing anything much in the way of competition and sexual selection, and luck of circumstances etc…
Nope, it's been done with a lot of organisms, including eukaryotes. I've done selection experiments with cereal mildews, and at work have been discussing experiments on chironimids. And selection experiments have been done on many more species:
For example, in the present symposium, we have papers about mice artificially selected for high voluntary wheel-running behavior (Rhodes et al., 2005; Swallow et al., 2005) and for basal metabolic rate (Konarzewski et al., 2005), rats selected for high and low treadmill running performance (Koch and Britton, 2005), crickets selected for high or low wing morph frequency (Zera, 2005), and stalk-eyed flies selected for male eye span (Wilkinson et al., 2005).
There obviously are limits to what can be done in the lab - the generation time can't be too long, and you need to be able to keep the species in the lab (so blue whale selection experiments are a few years off), but that still leaves a lot of species that can be worked with. BTW, if pone wanted to look at fitness of fruit flies in the wild, one could simply collect them from the wild, and not use lab stocks.Bob O'H
November 4, 2014
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Or are you talking about something like fruit flies, with all kinds of cross linked genes, where its almost impossible to draw conclusions about fitness in the wild?phoodoo
November 4, 2014
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Bob, Ok, let's do flush this out. First, I assume that all you can really test in a lab is bacteria, so you really aren't testing anything much in the way of competition and sexual selection, and luck of circumstances etc... But ok, you have one type of bacteria that has a certain mutation, and another bacteria with another mutation, and then you put them in a petri dish, and then what? You expose it to what you think might kill it? Some bacteria frequencies change (because they died) and some don't change much, because they didn't die. Is that it? The ones that died less are fit, right?phoodoo
November 4, 2014
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Bob O'H:
Certainly evolution can happen by loss of function, and I guess when evolution is quick (as in host-parasite/pathogen interactions) it can be a quicker way to evolve resistance (although loss of function can also cause a loss of fitness in the absence of the pathogen). But there are also gains of function, e.g. through duplication of a resistance gene, followed by its mutation.
Bob, always good to see you here. But let me point this out: via duplication, there is no net increase in information. Then, when there is a mutation, the vast majority of mutations are deleterious. How do you then say there is a gain of function? Don't the probabilities associated with mutations tell us that there is some loss of function in the mutated, duplicated "resistance" gene?PaV
November 4, 2014
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phoodoo @ 99 -
Bob, you also ignored the entire concept of function. Is there a meaning for gain of function or loss of function in the theory of evolution? How can there be? If something survives, that is all the function it needs.
Well, I guess you missed my post at 17. After that, my involvement in the discussions turned to specifics where function took a back seat. I'm happy to return to it later, but I'd rather wait until we've sorted out what fitness means.Bob O'H
November 4, 2014
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phoodoo @ 97 - First, I should be clear that I was trying to explain things simply, so you would understand the main points. It's not always easy to judge the optimal level of complexity in an explanation, and evidently I mis-judged it.
Now let’s be very clear here Bob, so you don’t accuse me of not understanding. When you say that fitness is the expected change in frequency and not the actual change, and then you say that someone can look at the expected (not the actual right??) HOW do you look at the expected change in a lab? You don’t. How do I know? Because you yourself said so:
You measure the actual change, yes. But you repeat the experiment. And the average change in frequency is the estimate of fitness. Because you have replicates, you have samples from the distribution, so you can use that to estimate the uncertainty in the estimate. Formally it gets a bit more complicated, but I hope you appreciate the idea, at least.Bob O'H
November 4, 2014
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“And that is important because macroevolution requires an increase in biological information.” ws:
Says who?
