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Genetic basis for human evolution

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kenneth558

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mark kennedy, I appreciate your heart, brother. I couldn't read in depth all your postings, but I didn't notice anywhere where you acknowledge divergent lineages between chimps and humans are TWO lineages, each diverging from supposed common ancestry in the same 4-5M years. Assuming we are comparing present-day genome base differences, half the base changes of divergence from common ancestor could appear in chimps' genome, half in humans' genome. Assuming equal rates for the two lineages means that HALF the base differences between chimps and humans had to occur in that 4-5M yrs in each lineage. If you already made this point, I'm sorry to interrupt. Of course, some unscrupulous evolutionists like to say we evolved from "common ancestors" when it suits their argument one day, then say we evolved from chimps themselves when it suits their argument the next day, so maybe this is a wasted post.

Have to get back to studying for boards.....
 
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Dannager

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kenneth558 said:
Of course, some unscrupulous evolutionists like to say we evolved from "common ancestors" when it suits their argument one day, then say we evolved from chimps themselves when it suits their argument the next day, so maybe this is a wasted post.
I'm not sure what you mean by this.
 
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mark kennedy

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shernren said:
Rushing for class now, but off the top of my head I'm thinking of flagella evolution:

http://en.wikipedia.org/wiki/Evolution_of_flagella

Regarding the origin of the individual protein components, an interesting paper on the evolution of dyneins[1][2] shows that the more complex protein family of cilial dynein has an obvious ancestor in a simpler cytoplasmic dynein (which itself appears to be a result of a four-fold duplication of a smaller motif). Long-standing suspicions that tubulin was homologous to FtsZ (based on very weak sequence similarity and some behavioral similarities) were confirmed in 1998 by the independent resolution of the 3-dimensional structures of the two proteins.

(emphasis added)

I see minor variations in the "very precise assembly instructions" producing a family of proteins from an ancestral protein here. There aren't really that few possible combinations of working codons, are there?

I think you might be talking about the chemical evolution of these proteins. My main point was that the assembly instructions must be precise. Just changing the protein does not get you anywhere, if they have to fold in order to fit hand in glove the two shapes must fit one another, obviously. If the first one is positivly charged the second one has to have a negative charge. If its an enzyme it generally matches the shape of the chemical that is its target.

Ok, on to symbiosis if that is where we are heading with this. Lynn Margulis proposed symbiotic relationships like large ancient cells swallowing up bacteria cells without digesting them. One scenerio has this resulting in mitochondrion. She managed to demonstrate that mitochondrial peoteins more closely resemble bacterial proteins than host cell proteins. This is suppose to explain the origin of complex biochemical systems? Before I ask you to elaborate on the, "cilial dynein has an obvious ancestor in a simpler cytoplasmic dynein", I have a little quote for you:

"The important question for us biochemists is, can symbiosis explain the origin of complex bichemical systems? Clearly it cannot. The essence of symbiosis is the joining two separate cells, or two separate systems, both of which are already functioning...Symbiosis theory may have important points to make about the development of life on earth, but it cannot explain the ultimate origins of complex systems." (Darwins Black Box, Michael Behe)

Now, if you would be kind enough to tell me how to compare cilial dynein to cytoplasmic dynein we can continue.



I don't get what you're trying to say.

That's one of the philosophical premises of natural selection, aka survival of the fittest. Let's let that go for now.



Mutations make new alleles.

Oh well, I was thinking Kerrmetric would be jumping in here but he is probably busy...or something. Anyway, lets talk about mutations making new alleles. The Chimpanzee Genome paper has an interesting sections on Human disease alleles.

"Starting with 12,164 catalogued disease variants in 1,384 human genes, we identified 16 cases in which the altered sequence in a disease allele matched the chimpanzee sequence..."

http://www.nature.com/nature/journal/v437/n7055/full/nature04072.html

There is allso a section on Human population genetics that follows this one.



I didn't say ID was an incredulous argument I said it was an argument-from-incredulity. And as far as I know ID really has no way to quantify "irreducible complexity" other than assigning a probability to the synergistic parallel evolution of multiple features required in an "irreducibly complex" system, and assuming that a system with a low enough probability must therefore be intelligently designed.

That's intelligent design allright, they take it down to the molecular mechanisms. At any rate, not ID scientists would ever hazard a challenge to common ancestory of humans and chimpanzees. Creationists tend to focus on the age of the earth, fossils and are quite found of emphasising human evolution. Obviously, I, being a creationist tend to drift toward the latter.

I have long wondered if ID was really what critics called it, creationism in disguise. I do hope that it is but we wont really know until we look at the biochemical basis for human evolution. Behe is into mitochondria and bacteria flaggelum, my big issue is the evolution of the human brian.

Why don't you see what you can do something with this post and we can talk some more.

Grace and peace,
Mark
 
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mark kennedy

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kenneth558 said:
mark kennedy, I appreciate your heart, brother. I couldn't read in depth all your postings, but I didn't notice anywhere where you acknowledge divergent lineages between chimps and humans are TWO lineages, each diverging from supposed common ancestry in the same 4-5M years. Assuming we are comparing present-day genome base differences, half the base changes of divergence from common ancestor could appear in chimps' genome, half in humans' genome. Assuming equal rates for the two lineages means that HALF the base differences between chimps and humans had to occur in that 4-5M yrs in each lineage. If you already made this point, I'm sorry to interrupt. Of course, some unscrupulous evolutionists like to say we evolved from "common ancestors" when it suits their argument one day, then say we evolved from chimps themselves when it suits their argument the next day, so maybe this is a wasted post.

