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Why Hasn't Malaria Won.


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#21 Bruce V.

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Posted 29 November 2007 - 11:41 PM

Hi Bruce,
First, I can't say I understand Behe's point so it is hard to criticize directly. However, I can say that if one were to look at animal breeds developed by artificial selection, I am fairly sure we can find lots of cases where the breeds differ by multiple mutations. However, it is always difficult to determine what mutations produce particular traits - so it is difficult to say something like "the new breed showed 4 mutations and 3 of those are beneficial".

Suppose you were a pigeon breeder trying to get a breed a fancy pigeon and after 200 generations you get this from a regular pigeon

Posted Image

Ok, now suppose you find that the new pigeon has 3 mutations in their genome. Were these beneficial? Did you need all three of the mutations to get this bird? You could try to do an experiment and change some of the genes back but that would take some clever gene splicing (but possible).

It is possible to also get these different mutations sequentially, which some might consider to be unsurprising micro-evolutionary steps.

I think Behe might be trying to argue that all three are unlikely to occur at the same time. But even there I would need to know the particular assumptions made. Suppose, for example, every new generation has 3 mutations on average at random places. Out of all the offspring with 3 mutations, I take the one I think looks pretty and allow those to breed. Ok, since at least one of those worked out, the answer is about 100% probability that the new breed will have 3 mutations.

None of this seems surprising to me. So I don't know what Behe finds surprising. I don't think he is arguing that plasmodia can't evolve resistance because we know it does. Is he suggesting that plasomodia is helped by God?

Behe appears to know the way most biologists believe information gets added to the genome. To quote Behe:

"Gene duplication is thought to be a major source of evolutionary innovation because it allows one copy of a gene to mutate and explore genetic space while the other copy continues to fulfill the original function."

So he seems to know how it works, but he doesn't think it is probable enough. Unfortunately, I don't get his math.

James

p.s. The Nova show used transcripts to show what Behe and other said in the trial so I am not sure if you suggesting the show was unfair or that the judge in the trial was unfair.

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Hi James,

I need to reread Behe' s book to make sure I am representing his thesis correctly. We may be talking apple's and oranges.

Is he suggesting that plasomodia is helped by God?


No, I don't think Behe is making a statement about God either way. He is making a case against macro-evolution: small changes x millions years = big change

From this web site I found and article that talks about mutation build up. The basic premise is that negative mutations greatly exceed positive ones that the mutation build up is negative. It is actually a case that we are regressing not evolving.

http://www.youngeart...on_article1.htm

This is important since evolution requires "beneficial" mutations to build up and outpace harmful mutations such that new features and organs can arise (I say "beneficial" loosely, since there are no known examples where a mutation added information to the genome, though there are some that under certain circumstances can provide a temporary or superficial advantage to a species[9]). If over time harmful mutations outpace "beneficial" ones to fixation, evolution from molecules-to-man surely cannot occur. This would be like expecting to get rich despite consistently spending more money than you make.


This may address that A B and C mutation statement you talked about earlier. This is what I think you where saying in my own words.

Mutation B hangs around not providing much benefit until mutation C happens. The combination of mutations B and C are far superior than mutation A.

The article states that negative mutations builds up much faster than positive ones. Hence, the effect of mutation build up is very negative.

#22 jamesf

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Posted 02 December 2007 - 10:58 AM

Hi James,

I need to reread Behe' s book to make sure I am representing his thesis correctly.  We may be talking apple's and oranges.
No, I don't think Behe is making a statement about God either way.  He is making a case against macro-evolution: small changes x millions years = big change

From this web site I found and article that talks about mutation build up.  The basic premise is that negative mutations greatly exceed positive ones that the mutation build up is negative.  It is actually a case that we are regressing not evolving.

http://www.youngeart...on_article1.htm
This may address that A B and C mutation statement you talked about earlier.  This is what I think you where saying in my own words. 

Mutation B hangs around not providing much benefit until mutation C happens.  The combination of mutations B and C are far superior than mutation A.

The article states that negative mutations builds up much faster than positive ones.  Hence, the effect of mutation build up is very negative.

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Hi Bruce,

One thing I would like to understand. Why do you believe that negative mutations would "build up"? Negative mutations can result in aborted fetuses, abnormalities, make you infertile, early death etc. The harmful mutated genes are removed from the gene pool in all these cases. They don't build up.

Positive mutations (like the recent mutations that confer lactose tolerance) can spread relatively quickly through the population because it confers an advantage to the offspring (your offspring have access to a new source of protein).

Most mutations are neutral. The last I read was that you probably have on the order of 100 mutations relative to your parents (changes in your genes that are found in neither of your parents). But I suspect you are doing fine.

In the example I gave above, mutation A was originally beneficial but the gene (call it Gene A) is no longer needed. So if the gene mutated again and created a new protein, it would likely be neutral (i.e. useless), but it could be helpful if some process in the body found some use for the new protein. However, if the new protein stopped some important process in the body, the owner would die, and the mutation would not be passed on.

Hope that helps.

#23 Bruce V.

