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Mitchondrial DNA

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gluadys

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Do you believe in God?

Yes.

If so then what do you feel His role in the universe is?

Actually, that is the question I am asking you. I infer from what you have said that you believe God has no role in the universe as long as it is functioning according to its created nature. Would you like to confirm or correct that inference?

I'll provide my answer when I have heard yours.

Well, I'm not going to jump thru a bunch of hoops just to satisfy your little fancy so let's focus on one or two areas. The modern evolutionary synthesis has a lot to say on mathematical population genetics. Then there is a lot on genetic drift, mutations or gene/allele flow. So where do you want to go with this?

Distribution of alleles and what brings about changes in that distribution.

BTW, how would I know if you even knew what you were talking about or not?

Same way I know about you.

Walt Brown's son's work may not be that far off. Look at this:

http://www.windsorpark.org.nz/Feature/Cytochrome divergence.asp

Yes, those figures are quite consistent with the predictions of cladistic evolution.

If you honestly believe they are a problem for evolution, I suggest you need to do some study of cladisitics.

Your statement concerning a mutation in a recessive or dominant gene is vague because it is a blanket statment and cannot apply to all mutations of recessive alleles.

Certainly, it can. All I am saying is that whether an allele is recessive or dominant does not determine whether a mutation in the allele is harmful, neutral or beneficial. The categories are independent of each other.

So it is erroneous to associate only harmful mutations with recessive alleles.
 
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sfs

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Do I care? No.

Tell you what. Work with the OP and find something good in it. It is proof that you are really engaged on the issue. Anyone can find a reason to attack relentlessly on any position. Once you take the other approach, there will be a basis to proceed.

Then I will care.
You will only care if your own statements are accurate if I go and engage in a discussion with someone else? Odd. I asked whether you cared because I wanted to know if it was worth the trouble to respond to your statements. You have answered my question.

I argue and fight with people for a living. I am more than able here, but would prefer not to.
I have zero interest in fighting. If I want fighting I'll listen to the Democratic campaign spokesmen, or to my kids.
 
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sfs

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Could you "briefly" explain how do we know it is pointing to a group of people rather than to one or two individuals? I hope you would NOT pointing me to a research reference. To me, that would be equal to not answering.
We know because changes to the size of a population affect the frequency spectrum of alleles (genetic variants) in the population. A constant-sized population has a characteristic shape of that spectrum, the result of neutral genetic drift. The spectrum for humans looks very much like that shape (especially for African populations). It takes a long time for genetic drift to create that distribution (a large fraction of the age of the DNA in that region, which will be hundreds of thousands of years for autosomal genes -- see my message #40), so it is reasonable to conclude that the population has had a reasonable size for those hundreds of thousands of years.

A dramatic increase in population from a tiny number would produce a very different spectrum; most alleles would be rare, except for whatever variants made it through the bottleneck, which would be at high frequency.
 
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sfs

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Well, I'm not going to jump thru a bunch of hoops just to satisfy your little fancy so let's focus on one or two areas. The modern evolutionary synthesis has a lot to say on mathematical population genetics. Then there is a lot on genetic drift, mutations or gene/allele flow.
Genetic drift, mutations and gene flow are part of population genetics.

So where do you want to go with this? BTW, how would I know if you even knew what you were talking about or not?
I'm not one of the original participants, and I don't want to go anywhere in particular. I just want to correct misstatements about genetics (and anything else I may happen to know about). As for how you can tell if I know what I'm talking about, I'll be happy to tell you how if you really want to know.

Walt Brown's son's work may not be that far off. Look at this:

http://www.windsorpark.org.nz/Feature/Cytochrome divergence.asp
Ouch. Those cytochrome C divergences from bacteria are all supposed to be the same. All of those species are equally distant from bacteria (that is, they have evolved for the same amount of time since they last shared a common ancestor with that bacterium).