Anyone with knowledge of biology. That leaves you out.Joe
November 4, 2014
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Bob, you also ignored the entire concept of function. Is there a meaning for gain of function or loss of function in the theory of evolution? How can there be? If something survives, that is all the function it needs. There is no such thing as gaining or losing function, if a system has no meaning, other than whatever survives works. If an albino is said to "lose" function by the normal person's language, that is not really true in the evolutionists view. Because, maybe albinos would be the best surviving allele in some conditions. In reality its just an extreme form of blue eyes. Are blue eyes also losses of function? How about white skin? Furless skin? Without a standard of "fit" everything is just increases or decreases in their frequency in a population. If most people are albinos, then that would be their function. If most people have blue eyes, that is their function. If most dogs that are bred have Hip Dysplasia, then that is its function. That is Fitness according to you!phoodoo
November 4, 2014
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Bob, You answer is very puzzling. Don't blame me if you answer as to what the meaning of fitness is is not clear. HOW do you determine the EXPECTED change in the frequency of phenotypes? I quote from YOU: "One way is by doing experiments – you take the phenotype into the lab and measure fitness and/or do selection experiments. If fitness means the EXPECTED change in frequency, and not the ACTUAL change in frequency, then that is not what you are measuring in the lab, you are measuring the actual change in frequency. You are being very imprecise with your language. Bob, it was you, and no one else, that said, "If someone looks at fitness in the lab and wants to use that to make predictions..." Now let's be very clear here Bob, so you don't accuse me of not understanding. When you say that fitness is the expected change in frequency and not the actual change, and then you say that someone can look at the expected (not the actual right??) HOW do you look at the expected change in a lab? You don't. How do I know? Because you yourself said so: "One way of thinking about it is that from a starting point, you run the tape of life for a generation a lot of times, and the fitness of an allele is the average in the change in its frequency." You also said: "Without getting into technical details, it’s the mean of a distribution." So you are measuring which alleles were successful most in the past, and the ones which were successful in the past, fall into the mean of the distribution. Correct me if YOU were wrong Bob.phoodoo
November 4, 2014
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Tim,
The easier pathway in both cases is the same: loss. That is what is at issue.
As I said earlier, the answer is no. Losing genomic information is going to reduce the size of the genotype network. A reduction in size will decrease the chance of finding a new phenotype within the network. Gene mutation ,whether neutral or beneficial helps in increasing the network size. When the network is large, in 1 dimension a new phenotype can found within 15 steps, as dimensions increases, the search space for new phenotype reduces drastically. You can calculate the search sphere volume for any dimension using the formula Pi^(d/2)/r(d/2+1) d = dimension, r=radius of search sphereMe_Think
November 4, 2014
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The bottom line is this: by ignoring all other narratives and looking only at numbers, we should find that in malaria the constant battle should produce novel information/function (whichever suits you) more immediately than loss of function.
Why?Bob O'H
November 4, 2014
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You said you determine what is the fittest phenotype by seeing where that phenotype falls with the mean of distribution in a population, right?
Err, no. Nothing of the sort, I'm afraid. Fitness is the (expected) change in frequency.