Actually, the common ancestor for chimpanzees and humans is supposed to be 5-6 Mya. There are no big differences for around 2 1/2 million years except for some highly simular features with real differences (robust vs gracial features, habitual bipedalism, precise vs merely opposable thumbs).

The biggest changes started with the Homo lineage and the brain (cranial capacity) started expanding like crazy. There is one school of thought that wants to make chimpanzees Homo troglodydes rather then Pan toglodytes. In other words they want us to be different species within the same genus. They base this on the simularity of the DNA in the comparative genomes that was supposedly 98% identical. It's not, it's 96% simular with most of the protein coding genes showing differences at an amino acid sequence level.

Have to get back to studying for boards.....

Cool, thanks for stopping in.

Grace and peace,
Mark
 
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shernren

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I think you might be talking about the chemical evolution of these proteins. My main point was that the assembly instructions must be precise. Just changing the protein does not get you anywhere, if they have to fold in order to fit hand in glove the two shapes must fit one another, obviously. If the first one is positivly charged the second one has to have a negative charge. If its an enzyme it generally matches the shape of the chemical that is its target.

Ok, on to symbiosis if that is where we are heading with this. Lynn Margulis proposed symbiotic relationships like large ancient cells swallowing up bacteria cells without digesting them. One scenerio has this resulting in mitochondrion. She managed to demonstrate that mitochondrial peoteins more closely resemble bacterial proteins than host cell proteins. This is suppose to explain the origin of complex biochemical systems? Before I ask you to elaborate on the, "cilial dynein has an obvious ancestor in a simpler cytoplasmic dynein", I have a little quote for you:

"The important question for us biochemists is, can symbiosis explain the origin of complex bichemical systems? Clearly it cannot. The essence of symbiosis is the joining two separate cells, or two separate systems, both of which are already functioning...Symbiosis theory may have important points to make about the development of life on earth, but it cannot explain the ultimate origins of complex systems." (Darwins Black Box, Michael Behe)

Now, if you would be kind enough to tell me how to compare cilial dynein to cytoplasmic dynein we can continue.

No, I was never going anywhere near Margulis' endosymbiosis ideas, and while it seems appropriate to posit such theories for the inclusion of the mitochondrion and chloroplast in modern cells those arguments for cilia seem less satisfactory. I meant that cilial ("axonemal") and cytoplasmic dyneins seem to have diverged from a common dynein protein. http://jcs.biologists.org/cgi/content/abstract/108/5/1883 : The trunk for all the cytoplasmic dynein heavy chain homologues diverged directly from the root of the phylogenetic tree, suggesting that the first dynein gene duplication defined two distinct functions as respective subfamilies. What is stated here seems to be that early on a dynein gene was duplicated, one set going on to give rise to the cytoplasmic dynein heavy chain and one to the cilial / axonemal dynein. More stuff on the dyneins:

http://chronicle.com/colloquy/2001/design/373.htm
[this seems to have been a very interesting discussion, when I have time I'm going to read through all 400+ posts here]

http://genetics.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pgen.0020001
[long technical paper, but there seem to be parallels made between cytoplasmic and axonemal dyneins all over the place.]

Oh well, I was thinking Kerrmetric would be jumping in here but he is probably busy...or something. Anyway, lets talk about mutations making new alleles. The Chimpanzee Genome paper has an interesting sections on Human disease alleles.

"Starting with 12,164 catalogued disease variants in 1,384 human genes, we identified 16 cases in which the altered sequence in a disease allele matched the chimpanzee sequence..."

http://www.nature.com/nature/journal...ture04072.html

There is allso a section on Human population genetics that follows this one.

Okay, I've looked through it, what specifically do you want to discuss? I'm not sure how to interpret Table 7, especially the column labeled "ancestral".
 
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mark kennedy

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shernren said:
No, I was never going anywhere near Margulis' endosymbiosis ideas, and while it seems appropriate to posit such theories for the inclusion of the mitochondrion and chloroplast in modern cells those arguments for cilia seem less satisfactory. I meant that cilial ("axonemal") and cytoplasmic dyneins seem to have diverged from a common dynein protein. http://jcs.biologists.org/cgi/content/abstract/108/5/1883 : The trunk for all the cytoplasmic dynein heavy chain homologues diverged directly from the root of the phylogenetic tree, suggesting that the first dynein gene duplication defined two distinct functions as respective subfamilies. What is stated here seems to be that early on a dynein gene was duplicated, one set going on to give rise to the cytoplasmic dynein heavy chain and one to the cilial / axonemal dynein. More stuff on the dyneins:

http://chronicle.com/colloquy/2001/design/373.htm
[this seems to have been a very interesting discussion, when I have time I'm going to read through all 400+ posts here]

http://genetics.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pgen.0020001
[long technical paper, but there seem to be parallels made between cytoplasmic and axonemal dyneins all over the place.]