Your statement concerning a mutation in a recessive or dominant gene is vague because it is a blanket statment and cannot apply to all mutations of recessive alleles. If a mutation occurrs on a dominant gene or recessive gene it can cause diseases such as Tay Sachs disease
http://en.wikipedia.org/wiki/GM2_gangliosidosis
I have not been following the discussion of dominant vs recessive. Technical correction, however. Genes are neither dominant nor recessive. A particular variant (allele) can be dominant or recessive (or other things) for a particular trait; it need not be the same for all traits. Thus, the allele (in the hemoglobin gene) that causes sickle cell disease also provides protection against malaria. That allele is dominant for malaria resistance but recessive for sickle cell disease.

Getting back to drosophila. The modality given for change in the biota is mutations yet in over 70 plus years and tens of thousands mutations later we still don't see anything but detrimental changes to this animal and no new genomic information as a result. Mutations have not been shown to be a good causitive agent for the diversity in the biota.
We routinely see new beneficial mutations in laboratory selection experiments, which can be done with insects, although they are a lot easier with microbes. For example, if you subject bacteria or malaria parasites in the lab to drugs that work against them, they will quickly develop all kinds of mutations that permit them to thrive even in the presence of the drug. We also routinely see mutations that increase the amount of information in the genome, that is, gene duplication events, in which a single gene ends up as two copies in the genome. Sometimes gene duplications are among the mutations that produce drug resistance; sometimes the duplicated genes acquire further mutations that give them slightly different functions, and permit them to survive even better.
 
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juvenissun

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We know because changes to the size of a population affect the frequency spectrum of alleles (genetic variants) in the population. A constant-sized population has a characteristic shape of that spectrum, the result of neutral genetic drift. The spectrum for humans looks very much like that shape (especially for African populations). It takes a long time for genetic drift to create that distribution (a large fraction of the age of the DNA in that region, which will be hundreds of thousands of years for autosomal genes -- see my message #40), so it is reasonable to conclude that the population has had a reasonable size for those hundreds of thousands of years.

A dramatic increase in population from a tiny number would produce a very different spectrum; most alleles would be rare, except for whatever variants made it through the bottleneck, which would be at high frequency.
Is there anywhere I can see a sample of the spectrum?

So, how do we estimate the number of that small group? What order of number are we talking about? How good (the resolution) is the correlation between the frequency and the size of the group ? Is it theoretically possible that we could pin the number down to a few individuals? What does it take to see that?

My guess is that what we can do now is not very good. I guess the number in the small group which we can see is about a few hundreds? But, is there any way on the observation of the frequency spectrum of alleles be improved, so we could narrow down the number further?

I might be off track. But as you said, you are here to make corrections. So, please do.
 
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sfs

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Is there anywhere I can see a sample of the spectrum?
Figure 2 in this paper shows the spectrum. for several populations. These data were collected in a way that emphasizes higher frequency alleles, so rare alleles don't really enter the picture. The dashed curve shows the distribution expected for a constant-sized population. The green line shows the distribution for an African population (Yoruba in Nigeria); it has the characteristic shape of a population that has increased in size. The red and blue curves represent non-African populations (European and East Asian); these show the effects of a moderate bottleneck.

Other questions I'll have to answer later.
 
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Jimlarmore

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Yes.
Actually, that is the question I am asking you. I infer from what you have said that you believe God has no role in the universe as long as it is functioning according to its created nature. Would you like to confirm or correct that inference?

I'll provide my answer when I have heard yours.

Sorry for the delay on posting. The server here at work cratered and my computer at home is not up and running yet after a fire at our home.

Since I gave up agnostism I studied the Bible. I did this after considering several world religions. The reason I settled on the Bible was because of the prophecies that are sustained by history. So, let me explain my position this way. I have faith in every aspect of what the Bible says. The Bible teaches God knows the beginning from the end. That to me means He stands outside of time. So He is what we call omnipotent. He knows everything so He is what we call omniscient, and last but not least He can be omnipresent. So given those set of parameters there is nothing that is not under God's direction. He has made natural laws that function according to His design whether or not that means He is directly involved with the beat of every insect's wing or not I don't know, but He surely could be.