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Posted 02 December 2007 - 03:39 PM

Hi Bruce,

One thing I would like to understand. Why do you believe that negative mutations would "build up"?  Negative mutations can result in aborted fetuses, abnormalities, make you infertile, early death etc. The harmful mutated genes are removed from the gene pool in all these cases. They don't build up.

Positive mutations (like the recent mutations that confer lactose tolerance) can spread relatively quickly through the population because it confers an advantage to the offspring (your offspring have access to a new source of protein).

Most mutations are neutral. The last I read was that you probably have on the order of 100 mutations relative to your parents (changes in your genes that are found in neither of your parents). But I suspect you are doing fine.

In the example I gave above, mutation A was originally beneficial but the gene (call it Gene A) is no longer needed. So if the gene mutated again and created a new protein, it would likely be neutral (i.e. useless), but it could be helpful if some process in the body found some use for the new protein. However, if the new protein stopped some important process in the body, the owner would die, and the mutation would not be passed on.

Hope that helps.

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Hi James,

From the article.

Let's first consider a recent study in the science journal Nature [4]. By comparing human and chimp differences in protein-coding DNA, the authors arrived at a deleterious (harmful) mutation rate for humans of U=1.6 per individual per generation . They acknowledged that this seemed too high, but quickly invoke something called "synergistic epistasis" as a just-so explanation (I'll address this later). The authors also acknowledged that favorable assumptions were used in their study. For example, they did not account for the impact of insertions/deletions, and mutations to non-genic sequences such as introns. When they accounted for the impact of these and other assumptions [7], they arrived at a mutation rate of U = 3.1, which they admitted was "remarkably high". Widely recognized geneticist James Crow in the same Nature issue concurred that the deleterious rate was more likely U=3.

Since the Nature study, a recent study published in the journal Genetics revealed that the rate was even more of an underestimate:

"The genomic deleterious mutation rate in humans was previously estimated to be at least 1.6 on the basis of an estimate that 38% of amino acid mutations are deleterious. The genomic deleterious mutation rate is likely much larger given our estimate that 80% of amino acid mutations are deleterious and given that it does not include deleterious mutations in noncoding regions, which may be quite common. [emphasis mine]." [6]

Using a straight extrapolation yields a mutation rate of U=3.4. What exactly does this mean, and why is this a serious problem for evolution? It is related to the renowned geneticist J.B.S. Haldane's reproductive cost problem that Walter Remine eloquently illuminated in "The Biotic Message"[8]. What we will determine is how many offspring are needed to produce one that does not receive a new harmful mutation during the reproduction process. This is important since evolution requires "beneficial" mutations to build up and outpace harmful mutations  such that new features and organs can arise (I say "beneficial" loosely, since there are no known examples where a mutation added information to the genome, though there are some that under certain circumstances can provide a temporary or superficial advantage to a species[9]). If over time harmful mutations outpace "beneficial" ones to fixation, evolution from molecules-to-man surely cannot occur. This would be like expecting to get rich despite consistently spending more money than you make.



#24 jamesf

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Posted 02 December 2007 - 10:56 PM

Hi James,

From the article.

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Well, I tried reading the original article and the genetics articles that responded - and the response to that. From reading these papers, all I can tell you is that the academic community is currently debating how to define a harmful mutation. Even the most recent papers are debating how one can evaluate fitness - especially when there are two mutations.

They also seem to be talking about those mutations 'which show a phenotypic effect' tend to be deleterious. Since most mutations do not show phenotypic effects, I can only assume that most (which do not show phenotypic effects) are neutral.

Certainly lots of debate out there in the academic community on this issue. Don't see a clean answer yet though. I'll try looking again.

Here are some examples.

Shaking the ‘deleterious mutations’ dogma?

Thomas BataillonE-mail The Corresponding Author
UMR 1097 ‘Diversité & Génomes des Plantes Cultivées’ INRA, Domaine de Melgueil, 34130, Mauguio, France
Available online 7 June 2003.

Estimating the genome-wide mutation rate and the distribution of mutation effects on fitness is important both for the evolution of s@x and the fate of small populations. To date, most studies have suggested that most mutations with phenotypic effects tend to be deleterious to fitness. However, Shaw et al., studying the effect of mutations on fitness in Arabidopsis thaliana, now suggest that mutations can often have beneficial effects. These findings have been questioned by Keightley and Lynch.


Nature Genetics 39, 555 - 560 (2007)
Published online: 18 March 2007 | doi:10.1038/ng1998
Distributions of epistasis in microbes fit predictions from a fitness landscape model
Guillaume Martin1,2, Santiago F Elena3 & Thomas Lenormand1
How do the fitness effects of several mutations combine? Despite its simplicity, this question is central to the understanding of multilocus evolution. Epistasis (the interaction between alleles at different loci), especially epistasis for fitness traits such as reproduction and survival, influences evolutionary predictions1, 2 "almost whenever multilocus genetics matters"3.



#25 Bruce V.

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Posted 03 December 2007 - 12:02 PM

Well, I tried reading the original article and the genetics articles that responded - and the response to that. From reading these papers, all I can tell you is that the academic community is currently debating how to define a harmful mutation. Even the most recent papers are debating how one can evaluate fitness - especially when there are two mutations.