Okay, I've looked through it, what specifically do you want to discuss? I'm not sure how to interpret Table 7, especially the column labeled "ancestral".

The evolution of cilium and bacteria flaggelum is as deep as the ocean. Behe discusses both at length and the basic premise is that genuine ancestoral forms are virtually nonexistant. You asked about Table 7.

Here they list the disease alleles that chimapnzees and humans have in common. The way I understand it is this is ground breaking research and this is just raw data. Comparing genomic sequencies and cracking the genetic code are two different things. What stood out in my mind is that of 12,164 disease variants in 1,384 human genes they only identified 16 cases that matched the chimpanzee.

It's human evolution that has my attention, particularly the genetic basis for the transition from apes. That is what I was looking at and for whatever reason, ID has no interest in it.
 
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mark kennedy

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gluadys said:
It is impossible to talk evolution without talking population genetics even when you are talking about populations of bacteria. It is key to understanding how changes in cells become changes in populations--and that is what evolution is: changes in populations which began as changes in cells.

Speaking of population genetics, there is a section in the Chimanzee genome paper"

"The chimpanzee has a special role in informing studies of humans population genetics, a field that is undergoing rapid expansion and acquiring new relevgance to human medical genetics. The chimpanzee sequence allows recognition of those human alleles that estimates of locat mutation rates, which serve as an important baseline in searching for signs of natural selection."

(Initial equence of the chimpanzee genome and comparison to the human genome, Nature, 2005, available online)



The genetic basis of evolution is not limited to the study of mutations and their impact on cells/organisms. It has to include the effect on populations and that means looking at the role of natural selection. You have never displayed any comprehension of how natural selection affects the distribution of mutations. Without that comprehension you have no way to grasp the genetic basis of evolution. Remember evolution is a species-wide process. You have to get above the level of impact on a cell or organism to look at what is happening to those genetic changes on a population basis.

Assuming that natural selection is a quantifiable event, how is it measured? Natural selection eliminates mutations through genetic drift most of the time. Some times one will slip through and become inheritable even having an effect on the gene flow. This is usually a profoundly bad thing and frankly, mutations as a vehicle of adaptation to me is absurd.




Well, in this case we are not looking at competition of one species with another, since chimps and humans have not been competing with each other directly (unless you count the current impact of human activity on chimp habitat which is reducing the population of chimps.)

For millions of years they shared the same environment in equatorial Africa. The migration of apes from that area of our supposed ancestors was 1 million years ago. They, like virtually all the Homo species coexisted for extensive periods of time.

So let's get back to what process was happening to change humans and human ancestors over the last 5 million years. The key here is to understand the process of change and divergence first. Then you have a basis for commenting on the amount of divergence. Right now, you claim the level of divergence is impossible, but you have nothing but your own incredulity as evidence for that claim.

That is simply not true and all the wrangling over semantics won't make it true. We now now what the divergance is, what we don't know is how it is possible for it to be fixed on that level given the time constraints. You should be incredulous when asked to accept the impossible, it only makes good sense.

If you learn the process of divergence, you may be able to put some teeth in your argument.

If you could apply that to human evolution we would both benefit I'm sure.


The process applies to all situations of divergence, not just this one. But it does apply to this one too. Now, just to check. Are you clear on the difference between changing alleles and changing the distribution of alleles? What does the latter phrase mean to you?

Changing alleles sounds like the genes have been altered while change in distribution means a rearrangment of existing alleles.


Next question: how is the distribution of a pair of alleles changed?

Meiosis and recombination, some of the traits are dominant and some are recessive. The dominant suppress the recessive ones but they can still be express. One of the goals of hybrids is to make the recessive traits more dominant. That's selective breeding and supposedly nature does something simular


What is the relationship between the distribution of an allele in the gene pool and the fixation of that allele in the genome?

When it becomes fixed it is no longer subject to genetic drift the way mutant alleles have to be. It can be a favorable trait or it can be a retrovirus. Polar bears are allways born with white coats, their ancestors probably where much darker. Through some genetic mechanism the way these genes are expressed changed in distribution and now have become fixed.

btw, it is permissible to answer "I don't know". I just want to avoid going over what you already know. But if the question mystifies you, I will explain.

I am not real sure what your point is but the terms you are using don't mystify me in the slightest.


In what sense do you mean "rare"? I think you are going off on a tangent here.

5% of what is about right?

98% of mutations are neutral, the vast majority of the balance are deleterious with a rare few being beneficial in their effect. The ones that effect populations probably effect less then 5%, good, bad or neutral.


This is what makes me think you are going off on a tangent. Do you not realize that if a mutation with a deleterious impact affects 5% of a population, then the beneficial impact of not having that mutation affects 95% of the population. The beneficial impact is dramatically higher, not lower. [/quote

It effects only 5% because only 5% have it to begin with. I think what you are trying to say is the natural selection is screening harmfull effects out.


Bottlenecks are not necessarily required. I grant that fixation is likely to occur more rapidly in a small population, but as long as there is a benefit to having a new variable, it will eventually fixate even in a larger population.

Bottlenecks tend to cut down the gene flow, adaptation is much more likely the result of triggered responses. There are genetic mechanisms that adapt living creatures to their environments. These mechanisms are their by design not some nebulas naturalistic process.