Distribution of alleles and what brings about changes in that distribution.

First off I've already alluded to this but I do not accept that mutation and natural selection is responsible for the diversity in the biota that we see. I think the primary genomes that exist contain a huge number of alleles many of which may not be functional until a stimulus of some kind requires that they be. Every hear of epigenetics? So based on that statement where do you want to go?


Yes, those figures are quite consistent with the predictions of cladistic evolution.

If you honestly believe they are a problem for evolution, I suggest you need to do some study of cladisitics.

I already have and it just does not work out to be a truely valid way of determining how the biota's diversity came about. There are too many unanswered questions that cladistics cannot answer. The primary one is that analogous morphologies are not produced by the same or similar allele in separate species. IOW, body parts like eyes legs or stomach are not made by the same allele's in different species.

Certainly, it can. All I am saying is that whether an allele is recessive or dominant does not determine whether a mutation in the allele is harmful, neutral or beneficial. The categories are independent of each other.

This is true however, the phenotypical expression of a mutation whether dominant or recessive is over 90% of the time harmful to the recipient of that mutation.

God Bless
Jim Larmore
 
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busterdog

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DNA analysis is used to confirm that there have been changes in both groups from the original parent group.

Yorkies and and Mastifs have different DNA. But, speciation is the issue. Reproduction is possible, but unlikely. Morphology, even enzymatic preferences, is consistent with variation within "kinds" as the YECs say, but isn't the "origin of species."
 
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gluadys

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Yorkies and and Mastifs have different DNA. But, speciation is the issue. Reproduction is possible, but unlikely. Morphology, even enzymatic preferences, is consistent with variation within "kinds" as the YECs say, but isn't the "origin of species."

You have to look not only at mating preferences, but also the possibility of indirect gene flow.

A mating between a Yorkie and a Mastiff may be unlikely, but gene flow between Yorkies and Mastiffs is both possible and likely because both are able and willing to mate with intermediate breeds and so contribute to the common gene pool of the species.

But where is the possibility of gene flow between the new fruit fly groups? They are already sister species having been derived from the same parent species. The only possible intermediate through which they could share genetic information is the parental species. So if they refuse to mate with each other and with the parent species--where is the possibility of gene flow from one group to the other?

If exclusive gene pools do not define species boundaries, what does?
 
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sfs

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I already have and it just does not work out to be a truely valid way of determining how the biota's diversity came about. There are too many unanswered questions that cladistics cannot answer. The primary one is that analogous morphologies are not produced by the same or similar allele in separate species. IOW, body parts like eyes legs or stomach are not made by the same allele's in different species.
You didn't address the point. Do you understand that the site you linked to was wrong? That the observed differences between the species they talk about are exactly what evolution would predict?
 
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busterdog

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You have to look not only at mating preferences, but also the possibility of indirect gene flow.

A mating between a Yorkie and a Mastiff may be unlikely, but gene flow between Yorkies and Mastiffs is both possible and likely because both are able and willing to mate with intermediate breeds and so contribute to the common gene pool of the species.

But where is the possibility of gene flow between the new fruit fly groups? They are already sister species having been derived from the same parent species. The only possible intermediate through which they could share genetic information is the parental species. So if they refuse to mate with each other and with the parent species--where is the possibility of gene flow from one group to the other?

If exclusive gene pools do not define species boundaries, what does?

No disagreement there.

However, the beef with Darwin and evolution is whether new genomes are created. No one argues with microevolution here.

First of all, none of your examples would indicate a change in the number of base pairs that are characteristic of a distinct species.

That is probably as good a boundard as there is between Darwinian evolution and the type of "evolution" that creationists are comfortable with. Yes there are changes in genes that affect mating. Call it a new species if you want. But, there is no successful mutation in evidence that is adding base pairs to genetic information.