  They also seem to be talking about those mutations 'which show a phenotypic effect' tend to be deleterious. Since most mutations do not show phenotypic effects, I can only assume that most (which do not show phenotypic effects)  are neutral.

  Certainly lots of debate out there in the academic community on this issue. Don't see a clean answer yet though. I'll try looking again.

Here are some examples.

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This is from memory, I will look it up and information you want validated.

The reason malaria mutations are interesting is because red blood cells are very unusual. Most type of cells contains many different kinds of proteins, no one of which overwhelms the cell. Because its job is to carry as much oxygen as it can from the lungs to the tissues, by contrast, the red blood cell is stuffed with one protein, hemoglobin: 90% of red blood cell proteins are hemoglobin. The high concentration of hemoglobin makes it lot easier for mutations (like shape) to have a noticeable effects. This is true for both the parasite and the host. This is why we have seen so many positive mutations (loosely defined) from malaria: The red blood cell system is not that complex relatively speaking.

The problem for beneficial mutations now is that life and become very complex. For a biological system to do its complex job is has a series of proteins that each does its part: like a computer code. If one protein mutates then its function changes or it ceases to do its part, then whole system looses continuity. For any mutation to be beneficial it requires that it integrate with the other proteins within the system. Therefore, to build a new and better system requires multiple mutations so that all the proteins work together. Here is the rub, most single mutations are rather rare and almost always negative: Any negative mutation breaks the system. The new system requires multiple positive mutations without any negative ones. You can’t build a system one piece at a time in small incremental steps: You need many changes all at once for it to work.

Have a good one,

Bruce

#26 jamesf

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Posted 03 December 2007 - 05:12 PM

This is from memory, I will look it up and information you want validated.

The reason malaria mutations are interesting is because red blood cells are very unusual.  Most type of cells contains many different kinds of proteins, no one of which overwhelms the cell.  Because its job is to carry as much oxygen as it can from the lungs to the tissues, by contrast, the red blood cell is stuffed with one protein, hemoglobin: 90% of red blood cell proteins are hemoglobin.  The high concentration of hemoglobin makes it lot easier for mutations (like shape) to have a noticeable effects.  This is true for both the parasite and the host.  This is why we have seen so many positive mutations (loosely defined) from malaria:  The red blood cell system is not that complex relatively speaking.

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Hi Bruce,
First off, with regard to malaria, most of our discussion has focused on the mutations of the malaria parasite - the plasmodium (not the human). And there is lots of work on how these parasites evolve when the humans take drugs that kill them. There seems to be lots of evidence that these parasites have developed mutations that can make them relatively immune to the drugs that are trying to kill them off. Human mutations that help humans resist malaria are a different issue - but we could go there too. Of course, human mutations are much slower. There are five mutations that humans have had in response to malaria that is argued make people more resistant.

Wikipedia has a nice description of those
http://en.wikipedia.org/wiki/Malaria

The problem for beneficial mutations now is that life and become very complex.  For a biological system to do its complex job is has a series of proteins that each does its part:  like a computer code.  If one protein mutates then its function changes or it ceases to do its part, then whole system looses continuity.  For any mutation to be beneficial it requires that it integrate with the other proteins within the system.  Therefore, to build a new and better system requires multiple mutations so that all the proteins work together.  Here is the rub, most single mutations are rather rare and almost always negative: Any negative mutation breaks the system. The new system requires multiple positive mutations without any negative ones.  You can’t build a system one piece at a time in small incremental steps:  You need many changes all at once for it to work.

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I think it is very important to recognize the major role of gene duplications. They come in many forms. But I think I will quote Behe since he said it perfectly well.

From Behe...
"Gene duplication is thought to be a major source of evolutionary innovation because it allows one copy of a gene to mutate and explore genetic space while the other copy continues to fulfill the original function."

So lets go through this. First a gene duplicates. The mutation is neutral because both genes continue to produce the same protein.

Second, another mutation changes the amino acids in one of the two genes. Four things can happen.
1. The new gene fails to produce a protein (no problem here since you have the other protein)
2. The new gene produces a new protein that is useless (again, no problem)
3. The new gene produces a protein that interferes with some other process
4. The new gene produces a protein that assists some other process

As long as 3 does not occur, then the animal continues to produce viable offspring. If 1,2 or 4 occur then to use Behe's phrase, the gene can continue to "explore genetic space while the other copy continues to fulfill the original function."

If one of the mutation succeeds during this "exploration".. Bingo! the animal wins and has more offspring than the neighbors and the gene spreads through the population.

I should also note that I have read a number of accounts suggesting that important genes often have 'backups' . Here is a quote from a recent article ....

http://www.bioone.or...e...MP]2.0.CO;2

“A key question in molecular genetics is why severe mutations often do not result in a detectably abnormal phenotype,” begins an article by Weizmann Institute of Science geneticists Ran Kafri, Arren Bar-Even, and Yitzhak Pilpel in the March issue of Nature Genetics. They then proceed to show how 40 different knockout mutations in yeast (Saccharomyces cerevisiae) are rescued by activation of functionally similar duplicate genes.