Also, what do you mean about a dog breed
I believe it's a standard term. But I think you need to understand the concept of fitness first, before discussing how it varies between breeds.Bob O'H
November 4, 2014
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Tim Well, this has certainly been entertaining, a little instructive and somewhat disappointing. Glad you were entertained but it's a pity you're so averse to being educated. You were so busy looking for anything to support your preconceived ideas on "information loss" you missed a lot of interesting science. Oh well. Like I noted above, the evidence is there for anyone to examine but first you have to want to learn.Enkidu
November 3, 2014
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Well Tim, in my opinion the topic is necessary large because its a big question. We don't really know what is meant by information of function. Is a particular feature or trait good or bad for an organism. In evolutionary theory, there is really no way of deciding what is good or bad, other than deciding what is frequent, and what is less frequent. The more frequent (by their definition) the more good (or fit) that trait is. I don't know if there is a definition of function, other than to say that something is either useful or not useful. I don't think you can call a sickle cell a function, rather it is the functioning (the operation of a known system) that has gone haywire (that is clearly a loss of function in my eyes) . It just so happens that they system that has stopped working as it (was designed to-haha) usually does, means that it is harder to get one type of disease which affects that system. Its probably harder to get lice if you have no hair, and harder to get gall stones if you were born without a gall bladder. Are those losses or gains in functionality. From my point of view (an ID perspective), its pretty clear that systems are made to work a certain way. Our nervous system, or respiratory system, or circulatory system, they have many parts, all which seem to have a very specific and useful purpose. And so if one part is broken, that to me is a loss of function. But from the Evolutionists standpoint, I don't think they can make that same claim. There is no such thing as a system. What looks like systems is really just an illusion, all are just separate parts that luckily happen to survive, if it turns out that it is lucky enough that one part can be useful with another part for further reproduction, that it sticks around. There is no such thing as a "broken" system, if nothing is really a system. When evolutionist talk of a system, really that is just convenient language, actually they are all just meaningless parts which just so happen to not destroy each other. So how can an evolutionist talk about gain of function or loss of function in any meaningful way, other than to say if something stays alive, it has function. That has been the whole point of my posts. If you take the evolutionists believe, there is no such thing as good or bad, fit or not fit (as ordinary people use the word fit) there is only more of one kind or less of one kind. That has been my point to Bob. If evolutionists start calling one trait good or bad, because it seems useful to a normal person, that is cheating-because to them, the best traits are simply the most frequent ones. I think they try to equivocate on this point, but it is still inescapable. They hedge this a bit by saying the ones they "expect" to be most numerous (how do they expect it, by counting the frequency of course). There is no system, there is no good or bad trait, there is no function, and non-function, there are only frequent ones, and less frequent ones. The frequent ones are best. How can you call something a system or a function, when it was never designed to be a system, it is just a random collection of parts, that happen to work sometimes.phoodoo
November 3, 2014
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Well, this has certainly been entertaining, a little instructive and somewhat disappointing. Entertaining Watching the back and forth erupt. Instructive A few good ideas from Jerry, Mark Frank, even Enkidu (once! ha!) and others. Disappointing The participants, so overly invested that they cannot but trot out the stories closest to themselves without going to the trouble to examine the OP closely. We were lectured on . . . types of selection, micro/macro, then nature of selection, the definition of selection, alleles, bottlenecks, information, function, and more. Read the OP folks, it is about number, simply put, more dogs than wolves. That's it. "In the world as it is," ideas such as environment, niche, and all of the above are distractions. Here is what we must look at: There are way more dogs than wolves. Because we are working under evolutionary stipulation, we must assume that modern wolves and the domesticated dog both have a common ancestor. The evolutionary narrative (correct me if I am wrong, but I am not) is that the domesticated dogs are descended from wolves. Among domesticated dogs, the referenced article describes a review of 800 studies. Now, I have not read the research in toto, but it is not in dispute that dogs have lost function in relation to wolves. The question that I left open was "do dogs exhibit increased (integrated) information" in comparison to wolves. But for malaria-sickle-trait-sickle-cell the story is clearer. Again, numbers don't lie. People who carry sickle-trait, "enjoy" loss of function, but this loss of function makes it difficult for good ol' plasmodium falciparum to hook onto cells. That, in turn, seems to