Breeding is dependent all types of morphology issues as chemical cues, if not colors for some animals. All these things can be changed by the deletion of information by mutation, but none of these things prove the possibility that amphibians can become lizards or mammals. Your example does not give any indication of bacteria beoming a multicellular organism, or fish becoming an amphibian.

Variations within a species that create distinct mating habits in certain populations is not proof that a new kind has been created.
 
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sfs

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First of all, none of your examples would indicate a change in the number of base pairs that are characteristic of a distinct species.
Changes in the number of base pairs is not characteristic of a distinct species. Individuals within a species (e.g. humans) differ quite a bit in how many base pairs they have, and distinct species can have very similar numbers of base pairs.
 
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busterdog

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Changes in the number of base pairs is not characteristic of a distinct species. Individuals within a species (e.g. humans) differ quite a bit in how many base pairs they have, and distinct species can have very similar numbers of base pairs.

OK.

But, if you can't cross the barrier of a new genome with a distinctly new number of base pairs, you can't exactly have classical Darwinian evolution.

All you can do is extrapolate from examples of so-called speciation.

Creationism (and ID) as a theory predicts that you will never find it. And you haven't. How is that for a successful theory!

Slightly different issue, but not really. The question is never answered by Dawkins:

http://www.youtube.com/watch?v=zaKryi3605g
 
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Jimlarmore

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You didn't address the point. Do you understand that the site you linked to was wrong? That the observed differences between the species they talk about are exactly what evolution would predict?

It depends on how you interpret the information. The differences of some species could be predicted, some not, but the modalities of mutation or natural selection most likely wouldn't accomplish it. Both working from a negativity perspective. For instance a gentleman who posted on the IC thread used the illustration that nearly all of the components of the flagellum are present in a TTSS system that functions completely differently in another species of bacterium. THis is somehow to show that IC is not valid . That the one could easily have given rise to the other. However, you won't find a type three secretorial system morphing into the vestigial, not quite functional, form of a flagellum. IOW, an intermediate form. As a matter of fact I don't think even with man's influence could you make a TTSS turn into a flagellum. Enlighten me if that has already been done. I"ve searched for a study on it but have not found it yet.

God bless
Jim Larmore
 
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sfs

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OK.

But, if you can't cross the barrier of a new genome with a distinctly new number of base pairs, you can't exactly have classical Darwinian evolution.
What is a "distinctly new number of base pairs"? Base pairs come in integral units, and a change of one base pair is a change to a distinctly new number. As I wrote, that happens all the time within a species, so why should there be a barrier when it comes to speciation.

In other words, what are you talking about?

All you can do is extrapolate from examples of so-called speciation.
Some instances of speciation involve the doubling of the number of base pairs. Does that count as a distinctly new number?

Creationism (and ID) as a theory predicts that you will never find it. And you haven't.
Go look up polyploid speciation. What you describe not only happens, it can happen in a single generation.

How is that for a successful theory!
About par for the course.
 
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sfs

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It depends on how you interpret the information. The differences of some species could be predicted, some not, but the modalities of mutation or natural selection most likely wouldn't accomplish it.
We're talking about this link that you posted, right? My question is, do you understand that the results they describe are to be expected from evolution? That is, that the bacterium's cytochrome C should show about the same divergence from all the species they compared it to? The authors of that web page obviously think evolution predicts something else, but I think they are wrong. What do you think evolution predicts about these divergences? Please be specific. If they should all be the same, why did you post the link? If they should be different, explain why they should be different.
 
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busterdog

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What is a "distinctly new number of base pairs"? Base pairs come in integral units, and a change of one base pair is a change to a distinctly new number. As I wrote, that happens all the time within a species, so why should there be a barrier when it comes to speciation.

In other words, what are you talking about?


Some instances of speciation involve the doubling of the number of base pairs. Does that count as a distinctly new number?