Gene duplication, long considered to be a key evolutionary mechanism, has been found to be a common phenomenon through genome sequencing. Large proportions of the genomes that have been sequenced (30 percent in S. cerevisiae; 65 percent in A. thaliana) have been found to contain duplicated, or paralogous, genes. Many duplicates are lost; yeast, for example, appears to have undergone duplication of the whole genome, with subsequent loss of most of the genetic redundancy. One way it is supposed that duplicates are stably maintained in the genome is that they undergo a division of labor, or subfunctionalization, often involving differential expression, soon after duplication.

Pilpel and colleagues mined the wealth of available yeast data for viable mutants lacking one of the members of duplicate gene pairs and examined the expression profiles of the paralogs. The more dispensable genes, that is, those with better backup, differ from their paralogs in their expression. When both are present, they tend not to be coexpressed. When one is absent, the other is up-regulated to back up the missing gene.


p.s. in my way of thinking, a gene which duplicates then mutates to produce a new protein, adds information. But I use the classic academic definition of information. I can't say I understand the other definitions.

#27 Bruce V.

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Posted 05 December 2007 - 09:13 AM

Hi Bruce,
First off, with regard to malaria, most of our discussion has focused on the mutations of the malaria parasite - the plasmodium (not the human). And there is lots of work on how these parasites evolve when the humans take drugs that kill them. There seems to be lots of evidence that these parasites have developed mutations that can make them relatively immune to the drugs that are trying to kill them off. Human mutations that help humans resist malaria are a different issue - but we could go there too. Of course, human mutations are much slower. There are five mutations that humans have had in response to malaria that is argued make people more resistant.

Wikipedia has a nice description of those
http://en.wikipedia.org/wiki/Malaria
I think it is very important to recognize the major role of gene duplications. They come in many forms. But I think I will quote Behe since he said it perfectly well.

From Behe...
"Gene duplication is thought to be a major source of evolutionary innovation because it allows one copy of a gene to mutate and explore genetic space while the other copy continues to fulfill the original function."

So lets go through this. First a gene duplicates. The mutation is neutral because both genes continue to produce the same protein.

Second, another mutation changes the amino acids in one of the two genes. Four things can happen.
1. The new gene fails to produce a protein (no problem here since you have the other protein)
2. The new gene produces a new protein that is useless (again, no problem)
3. The new gene produces a protein that interferes with some other process
4. The new gene produces a protein that assists some other process

As long as 3 does not occur, then the animal continues to produce viable offspring. If 1,2 or 4 occur then to use Behe's phrase, the gene can continue to "explore genetic space while the other copy continues to fulfill the original function."

If one of the mutation succeeds during this "exploration".. Bingo! the animal wins and has more offspring than the neighbors and the gene spreads through the population.

I should also note that I have read a number of accounts suggesting that important genes often have 'backups' . Here is a quote from a recent article ....

http://www.bioone.or...e...MP]2.0.CO;2
p.s. in my way of thinking, a gene which duplicates then mutates to produce a new protein, adds information. But I use the classic academic definition of information. I can't say I understand the other definitions.

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Hi James,

I have been busy so I have not been able to reply on this- it may take me a few days.

The question we were discussing was: How do positive mutations build up so that one day they can evolve into a new system?

Is the best answer gene duplication? If so, I will attempt to address this in a few days.

What Behe was doing was not addressing each and every kind of mutation. He was looking looking at it empirically. That is, for every ~10^12 malaria we, on average, have a beneficial mutation (loosely defined): for 2 mutations it is ~10^20. Sometimes there are so many variables you have to look at it empirically to get a realistic picture. From what I have read, the mutation "build up" has been limited in malaria from an empirical standpoint: In other words, it does not look like malaria is poised to have a macro evolutionary change. IMO the staggering numbers of malaria should have produced something more from an evolution standpoint.

Theoretically speaking, DNA duplication could work, but has it?

Cheers,

Bruce

#28 Bruce V.

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Posted 06 December 2007 - 12:56 PM

Hi Bruce,
First off, with regard to malaria, most of our discussion has focused on the mutations of the malaria parasite - the plasmodium (not the human). And there is lots of work on how these parasites evolve when the humans take drugs that kill them. There seems to be lots of evidence that these parasites have developed mutations that can make them relatively immune to the drugs that are trying to kill them off. Human mutations that help humans resist malaria are a different issue - but we could go there too. Of course, human mutations are much slower. There are five mutations that humans have had in response to malaria that is argued make people more resistant.

Wikipedia has a nice description of those
http://en.wikipedia.org/wiki/Malaria
I think it is very important to recognize the major role of gene duplications. They come in many forms. But I think I will quote Behe since he said it perfectly well.

From Behe...
"Gene duplication is thought to be a major source of evolutionary innovation because it allows one copy of a gene to mutate and explore genetic space while the other copy continues to fulfill the original function."

So lets go through this. First a gene duplicates. The mutation is neutral because both genes continue to produce the same protein.