increase "function" i.e. people with sickle trait get less malaria -- and that is rather functional, indeed. The bottom line is this: by ignoring all other narratives and looking only at numbers, we should find that in malaria the constant battle should produce novel information/function (whichever suits you) more immediately than loss of function. Or, perhaps in dogs we should see more novel information/function (whichever suits you) in comparison to wolves. We don't. The easier pathway in both cases is the same: loss. That is what is at issue. I am the first to admit it. These are only two (very different) examples, and I appreciate Mark Frank's discussion of information/function and even Enkidu and the ring-species of salamanders. Not too surprisingly, I find these only as convincing as an evidence of species formation to the extent that I have assumed evolution's ability to create information -- extrèmement limité.Tim
November 3, 2014
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Bob, I am trying to stick with your definition of fitness, but that is a little hard to do, because it seems to keep changing. You said you determine what is the fittest phenotype by seeing where that phenotype falls with the mean of distribution in a population, right? So that is how you "expect" the phenotype to be the fittest, by virtue of the fact that it is most prevalent. Is this not what you said or meant? So new phenotypes would never be the most prevalent initially, so initially you must describe it as being less fit, correct? Because the definition of fitness is not some vague feelings about good, or worthy, its decided by a popularity contest within the population, correct? Also, what do you mean about a dog breed? Are you using a new definition of the concept of a dog breed to mean a new species? How do you classify them as different populations rather than simply different phenotypes? If there are less American Huskies than dachshunds, are the dachshunds a more fit animal? Or is what you are really saying is we get to first decide our population size and criteria, and only then do we decide what is the most common phenotype within a population which we just selected for measuring?phoodoo
November 3, 2014
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jerry This is all micro evolution and while interesting is not what the real evolution debate is about. For that we need massive creation of new functional variation. The question is what can do this. Science has known the answer for over 60 years. It's the genetic variations that occur in a population every generation with the resulting phenotypes filtered by environmental selection pressures and which are passed on to new generations as heritable traits. Also called evolution. It's been empirically observed in the lab and in the field, confirmed with computer modeling and the functioning of genetic algorithms. You can learn about it any any decent college or university. This is nonsense. I have been reading about ID for over 15 years and never saw this. The waffling over "information" and "function" in this dog breeding is a perfect example. CSI is another - a vaguely defined term with no objective way to identify or quantify it. There are no examples of a new species being created through random variation. Lots of speculation. But no good evidence. Except the scientific literature has tons of such evidence. Observed incipient speciation in ring species like the Ensatina family of salamanders is a good example.
Incipient species formation in salamanders of the Ensatina?complex Abstract: The Ensatina eschscholtzii complex of plethodontid salamanders, a well-known “ring species,” is thought to illustrate stages in the speciation process. Early research, based on morphology and coloration, has been extended by the incorporation of studies of protein variation and mitochondrial DNA sequences. The new data show that the complex includes a number of geographically and genetically distinct components that are at or near the species level. The complex is old and apparently has undergone instances of range contraction, isolation, differentiation, and then expansion and secondary contact. While the hypothesis that speciation is retarded by gene flow around the ring is not supported by molecular data, the general biogeographical hypothesis is supported. There is evidence of a north to south range expansion along two axes, with secondary contact and completion of the ring in southern California. Current research targets regions once thought to show primary intergradation, but which molecular markers reveal to be zones of secondary contact. Here emphasis is on the subspecies E. e. xanthoptica, which is involved in four distinct secondary contacts in central California. There is evidence of renewed genetic interactions upon recontact, with greater genetic differentiation within xanthoptica than between it and some of the interacting populations. The complex presents a full array of intermediate conditions between well-marked species and geographically variable populations. Geographically differentiated segments represent a diversity of depths of time of isolation and admixture, reflecting the complicated geomorphological history of California. Ensatina illustrates the continuing difficulty in making taxonomic assignments in complexes studied during species formation
The evidence is there for anyone to examine but first you have to want to learn.Enkidu
November 3, 2014
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It’s pretty common practice in the ID world to never define their terms so there’s always plenty of wiggle room.