Its been asked, but not answered. Or rather, every time it has been asked, your answer has been irrelevant to the question. You go off onto the same tangent as you do here talking about the deleterious impact of harmful mutations on the individuals who carry them. You totally lose focus of the fact that evolution happens to species, not individual cells or organisms.

You seem to have a problem relating this to human evolution. This happens on a subcellular biochemical level, in nature this happens without the genes being substantially altered. The only things that needs to change is how they are expressed, not the amino acid sequence. Mutations almost always result in a net loss of information.

You say "there is not earthly way of measuring the rate" but you don't say which rate you are speaking of. Is it the rate of mutations per cell replication? Is it the ratio of harmful/beneficial mutations per 1 million mutations? Is it the ratio of harmful to beneficial mutations that affect a cell or organism? Or is it the rate at which a particular harmful mutation shows up in a species?

Mutations are not the cause of adapations, if anything they are the consequence. The overwhelming majority of changes in the structure of genes are harmfull, sooner or later you will have to come to terms with this.


I am not confusing anything. In the first place, all mutations are modifications of existing genes. Not every genetic modification, however, is expressed as a modification of the organism that carries it.

Sure, if it is the gene that is being changed. Genetic modifications could be anything from a change in gene expression to gene duplications and other gross structural changes.

When the genetic modification (aka mutation) is expressed as a cellular or organic modification, it is called a variation. If the variation increases the fitness level of the organism, it is an adaptation.

A mutation is not nessacary for an adaptation. You are still accepting that mutations drive evolution. The reason this has become such dogma is because that is the only way you could get single common ancestory. Normal adaptation is caused by existing genetic mechanism that are permenantly fixed. There is no reason for nature to get creative, God has allready done that.




I've got news for you. Have you ever heard of reproduction? Really, Mark, how did you think changes in genetic codes are spread?

Yes, through recombination during meiosis not mutations. That is not big news for me, what may come as a big shock to you when you realize it is, mutations have nothing to do with it.



Do you remember reminding me that cells as well as multicellular organisms are populations?

Yes

Well genes are populations too.

Of course they are.

They also replicate and they compete with each other to replicate more of themselves. And natural selection affects the outcome of that competition too. So it is a genetic mechanism. And if the effect of natural selection is directly on cells or organisms, it is still also indirectly on genes. So how can it not be a genetic mechanism.

Apparently natural selection knows no bounds. It can be applied to any mechanism, it is utterly transendant.




You are right, it is not a thinking process, and when it is spoken of anthropomorphically, as it often is, it is a personification.

It is a personification of natural laws and mechanisms. Ultimatly it is a personification of an unconcious designer, it allways has been.


Those who think of natural selection in this way do not understand it. It is not a force. It is more like an algorithm. The force involved is environmental pressure aka selective pressure. But that force is highly variable and may even be absent. Nothing decrees that a species must evolve in the absence of environmental pressure. And since evolution also depends on the presence or new occurrence of variation (which in turn depends on genetic change) it is possible that no adaptive evolution will occur even in the face of environmental pressure.




Could you clarify what you mean by this?

Pragmatism is the same philisophical system of thought that produced natural selection. Evolution transends legal, political, social, known history and even religion, in all tiers of modern thought. It is metaphysics not natural science.






And the theory of evolution does not predict a complete change into another kind.

It does not predict it, it assumes it and just projects it over incomprehisable periods of time.



What study backs up this statement?

It is supported by the raw data of virtually all of them.


No wonder you think fixation is impossible. This is the meaning of fixation---the elimination of alternative alleles in favour of the most adaptive one, which becomes the species norm. Early tetrapods had six, seven or eight digits, but those alternatives were eliminated in favour of the pentadactyl limb, which humans still retain as the species norm.

It was not retained by some nebulas naturalistic process. We have that in common because they were designed to do simular things. Homology is such an overworked concept, that's what happens when a priori assumptions are taken too far.



You have it backwards. The Ka/Ks ratio is a measure of natural selection. When it is greater than 1, it is an indication of adaptive selection and therefore of a beneficial mutation.

Glad you understand that, it will be important later.


I should hope it does. But apparently you did not understand it.

It's not what I understand that is important here but what I refuse to accept as a self evident fact.

Try this. Changes at an amino acid sequence level occur one gene at a time. Gross structural changes like gene duplications occur in one chromosome at a time.

I'm with you so far.

Both occur in one cell at a time.

Ok

Evolution occurs when these changes spread to other cells or organisms in the population.

Here we go...

Natural selection is what governs the distribution of these changes from the single gene or chromosome in which they first occurred to the genes and chromosomes in other cells and organisms.

Natural selections does not govern anything. It preserves what is allready there and providing an advantage or disadvantage. It's an end result, not a real process.

So let's start with a simple question. In bacterial cell #9277 out of a population of 500 million cells, an amino acid sequence is changed. How is that change spread to two cells?

What happens is that a population of cells have a small subset of cells that have spontaneous mutation(s). Most of the time the cannot compete but if the resources dwindle if provides a slight edge for #9277. This will be of benefit only while their is scarcity but when resources return #9277 will fade away.