Second, another mutation changes the amino acids in one of the two genes. Four things can happen.
1. The new gene fails to produce a protein (no problem here since you have the other protein)
2. The new gene produces a new protein that is useless (again, no problem)
3. The new gene produces a protein that interferes with some other process
4. The new gene produces a protein that assists some other process

As long as 3 does not occur, then the animal continues to produce viable offspring. If 1,2 or 4 occur then to use Behe's phrase, the gene can continue to "explore genetic space while the other copy continues to fulfill the original function."

If one of the mutation succeeds during this "exploration".. Bingo! the animal wins and has more offspring than the neighbors and the gene spreads through the population.

I should also note that I have read a number of accounts suggesting that important genes often have 'backups' . Here is a quote from a recent article ....

http://www.bioone.or...e...MP]2.0.CO;2
p.s. in my way of thinking, a gene which duplicates then mutates to produce a new protein, adds information. But I use the classic academic definition of information. I can't say I understand the other definitions.

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Hi James,

One of the best evidences for gene duplication is the arctic fish (nonothenoids). In the arctic, salt water temperature goes below freezing point of the blood of this fish. Why doesn’t the fish’s blood freeze? Ice needs a crystal seed to start; once a seed is started the tiny crystals form rapidly. These fish have evolved, by gene duplication, an antifreeze which sticks to the seed crystals and prevents them from growing. These antifreeze proteins are similar to this fish’s digestive enzyme. Both portions had a certain 9 letter sequence, but in the antifreeze gene the 9-nucleotide region was repeated may times. When the digestive enzyme was copied, the process stuttered, creating multiple copies. Later these duplicate genes had a further deletion mutation which created a stable antifreeze protein(s) that gave this arctic fish a competitive advantage.

Looks good so far, but this example also underscores the limits of random mutation rather than its potential. It turns out that the antifreeze protein in Antarctic fish is not really a discrete structure comparable to, say, hemoglobin. Hemoglobin and almost all other proteins are coded by single genes that produce proteins of definite length. This mutation looks like genetic junk: There are multiple genes of different lengths, all of which produce amino acid chains that get chopped up into smaller fragments of differing lengths. In fact, the Antarctic protein appears not to have any definitive structure. Its amino acid chain is floppy and unfolded, unlike the very precisely folded shapes of most proteins. Nor do these proteins interact with other proteins and they are not building new molecular machinery or systems.

(MOST OF THIS INFORMATION IS FROM “THE EDGE OF EVOLUTION” page 80-81 by Michael Behe. I shortened and paraphrased it in my own words.

The questions I have about gene duplication are:
1. Isn’t gene duplication usually genetic junk that causes problems and not solutions, like Huntington’s disease?
2. Doesn’t DNA show a high degree of complexity or aperiodicity, not redundant order like what you would expect to see with gene duplication?

#29 jamesf

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Posted 08 December 2007 - 10:36 PM

The questions I have about gene duplication are:
1. Isn’t gene duplication usually genetic junk that causes problems and not solutions, like Huntington’s disease?
2. Doesn’t DNA show a high degree of complexity or aperiodicity, not redundant order like what you would expect to see with gene duplication?

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Hi Bruce,
Been traveling, so my responses are a bit slow
1. As far as the first question, many many mutations are neutral. Go to google and try typing in "neutral mutations" or "gene duplication", or "chromosome duplication" and you will find lots of websites and lots of papers on the subjects.

Here are a couple links
http://en.wikipedia....us_substitution
http://en.wikipedia....wiki/Polyploidy
http://findarticles....110/ai_78334664

Some mutations in the base pairs with a gene does not change the amino acid that is created with the gene. Since the amino acid is the same, the protein that is produced is the same. These neutral mutations are one of the ways geneticists determine the evolutionary distance between two species. Some genes are crucial to organisms, so if the mutation is not neutral then the organism dies. If the mutation is neutral then it is passed down to the offspring. By looking at the number of neutral mutations in these genes and knowing the average rate of mutation, one can get a handle on how many generations separate two species of sparrow - or separate two species of primate.

Here is a related link.
http://biology.plosj...al.pbio.0020207

There are many kinds of gene duplication and chromosome duplication. Chromosome doubling is relatively common in plants and is often encouraged by plant breeders to create new plant varieties. Here is a nice link

http://www.ces.ncsu..../polyploidy.htm

As you can read, in the 1930s some plant breeders learned how to help produce these polyploidal plants (with duplicate genes and chromosomes). Yes, the duplicate genes can be harmful, but they can also be quite beneficial. Here is a quote from the above link.

Plants with increased ploidy levels are often apparent by their distinct morphology. Increasing ploidy often results in increased cell size that in turn results in thicker, broader leaves and larger flowers and fruit. Shoots are often thicker and can have shortened internodes and wider crotch angles. Plants with high ploidy levels (e.g. octaploids) can have distorted growth and reduced growth rates.



Well, there's a bit to read there. And I can not say I am an expert at this stuff, but I can try to help with it.

James

#30 Bruce V.

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Posted 10 December 2007 - 01:57 PM

Hi Bruce,
  Been traveling, so my responses are a bit slow
1. As far as the first question, many many mutations are neutral. Go to google and try typing in "neutral mutations" or "gene duplication", or "chromosome duplication" and you will find lots of websites and lots of papers on the subjects.