This is nonsense. I have been reading about ID for over 15 years and never saw this. It is one thing to take someone who might not know too much and use their ignorance as an example then to make such an absurd statement about ID in general. It is much more common for anti ID people to switch meaning or divert from the real issue with irrelevant examples. I cannot tell the number of times when someone who is pro naturalistic evolution to use microbe changes as examples of evolution. Then there are the moths and finches, which also are not examples of meaningful change. There are no examples of a new species being created through random variation. Lots of speculation. But no good evidence.jerry
November 3, 2014
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I believe we can safely assume that a typical dog breed results from a loss of alleles. So we can say there is loss of information since there are fewer alleles in this particular population when breeding is controlled by humans. This does not mean that there is necessarily a loss of function in the breed. In fact there may a tremendous gain in some function. After all what was the purpose of the breeding? (Since nearly all dogs can inner breed, gene flow could restore all lost alleles and the other characteristics that come with the restored array of alleles.) So loss of information does not necessarily equate with no gain of function. There may be some function lost but there may be a tremendous increase in some other function. Now this is artificial selection but it does not mean that in the wild there may also be circumstances where some function is gained while at the same time there is a corresponding loss of alleles. That is what natural selection mostly is. And this can lead to extinction when the environment changes as other functions which are necessary for survival in the new environment have been lost and are no longer possible due to a reduced gene population. This is all micro evolution and while interesting is not what the real evolution debate is about. For that we need massive creation of new functional variation. The question is what can do this.jerry
November 3, 2014
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rhampton7 Do we know for certain that all of these animals exhibit only loss of information? Because if some of them show a gain in information/function, then the point about dog breeds falls apart. We'll never know because there is no clear objective quantitative determination of either information of function. There's certainly a loss of overall genetic diversity in each specialized breed but is that the same thing? Take the dachshund as an example. It was bred specifically to have short legs so it could go into animal burrows and flush out prey. Seems to me that's a gain of function. But an IDer will then argue it lost the ability to jump high fences so it lost function. There's no objective way to tell what's a gain and what's a loss. It's pretty common practice in the ID world to never define their terms so there's always plenty of wiggle room.Enkidu
November 3, 2014
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All I am asking is this: in the light of these two narratives, one where phenotype-change is sought and one where genotype is studied, does natural selection whether process or result, for crying out loud suggest that evolution is a producer of novel information in the long term?
Dog breeds aren't the only example of micro-evolution within Canidae. That's why I asked, in the previous thread, if the African Wild Dog (Lycaon pictus) was examined. Like dogs, wolves, coytoes, dingos, and some jackals, it too has 78 chromosomes. As you can see in the link, there are quite a number of species and sub-species. Do we know for certain that all of these animals exhibit only loss of information? Because if some of them show a gain in information/function, then the point about dog breeds falls apart.rhampton7
November 3, 2014
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Tim @ 71 -
All I am asking is this: in the light of these two narratives, one where phenotype-change is sought and one where genotype is studied, does natural selection whether process or result, for crying out loud suggest that evolution is a producer of novel information in the long term? I guess I was under the impression that it was all about little easy steps and that the easiest step with the “most fit” outcome is “always” “selected”. Here the easiest step is either loss of function or loss of genetic information. What gives?
First, I'd rather not get into the endless debates about what is information, so I'll assume you are equating loss if information with loss of function. My apologies if this causes problems, but it seems to be a reasonable interpretation of what you're arguing. Anyway, selection will act on the variation that's available. But it is mutation (and recombination and other processes, but let's stick to mutation to simplify things) that initially creates the variation. Thus selection will act on new functions if mutation create function, and conversely if mutation destroy function then selection will act on this reduced function. As it's usually easier to destroy or create, mutation will tend to act to reduce function. And often this reduced function reduces fitness, so these tend to get weeded out. But sometimes removing a function can increase fitness. This would be particularly common in a new environment, for example when a human goes "oh, that looks nice", or when a pathogen has evolved a new virulence. So if there is a gain of function, selection can act on it. And there are are examples of the evolution of a gain in function.Bob O'H
November 3, 2014
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Joe@20: "And that is important because macroevolution requires an increase in biological information." Says who? Getting back to dogs. If the only evidence we had of modern dog breeds were fossils, they would be classified as several different species. If you saw numerous fossils of old bull mastiffs, and numerous fossils of old chihuahuas, without knowing the history, you would assume different species, maybe different genera (OK, any sane person would). And these huge differences were the result of reduced information (variation) at least at the breed level. But for any individual dog, the amount of information has not changed much, if any.william spearshake
November 3, 2014
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phoodoo @ 51 -
How can you take the phenotype into the lab and do experiments, when the conditions in the lab are totally different from the conditions in nature. And furthermore there is no “standard” condition . Every instance, and every location is a different challenge for survival.