Go look up polyploid speciation. What you describe not only happens, it can happen in a single generation.


About par for the course.

You don't say?

Sort of like the guy on youtube you tries to support Dawkins with the Downs Syndrome example?

Why do you guys do this so consistently? Again and again and again. You know what the question is and yet you try jerk us creationists around.

Sarfati explains that your polyploidy is not beneficial mutation. It is not evolution. It is not a new genome.

And you alreay know what I am talking about.


Gene duplication, polyploidy, insertions, etc. do not help — they represent an increase in amount of DNA, but not an increase in the amount of functional genetic information—these create nothing new. Macroevolution needs new genes (for making feathers on reptiles, for example).
In plants, but not in animals (possibly with rare exceptions), the doubling of all the chromosomes may result in an individual which can no longer interbreed with the parent type—this is called polyploidy. Although this may technically be called a new species, because of the breeding isolation, no new information has been produced, just repetitious doubling of existing information. If a malfunction in a printing press caused a book to be printed with every page doubled, it would not be more informative than the proper book. (Brave students of evolutionary professors might like to ask whether they would get extra marks for handing in two copies of the same assignment.)
Duplication of a single chromosome is normally harmful, as in Down’s Syndrome. Insertions are a very efficient way of completely destroying the functionality of existing genes. Biophysicist Dr Lee Spetner in his book Not By Chance (see graphic, right) analyses examples of mutational changes that evolutionists have claimed to have been increases in information, and shows that they are actually examples of loss of specificity, which means they involved loss of information (which is to be expected from information theory).
The gene duplication idea is that an existing gene may be doubled, and one copy does its normal work while the other copy is redundant and non-expressed. Therefore it is free to mutate free of selection pressure (to get rid of it) . However, such ‘neutral’ mutations are powerless to produce new genuine information. Dawkins et al. point out that natural selection is the only possible naturalistic explanation for the immense design in nature (not a good one, as Spetner et al. have shown). The proposal is that random changes produce a new function, then this redundant gene becomes expressed somehow, thus comes under the selective process and is tuned.
It’s all a lot of hand-waving. It relies on a chance copying event, genes somehow being switched off, randomly mutated to something approximating a new function, then being switched on again so natural selection can tune it.
Furthermore, mutations do not just occur in the duplicated gene; they occur throughout the genome. Consequently, all the deleterious mutations have to be eliminated by the death of the unfit. Mutations in the target duplicate gene are extremely rare—it might represent only 1 part in 30,000 of the genome of an animal. The larger the genome the bigger the problem. This is because a larger the genome, the lower the mutation rate that can be sustained without error catastrophe, which means one has to wait longer for any mutation, let alone a desirable one, in the duplicated gene. There just has not been enough time for such a naturalistic process to account for the amount of genetic information that we see in living things.
Dawkins and others have recognised that the ‘information space’ possible within just one gene is so huge that random changes without some guiding force could never come up with a new function. There could never be enough experiments (mutating generations of organisms) to find anything useful by such a process. Note that an average gene of 1,000 base pairs represents 41000 possibilities — that is 10602 (compare this with the number of atoms in the universe estimated at ‘only’ 1080). If every atom in the universe were an experiment every millisecond for the supposed 15 billion years of the universe, this could only try a maximum 10100 of the possibilities. So such a ‘neutral’ process cannot find any sequence with specificity (usefulness), even allowing for the fact that there may be more than just one sequence that is functional to some extent.
So Dawkins and company have the same problem as the neutral selection theory advocates. Increasing knowledge of the molecular basis of biological functions has exploded the known ‘information space’ such that mutations and natural selection, with or without gene duplication, or any other known natural process, cannot account for the irreducibly complex nature of living systems.

http://www.answersingenesis.org/home/area/bios/

Is there one example of polypoidy in a trillion that might possibly beneficial and reproducible? I know Darwin likes and thrives on the long odds. But, lets see just one of those horses payoff.
 
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