Here are a couple links
http://en.wikipedia....us_substitution
http://en.wikipedia....wiki/Polyploidy
  http://findarticles....110/ai_78334664

Some mutations in the base pairs with a gene does not change the amino acid that is created with the gene. Since the amino acid is the same, the protein that is produced is the same. These neutral mutations are one of the ways geneticists determine the evolutionary distance between two species. Some genes are crucial to organisms, so if the mutation is not neutral then the organism dies. If the mutation is neutral then it is passed down to the offspring.  By looking at the number of neutral mutations in these genes and knowing the average rate of mutation, one can get a handle on how many generations separate two species of sparrow - or separate two species of primate.

Here is a related link.
http://biology.plosj...al.pbio.0020207

There are many kinds of gene duplication and chromosome duplication. Chromosome doubling is relatively common in plants and is often encouraged by plant breeders to create new plant varieties. Here is a nice link

http://www.ces.ncsu..../polyploidy.htm

As you can read, in the 1930s some plant breeders learned how to help produce these polyploidal plants (with duplicate genes and chromosomes). Yes, the duplicate genes can be harmful, but they can also be quite beneficial. Here is a quote from the above link.

Plants with increased ploidy levels are often apparent by their distinct morphology. Increasing ploidy often results in increased cell size that in turn results in thicker, broader leaves and larger flowers and fruit. Shoots are often thicker and can have shortened internodes and wider crotch angles. Plants with high ploidy levels (e.g. octaploids) can have distorted growth and reduced growth rates.



Well, there's a bit to read there. And I can not say I am an expert at this stuff, but I can try to help with it.

James

View Post


Hi James,


Evolution use the fossil record and DNA sequencing as proof of morphological changes. This is good science because it shows it happened somehow. However, IMO evolutionist have not explained the cause of this morphological change. They have theories and hypothesis but no proof. For example, small incremental steps are not a viable mechanism for large morphological changes. They have new theories that explain how large changes can happen all at once. For example,

1. Mutation of the DNA switch: The switch mutation affects the way whole groups of genes are affected by one mutation. (Evo-devo)
2. That there is part of our DNA that we thought wasn’t used. Rather, some believe it is used and is like an empty hard drive. It builds up information until it becomes useful.
3. Gene or DNA duplication: This is similar, because this duplicated DNA can build up useful mutations and has some starting point. This has been discussed some above.
4. Early mutations. A mutation early in an embryo’s development process has a better chance of causing morphological changes rather than mutations latter in the embryonic process.


According to scenarios 2-3, non-coding sections of the genome, or duplicated sections of coding regions, can experience a protracted period of “neutral evolution” during which alterations in nucleotide sequences have no discernible effect on the function of the organism. Eventually, however, a new gene sequence will arise that can code for a novel protein. At that point, natural selection can favor the new gene and its functional protein product, thus securing the preservation and heritability of both.


Stephen Myer quote from this article


This scenario has the advantage of allowing the genome to vary through many generations, as mutations “search” the space of possible base sequences. The scenario has an overriding problem, however: the size of the combinatorial space (i.e., the number of possible amino acid sequences) and the extreme rarity and isolation of the functional sequences within that space of possibilities. Since natural selection can do nothing to help generate new functional sequences, but rather can only preserve such sequences once they have arisen, chance alone--random variation--must do the work of information generation--that is, of finding the exceedingly rare functional sequences within the set of combinatorial possibilities. Yet the probability of randomly assembling (or “finding,” in the previous sense) a functional sequence is extremely small.


One problem with the isolated DNA strands, items 2 and 3, it that it relies on random mutation alone. There is no survival of the fittest mechanism. We have to wait until the whole process is finished by completely random events. In this way, James, the process resembles abiogenesis rather than a typical evolutionary process. They do the mathematics which shows absurd improbabilities. Dawkins has noted that scientific theories can rely on only so much “luck” before they cease to be credible.


Stephen Myer quote from this article


Thus, although this second neo-Darwinian scenario has the advantage of starting with functional genes and proteins, it also has a lethal disadvantage: any process of random mutation or rearrangement in the genome would in all probability generate nonfunctional intermediate sequences before fundamentally new functional genes or proteins would arise. Clearly, nonfunctional intermediate sequences confer no survival advantage on their host organisms. Natural selection favors only functional advantage. It cannot select or favor nucleotide sequences or polypeptide chains that do not yet perform biological functions, and still less will it favor sequences that efface or destroy preexisting function.

Evolving genes and proteins will range through a series of nonfunctional intermediate sequences that natural selection will not favor or preserve but will, in all probability, eliminate (Blanco et al. 1999, Axe 2000). When this happens, selection-driven evolution will cease. At this point, neutral evolution of the genome (unhinged from selective pressure) may ensue, but, as we have seen, such a process must overcome immense probabilistic hurdles, even granting cosmic time.


In my own words, negative mutations add up and are cumulative in any isolated stand of DNA. The mutations end up destroying the genes functionality and its specific folding that made it functional. Also, the new protein has to fit into a new system or creating a new system by pure random events. Again, we do not have a survival of the fittest mechanism in isolated DNA. This adds a significant hurtle to the isolated DNA scenarios.