How does natural selection account for these adaptive changes adequately without a common ancestor? How is that possible?

It does not account for the single common ancestor, it assumes one for everything.

If I could build a time machine I would go back and plead with Darwin to call it natural preservation of favored traits. Selection is such a bad term, nature does not select anything. Mutations are screened by enzymes that are designed to eliminate errors in the genetic code. There is no real selection process, just an intelligently designed system.


Natural selection is not simple, it is an assumption of a self existing, a priori fact. I believe that now more then ever, I see it every time I come on here and it is stubborn. I have one to, In the begining God created Adam and Eve and Adam is our single common ancestor.

Sorry but I had to shorten this a bit. I tried to keep the more substantive points.

Grace and peace,
Mark
 
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gluadys

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mark kennedy said:
Assuming that natural selection is a quantifiable event, how is it measured?

Maybe someone who is more knowledgeable in the mathematics of biology can answer that. I am not sure if the darwin is the relevant unit or not.


Natural selection eliminates mutations through genetic drift most of the time.

Actually genetic drift refers to the fixation of alleles that is not due to natural selection. Natural selection is the most important driver of evolution, but not the only one.

Some times one will slip through and become inheritable even having an effect on the gene flow.

Please clarify. One [what?] will slip through [what?] and become inheritable?

What do you mean by "have an effect on the gene flow".

As far as I can see, none of this relates to natural selecion.


For millions of years they shared the same environment in equatorial Africa. The migration of apes from that area of our supposed ancestors was 1 million years ago. They, like virtually all the Homo species coexisted for extensive periods of time.

But note that it was the other Homo species that became extinct, not the chimpanzees. This indicates that competition was more intense among the various Homo species than between humans and chimpanzees. This is what we would expect when natural selection is applied to inter-species competition.


We now now what the divergance is,

Knowing what the level of divergence is is a different matter than understanding the process of divergence. You need to understand the process before you can make proclamations as to whether the level of divergence outruns the capabilities of the process.

The process is what I am concentrating on. I will leave the more mathematically inclined to figure out whether the process is capable of producing the observed level of divergence between chimps and humans in the available time-frame.

What I do know is that if you do not relate the level of divergence to the process of divergence, there is no framework within which to judge whether or not the level of divergence is possible or not.

So, back to process...


Changing alleles sounds like the genes have been altered

Correct. Note that the gene alteration occurs only in one cell/organism out of the total population. This means that none of the other members of the population have an altered gene. Just the one individual in whom the alteration occurs.

What this means for the population as a whole is that this gene now exists in the gene pool in two forms, each form being called an allele. One of these alleles is located in one member of the population. The other shows up in all other members of the population.

Now, supposing the altered gene confers a benefit on the one member of the population who carries it, how does it spread from a single member of the population to all the other members of the population?

while change in distribution means a rearrangment of existing alleles.

Possibly, but given your past record, I don't think so. Where are you supposing that this re-arrangement of existing alleles takes place?


Meiosis and recombination,

No, this is not the process of changing the distribution of alleles in a population. And given your reverence for Mendel you should know better. Mendelian inheritance, when unaffected by natural selection, preserves the status quo distribution of alleles. It does not change it.

The recombination of genetic material in meiosis only affects the distribution of the alleles in the germ cells to the gametes, and the probable proportional distribution of those alleles in the offspring of the parents whose germ cells were transformed into gametes.

This recombination which takes place in individual parental germ cells is not sufficient to affect the distribution of alleles in the gene pool of the whole population.

Evolution is a species-wide phenomenon. The change in distribution you need to look at is not the re-arrangement which occurs in meiosis, but the redistribution of alleles in the gene pool of the whole population.

How does that occur? Hint: it has nothing to do with dominanct and recessive alleles. Both dominant and recessive alleles can spread through a population when they are beneficial and can be purged from a population when they are harmful.

One of the goals of hybrids is to make the recessive traits more dominant.

No, the goal of hybridization is to bring together desirable alleles which currently exist in separate breeds. It seems to me that you are confusing "dominant and recessive" with "more or less prevalent" and even with "more or less beneficial". "Dominant and recessive" refers only to which allele is more likely to be expressed in an individual which is heterozygous i.e. carries both the dominant and recessive allele of a gene. In a population it is possible for the dominant allele to be very rare. Especially when its effect is deleterious.


That's selective breeding and supposedly nature does something simular.

Hybridization is part of selective breeding, but the reason it is called selective breeding is because a selection is made among candidates for breeding as to which will be allowed to breed and with whom. Hybridization is not effective in producing a new breed unless it is followed up by selection.

Similarly in nature. Hybridization occurs, but it is rarely the means of producing a new breed or species. Most natural hybrids are incapable of viable reproduction. So most production of new species does not rely on hybridization at all, but only on selection. And even when hybridization is a factor, it has to be supported by selection.


When it becomes fixed it is no longer subject to genetic drift the way mutant alleles have to be.

This is insufficiently explicit for me to decide whether it answers the question. The elaboration, re polar bears does not help. But lets use it to set up the question again.

Today all polar bears are born with white fur. You agree that probably their ancestors did not have white fur. Would you agree this implies a transition period from a population in which white fur was rare, possible even non-existent, to one in which white fur is the fixed trait of the species? In short, the appearance of white fur must have changed over generations from rare, to occasional, to about equal with darker fur, to more frequent than darker fur, to predominant, to sole existing fur colour in the species.