This is a bit extreme! Yes, there are differences between the lab and the field, but there are also similarities. If someone looks at fitness in the lab and wants to use that to make predictions about the field then they have to make the argument. There are a few lines of argument possible, e.g. that the trait is the sort that would not be strongly affected by the environment, or the experiment could be done under different conditions, which represent variation that is likely to be important for selection. Also, predictions from lab-based experiments could be compared to field data. phoodoo @ 52 -
If the phenotypes of a dog are selected by man, is that a fit phenotype or an unfit phenotype by definition? Since there are so many phenotypes of dogs, is there only one phenotype (the one that sits at the mean of your statistical distribution) that is “fit” while the rest are luck, or whatever you want to call those that aren’t within the mean?
If the phenotypes are selected by man, then they are fitter. The fact that we have ended up with dogs with different phenotypes just means that we have applied different selection pressures on different dogs. So the fitness of one particular trait will depend on the breed it finds itself in. phoodoo @ 53 -
And, if we play your numbers game a little further, EVERY new phenotype is by definition less fit, as they fall well below the mean.
I'm sorry, I don't understand this point. If the expected change in frequency is positive, then a phenotype is more fit by definition, regardless of whether the initial frequency is low or high. I suspect you are confusing the change in frequency with the frequency itself.Bob O'H
November 3, 2014
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Tim, Delete my comment 75. My iPad is not behaving very well. It is a duplicate. When you delete it, delete this request.jerry
November 3, 2014
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Readers should be aware that not only have the formation of new alleles (= new information) been empirically observed the formation of novel genes has been studied in detail. There are many instances of relatively young novel genes and their regulatory control which have been identified. The genetic mechanisms for the formation of both new alleles and novel genes are well known.
Readers should also note that none of this disagrees with anything I have said nor does it in anyway contradict ID. Here is the last paragraph of the paper which is essentially the same as what I said.
Ultimately, differences observed between species are due to differences at the genome level. Genomic studies are revealing the extent of these differences—in gene number, in encoded functions, in expression—and are also revealing the mechanisms involved in the evolution of genomes. The analysis of particular newly evolved genes provides information in finer detail, which hopefully can be generalized and help to understand the evolution of new genes and new functions. Equally as important as the formation of new coding sequences is the formation of regulatory regions responsible for new patterns of expression as well as the processes leading to spread and maintenance of the novel gene in the population. Bacterial genome studies have made very clear that, at least in bacterial species, a great part of the genes are not shared by all individuals of a species [75]. Different strains of the same species share a core genome containing genes present in all strains; however there is also a pan-genome consisting of genes present in only a subset of strains. As more complete genome sequences become available, we will be able to determine if similar patterns are observed in eukaryotes.
Within these changes to genomes environmental and reproductive pressures work to change allele frequencies. The result is called natural selection.jerry
November 3, 2014
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Mark FRank:
If you accept common descent (and I imagine that includes everyone in this particular discussion) then there is absolutely no question that novel alleles have been created many, many times in the past. That is the only way to get from a bacterium to a mammal.
You cannot assume the very thing that you are trying to test.
I would argue that the path from wolf to dog is not a loss of function, but it doesn’t matter.
Wolf vs dog, wolf wins. For dogs that's a loss :)Joe
November 3, 2014
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Alan Fox:
It’s the ratcheting RV+NS+RV+NS+RV+NS+etc that gives the evolutionary process its power to change.
Power to change allele frequency. Drift does that too. You need much more than changing allele frequency to explain the diversity of life.Joe
November 3, 2014
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This paper indicate how genetic changes in domestic dogs are apparently linked to how they interact with humans. Loss of information? Hard to see it that way.Alan Fox
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