I can go into scenarios 1 and 4 later. I am tired now.

Bruce

#31 jamesf

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Posted 14 December 2007 - 09:38 AM

Hi James,
Evolution use the fossil record and DNA sequencing as proof of morphological changes.  This is good science because it shows it happened somehow.  However, IMO evolutionist have not explained the cause of this morphological change.  They have theories and hypothesis but no proof. 

View Post


Hi Bruce,
First off, it is important to remember that science almost never works by using "proofs". Science is a competition between theories. The best theory is the one that accounts for the most data without conflicting with accepted facts. The theory of gravity, molecular theory, gas theories etc are simply the best account of data. Scientists are constantly battling to make their theory the accepted theory in their field. It might take 30 years for a theory to become accepted after it is first proposed and many many battles. But evidence and mathematical proofs are used to to support the highest achievement: to have the accepted theory.

For example, small incremental steps are not a viable mechanism for large morphological changes.  They have new theories that explain how large changes can happen all at once. 

View Post


This first statement goes against most all evolutionary theorists. The general view is most all large changes have followed from a series of smaller morphological changes. Suppose we have an animal evolve from a squirrel to a flying squirrel (a glider) then it evolves towards a bat-like creature that can flap its wings. The standard argument is that all such changes involve relatively small incremental changes.
There have been some major genetic changes in the history of vertebrates. Chromosome doubling, chromosome fusing etc. But these kinds of changes are relatively rare and most of these "experiments" as with Down's syndrome do not result in offspring that pass on the genes. Some minor genetic changes do produce large morphological changes (e.g., extra fingers in the Amish). However, if these are 'negative' mutations and reduce the chances of having offspring, they do not accumulate. They are quickly removed from the gene pool.



  They have new theories that explain how large changes can happen all at once.  For example,

1. Mutation of the DNA switch:  The switch mutation affects the way whole groups of genes are affected by one mutation.  (Evo-devo)
2. That there is part of our DNA that we thought wasn’t used.  Rather, some believe it is used and is like an empty hard drive.  It builds up information until it becomes useful.
3. Gene or DNA duplication: This is similar, because this duplicated DNA can build up useful mutations and has some starting point.  This has been discussed some above.
4. Early mutations.  A mutation early in an embryo’s development process has a better chance of causing morphological changes rather than mutations latter in the embryonic process.
According to scenarios 2-3, non-coding sections of the genome, or duplicated sections of coding regions, can experience a protracted period of “neutral evolution” during which alterations in nucleotide sequences have no discernible effect on the function of the organism. Eventually, however, a new gene sequence will arise that can code for a novel protein. At that point, natural selection can favor the new gene and its functional protein product, thus securing the preservation and heritability of both.

View Post


All of these have been proposed, although I wouldn't phrase them this way. Because of gene duplication there are lots of extra genes. I have seen a lot of work on how the system can switch these on and off. If a protein that is needed by an organism does not appear because of a mutation, then other 'backup' genes appear to get switched on in an effort to get the necessary protein (this was mentioned in one of my previous posts).

Your point 2 is related to point 1. There are many old genes hanging around that are switched off. They can be switched on. There was the study that showed that it was possible to get chickens to produce teeth. This wasn't a new gene that suddenly appeared and produced all the necessary proteins for teeth. Rather the argument was that this gene had been switched off millions of years ago, but was still sufficiently functional. If the environment changed and teeth became useful to chickens again, the very rare mutation that switched this gene back on, could multiply in the gene pool.
However, it is important to recognize that this gene may have been 'latent'. That is, as long as the gene that signals the start of production for a normal beak was working, the gene that signaled the start of the tooth gene would be switched off. However, if a mutation in the normal gene occured, the back up gene for teeth would be switched on. If this was the case, then one does not require a mutation in 'just the right place' to get this gene functional.

And yes, your point 4 is an interesting direction and the subject of a lot of papers and books. Mutations that affect early development are usually much more severe and more likely to be fatal. For this reason, it is argued that early developmental stages for most vertebrates are so similar (although the similarity was exagerated by Haeckel)

They do the mathematics which shows absurd improbabilities.  Dawkins has noted that scientific theories can rely on only so much “luck” before they cease to be credible.
....

In my own words, negative mutations add up and are cumulative in any isolated stand of DNA.  The mutations end up destroying the genes functionality and its specific folding that made it functional.  Also, the new protein has to fit into a new system or creating a new system by pure random events.  Again, we do not have a survival of the fittest mechanism in isolated DNA.  This adds a significant hurtle to the isolated DNA scenarios.

View Post


First, when other people do the mathematics, they no longer seem absurd. If mutation is "negative" then it reduces the chance the organism will have fertile offspring. This quickly removes the negative mutation from the gene pool. I don't understand why you think they will 'build up'.

Second, it is important to remember that evolution does not have a target in mind. Imagine calculating two probabilities.

Probability A. This is chance of particular mutation on a particular gene that produces a very specific desired effect. This is what creationists often measure and argue is too rare. This is the probability of a very specfic mutation.