If you agree with this scenario, how does this happen?


Through some genetic mechanism the way these genes are expressed changed in distribution and now have become fixed.

The genetic mechanism is mutation. A mutation in the genes producing melanin and/or other pigments for fur colour suppressed the production of the pigment. Result: white fur.

Now what mechanism changed the distribution of the mutated gene so that this mutation became fixed?


98% of mutations are neutral, the vast majority of the balance are deleterious with a rare few being beneficial in their effect.

Ok. This is the rate of neutral:deleterious:beneficial mutations among all mutations. But the 5% I was referring to is a different rate.

It is a rate at which one mutation may show up in a population. Different mutations, such as those for albinism or microcephaly or six fingers instead of five each turn up consistently at a measurable rate in the human population. Each turns up at a different rate. Possibly as high or even higher than 5%, possibly as low or even lower than 0.5%.

In any case, how often a mutation, or more precisely, a trait based on a mutation, shows up in a population is a totally different concept from how often a mutation is deleterious or beneficial.

Are you clear on the difference?


The ones that effect populations probably effect less then 5%, good, bad or neutral.

No, you have tried to assimilate one rate with one application to a totally different rate applying to a different matter. The rate of deleterious mutations per all mutations is not correlated to the rate at which one deleterious mutation may occur in a population. Keep your rates separate.

That is why I asked you to be specific about which rate you were referring to.



It effects only 5% because only 5% have it to begin with. I think what you are trying to say is the natural selection is screening harmfull effects out.

No, natural selection does not screen out harmful effects. An organism carrying a mutation with deleterious effects will experience the deleterious effects. But natural selection does affect the distribution of the mutation.

So the question is: if a deleterious mutation is found in 5% of the population now, what keeps it from spreading to 6% of the population in the next generation, and 10% a few generations later, and even to more than 50% of the population eventually. Why do deleterious mutations not become more common generation after generation?

(Again, note, this is not a question about the overall rate of deleterious mutations vis-a-vis neutral and beneficial mutations. It is a question about the rate of occurance of one mutation on a population basis.)


Bottlenecks tend to cut down the gene flow,

I am not sure that is true, but in any case it is irrelevant. It does make me wonder if you understand what gene flow refers to. Would you care to explain gene flow as you understand it?

adaptation is much more likely the result of triggered responses.


Can you clarify what a triggered response is and what the "trigger" would be?

There are genetic mechanisms that adapt living creatures to their environments.

Mutation is such a genetic mechanism. But on its own, it does not produce adaptation. Natural selection is needed to make the adaptation effective in the species.

What other genetic mechanisms did you have in mind?

I need to break this response into two parts. Sorry.
 
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gluadys

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Response continued.


markkennedy said:
You seem to have a problem relating this to human evolution. This happens on a subcellular biochemical level, in nature this happens without the genes being substantially altered.

No, you are completely wrong here, except in reference to the evolution of genes themselves. The evolution of species does not occur on a subcellular biochemical level. It occurs on a population level.

The only thing relevant to the evolution of a species that occurs on a subcellular biochemical level is mutation, and I agree, most mutations do not substantially alter the genes in which they occur. However, a substantial alteration of the gene is not necessary for it to have a substantial effect. If it is a gene regulating the activity of other genes, it can have a very substantial effect even if the alteration in the gene is not at all substantial.

I realize that your primary interest is in biochemical changes. But as long as you keep your eye focused on changes in genes, you will not understand how species change occurs. That requires a focus on the population.


Mutations are not the cause of adapations, if anything they are the consequence.

Mutations are not the consequence of adaptations. They are the consequence of copying error, radiation, exposure to mutagenic chemicals, etc.

Adaptation is the consequence of natural selection, not of mutation per se.


The overwhelming majority of changes in the structure of genes are harmfull, sooner or later you will have to come to terms with this.

No, they are neutral as you have already said. 98% of changes at neutral. The majority of non-neutral changes are deleterious. We do not disagree on this point.


Sure, if it is the gene that is being changed. Genetic modifications could be anything from a change in gene expression to gene duplications and other gross structural changes.

Correction noted. We do get overly focused sometimes on one kind of change when there are others, such as chromosomal rearrangements that are also pertinent. Similarly, we tend to focus on natural selection even though it is not the only driver of evolution, sexual selection and genetic drift being also important.



A mutation is not nessacary for an adaptation. You are still accepting that mutations drive evolution.

Actually, I am insisting that natural selection, not mutation, is the driver of evolution.

In a sense you are right that a mutation is not necessary for an adaptation. That is because the mutation need not be novel in the generation in which it becomes adaptive.

Consider this scenario. Jeb McWhirter was conceived in 1790. The sperm involved in this conception carried a copy of his father's genetic information. But it was not a perfect copy. There was a copying error in one gene which made it slightly different from the original gene carried by his father's germ cell. Jeb carries a mutation.

Agreed?

Before he died, Jeb fathered 10 children. Since there is a 50-50 chance that he will pass on the mutated gene from his father to each of these children (the others will receive the unmutated gene from his mother), it is not unreasonable to suppose that 3 of his surviving children inherit the mutated gene.

So now the mutated gene exists in three people. Note, however, that we are not supposing that this gene is further mutated. It is an exact copy of Jeb's gene. But it is different from that of Jeb's father.

Now let us suppose that 2 of these 3 children also have families: 5 in one and 8 in the other. Again, there is a 50% chance that each will receive the mutated gene that first showed up in Jeb. Let's say that 3 in the family of 5 and 6 in the family of 8 inherit this particular gene. Again we suppose no new mutation in this gene in this generation. But now we have 9 people carrying the gene that mutated as their grandfather was conceived.

What do we call this inherited mutated gene? It is not itself a mutation, since there is no change from Jeb to his children or grandchildren. It is an allele i.e. one variant of a gene within a population.

Mutations are the source of alleles. An allele may be neutral or even slightly harmful when it first shows up in a population. But under changed environmental pressures, it can become adaptive.

When creationists say that evolution does not require mutations, they are right in the sense that the selection may be of an allele that already exists in the population (e.g. an allele that confers resistance to pesticide). What they overlook is that the allele exists because a mutation occurred in a previous generation and has been inherited as a neutral mutation from one generation to the next over many generations.


Normal adaptation is caused by existing genetic mechanism that are permenantly fixed.

What existing genetic mechanism are you referring to? And are you saying the mechanism is fixed? Or the adaptation?

There is no reason for nature to get creative, God has allready done that.

Is it unthinkable that God created nature to be creative? Did God not create humans to be creative? Why not nature in general?

Yes, through recombination during meiosis not mutations. That is not big news for me, what may come as a big shock to you when you realize it is, mutations have nothing to do with it.

Well, I am glad you have heard of reproduction. Yet you never seem to take it into account. I am not being facetious here as you may suppose. Reproduction is key to understanding natural selection and evolution.

You are right. Mutations have nothing to do with the spread of mutations through a population. Reproduction is the means of distribution, as in the case of Jeb McWhirter's family above. Mutations do not engineer their own distribution.

But since we are now agreed on reproduction as the method by which mutations are dispersed into a population, why do you claim that the process of "getting these changes in the respective genetic codes has remained elusive to the point of being impossible"?

What is so elusive and impossible about reproduction?


Pragmatism is the same philisophical system of thought that produced natural selection. Evolution transends legal, political, social, known history and even religion, in all tiers of modern thought. It is metaphysics not natural science.

Oh, the grand evolutionary scenario of creationist invention. Not science, then.


It does not predict it, it assumes it

No, evolution neither predicts nor assumes change into a completely different kind.


It is supported by the raw data of virtually all of them.

Please provide a specific example.


Natural selections does not govern anything. It preserves what is allready there and providing an advantage or disadvantage. It's an end result, not a real process.

Well let's not get hung up on semantics. The preservation of what is already there and providing an advantage is what I meant by "governing the distribution" of alleles.



What happens is that a population of cells have a small subset of cells that have spontaneous mutation(s). Most of the time the cannot compete but if the resources dwindle if provides a slight edge for #9277. This will be of benefit only while their is scarcity but when resources return #9277 will fade away.

In the first place I did not specify that #9277 received any benefit from the mutation. Let's assume one that is neutral in regard to fitness.

Second, I did specify that #9277 is one bacterium in a population of bacteria. So, in this case, the small subset consists of one bacterium. Not 50 or 15 or 5---just one.

Finally, let's remember we are speaking of a population of bacteria. The typical life-span of bacteria is on the order of 10-20 minutes. So #9277 is going to be gone in 20 minutes anyway. And not by fading away. Individuals do not fade away. They are alive or they are not alive. Period.

So, after #9277 is no more, what has happened to the mutated gene it carries? Does it still exist in the population? If so, how?

If I could build a time machine I would go back and plead with Darwin to call it natural preservation of favored traits. Selection is such a bad term, nature does not select anything.

I agree. "Natural selection" is not the best description of the process. And it lends itself to unwarranted anthropomorphic descriptions involving goals and purposes that are not part of the natural process.


Mutations are screened by enzymes that are designed to eliminate errors in the genetic code. There is no real selection process, just an intelligently designed system.

You are describing the sub-cellular corrective mechanisms that prevent most mutations from getting into the zygote. Obviously natural selection only applies to those mutations which slip through the correction process and do appear in the zygote.

Sorry but I had to shorten this a bit. I tried to keep the more substantive points.

No problem. You only missed one substantive question. See below.


gluadys said:
mark said:
I think the obvious answer is the natural selection eliminates them.
OK, you have named the process. Now describe it. How does natural selection eliminate deleterious mutations from a population (or as is more usual, keep them restricted to a small proportion of the population.)
 
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rmwilliamsll

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Assuming that natural selection is a quantifiable event, how is it measured?




Maybe someone who is more knowledgeable in the mathematics of biology can answer that. I am not sure if the darwin is the relevant unit or not.


it is possible that you are looking for W.
see: http://evolgen.blogspot.com/2005/12/mean-fitness-genetic-load-and.html
it is part of a nice series on detecting natural selection pressure and is written to a popular level. worth time to investigate.
 
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gluadys

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rmwilliamsll said:
Assuming that natural selection is a quantifiable event, how is it measured?




Maybe someone who is more knowledgeable in the mathematics of biology can answer that. I am not sure if the darwin is the relevant unit or not.


it is possible that you are looking for W.
see: http://evolgen.blogspot.com/2005/12/mean-fitness-genetic-load-and.html
it is part of a nice series on detecting natural selection pressure and is written to a popular level. worth time to investigate.

I think you are right. I remember lucaspa directing a creationist to that equation nearly 2 years ago.
 
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mark kennedy

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rmwilliamsll said:
Assuming that natural selection is a quantifiable event, how is it measured?




Maybe someone who is more knowledgeable in the mathematics of biology can answer that. I am not sure if the darwin is the relevant unit or not.


it is possible that you are looking for W.
see: http://evolgen.blogspot.com/2005/12/mean-fitness-genetic-load-and.html
it is part of a nice series on detecting natural selection pressure and is written to a popular level. worth time to investigate.

Actually it is the 'Ka/Ks ratio that is the classical measure of the overall evolutionary constraint on a gene, where Ka/Ks < 1 it indicates that a substantial proportion of amino acid changes must have been eliminated by purifying selection. Under the assumption that symonymous substitutions are netral, Ka/Ks > 1 implies, but is not a necessary condition for, adaptive or positive selection. (Paraphrased from the Chimpanzee Genome paper cited and linked in the OP)

They use it with regards to:

Gene Evolution
Average rates of evolution
Rapid evolution of individule genes
Variation in evolutionary rate across physically linked genes and
Variation in evolutionary rate across functionally related genes.

That's how natural selection is measured when looking at the genetic basis for human evolution.
 
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gluadys

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mark kennedy said:
Actually it is the 'Ka/Ks ratio that is the classical measure of the overall evolutionary constraint on a gene, where Ka/Ks < 1 it indicates that a substantial proportion of amino acid changes must have been eliminated by purifying selection. Under the assumption that symonymous substitutions are netral, Ka/Ks > 1 implies, but is not a necessary condition for, adaptive or positive selection. (Paraphrased from the Chimpanzee Genome paper cited and linked in the OP)

They use it with regards to:

Gene Evolution
Average rates of evolution
Rapid evolution of individule genes
Variation in evolutionary rate across physically linked genes and
Variation in evolutionary rate across functionally related genes.

That's how natural selection is measured when looking at the genetic basis for human evolution.

The Ka/Ks ratio refers to the evolution of a gene. The W equation refers to the changing frequency of alleles in a population.

Each is applicable in its proper scenario. But don't confound them as if they are referring to the same thing.
 
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shernren

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Here they list the disease alleles that chimapnzees and humans have in common. The way I understand it is this is ground breaking research and this is just raw data. Comparing genomic sequencies and cracking the genetic code are two different things. What stood out in my mind is that of 12,164 disease variants in 1,384 human genes they only identified 16 cases that matched the chimpanzee.

Did you expect that there should be more cases that match? Why?
 
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mark kennedy

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shernren said:
Did you expect that there should be more cases that match? Why?

I see a huge amont of differences between humans and apes. That is just one that I found particularly wide in its scope. The differences reflect a fundamental difference in human physiology or environment according to the paper. I would take this as an indication that the physiology is fundamentally different since few disease risk factors have been firmly established.

This is one of many fundamental differnces between humans and chimpanzees that make me highly skeptical of common ancestory.
 
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mark kennedy

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gluadys said:
The Ka/Ks ratio refers to the evolution of a gene. The W equation refers to the changing frequency of alleles in a population.

Each is applicable in its proper scenario. But don't confound them as if they are referring to the same thing.

That's true and the way the ratio is identified depends on what is being compared. It's just that I keep seeing this kind of ratio in the genetics papers and variations on this approach.
 
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gluadys

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mark kennedy said:
That's true and the way the ratio is identified depends on what is being compared. It's just that I keep seeing this kind of ratio in the genetics papers and variations on this approach.

My point is that there are two different ratios for two different comparisons.

One (Ka/Ks) deals with the ratio of synonymous and non-synonymous mutations in genes.

The other (W equation) deals with the relative fitness of different gene combinations, irrespective of mutations.
 
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shernren

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I see a huge amont of differences between humans and apes. That is just one that I found particularly wide in its scope. The differences reflect a fundamental difference in human physiology or environment according to the paper. I would take this as an indication that the physiology is fundamentally different since few disease risk factors have been firmly established.

This is one of many fundamental differnces between humans and chimpanzees that make me highly skeptical of common ancestory.

Interesting. Now can you quantify "huge difference"? :p Sorry, it's just how I work. I'm a numbers person and numbers make scientific predictions tangible for me.

In the first place, we are not told what genetic sequences were looked for and so we don't know that these genetic diseases are actually fundamental differences to the human physiology on a basic level. For all you know, 200 of those may have been suspected factors of, say, male pattern baldness, etc. The fact that the human genome has some differences in coding shouldn't come as a surprise.

Honestly I don't know enough to show that your interpretation is implausible, but I think mine is plausible. At any rate the researchers don't seem to reach the conclusion you imply, whatever their motives in doing so.
 
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