Probability B. This is the chance that a mutation in a gene causes the system to produce a new protein that can be used by the body somewhere in its lifetime and therefore slightly improves the chance of producing fertile offspring.

Probability B is much much greater than probability A since B allows for any useful protein while probability A allows for only one specified protein. If one was to start with squirrels 10 million years ago, we could try to calculate the probability that the flying squirrel would evolve with the exact genome we see today. Virtually every evolutionary theorist would agree that the particular mutations we see today would be extremely unlikely. But this is the wrong number to calculate. What we want to know is the probability that some set of mutations would allow for any new species of squirrel that was relatively successful in its environment. Evolutionary theorists would argue that this is quite likely, but it would be very difficult to make any predictions as to what sort of mutations that new species would have.

It is not easy to calculate B because we would need to know all the possible proteins that can be created with a mutation to each gene and then calculate the probability that some process somewhere in the body could use the new protein. If the mutation is negative, the organism dies and nothing is passed on, so it doesn't accumulate. Only the positive or neutral mutations are passed on. The positive mutations accumulate, the negative mutations are removed

James
(still traveling, so I am afraid I will remain slow to respond)

#32 Bruce V.

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Posted 17 December 2007 - 06:08 PM

Hi Bruce,
First off, it is important to remember that science almost never works by using "proofs". Science is a competition between theories. The best theory is the one that accounts for the most data without conflicting with accepted facts. The theory of gravity, molecular theory, gas theories etc are simply the best account of data. Scientists are constantly battling to make their theory the accepted theory in their field. It might take 30 years for a theory to become accepted after it is first proposed and many many battles. But evidence and mathematical proofs are used to to support the highest achievement: to have the accepted theory.
This first statement goes against most all evolutionary theorists. The general view is most all large changes have followed from a series of smaller morphological changes. Suppose we have an animal evolve from a squirrel to a flying squirrel (a glider) then it evolves towards a bat-like creature that can flap its wings. The standard argument is that all such changes involve relatively small incremental changes.
  There have been some major genetic changes in the history of vertebrates. Chromosome doubling, chromosome fusing etc. But these kinds of changes are relatively rare and most of these  "experiments" as with Down's syndrome do not result in offspring that pass on the genes. Some minor genetic changes do produce large morphological changes (e.g., extra fingers in the Amish). However, if these are 'negative' mutations and reduce the chances of having offspring, they do not accumulate. They are quickly removed from the gene pool.
All of these have been proposed, although I wouldn't phrase them this way. Because of gene duplication there are lots of extra genes. I have seen a lot of work on how the system can switch these on and off. If a protein that is needed by an organism does not appear because of a mutation, then other 'backup' genes appear to get switched on in an effort to get the necessary protein (this was mentioned in one of my previous posts).

Your point 2 is related to point 1. There are many old genes hanging around that are switched off. They can be switched on. There was the study that showed that it was possible to get chickens to produce teeth. This wasn't a new gene that suddenly appeared and produced all the necessary proteins for teeth. Rather the argument was that this gene had been switched off millions of years ago, but was still sufficiently functional. If the environment changed and teeth became useful to chickens again, the very rare mutation that switched this gene back on, could multiply in the gene pool.
  However, it is important to recognize that this gene may have been 'latent'. That is, as long as the gene that signals the start of production for a normal beak was working, the gene that signaled the start of the tooth gene would be switched off. However, if a mutation in the normal gene occured, the back up gene for teeth would be switched on. If this was the case, then one does not require a mutation in 'just the right place' to get this gene functional.

  And yes, your point 4 is an interesting direction and the subject of a lot of papers and books. Mutations that affect early development are usually much more severe and more likely to be fatal. For this reason, it is argued that early developmental stages for most vertebrates are so similar (although the similarity was exagerated by Haeckel)
First, when other people do the mathematics, they no longer seem absurd. If mutation is "negative" then it reduces the chance the organism will have fertile offspring. This quickly removes the negative mutation from the gene pool. I don't understand why you think they will 'build up'.

Second, it is important to remember that evolution does not have a target in mind. Imagine calculating two probabilities.

Probability A. This is chance of particular mutation on a particular gene that produces a very specific desired effect. This is what creationists often measure and argue is too rare. This is the probability of a very specfic mutation.

Probability B. This is the chance that a mutation in a gene causes the system to produce a new protein that can be used by the body somewhere in its lifetime and therefore slightly improves the chance of producing fertile offspring.

Probability B is much much greater than probability A since B allows for any useful protein while probability A allows for only one specified protein. If one was to start with squirrels 10 million years ago, we could try to calculate the probability that the flying squirrel would  evolve with the exact genome we see today. Virtually every evolutionary theorist would agree that the particular mutations we see today would be extremely unlikely. But this is the wrong number to calculate. What we want to know is the probability that some set of mutations would allow for any new species of squirrel that was relatively successful in its environment. Evolutionary theorists would argue that this is quite likely, but it would be very difficult to make any predictions as to what sort of mutations that new species would have.

It is not easy to calculate B because we would need to know all the possible proteins that can be created with a mutation to each gene and then calculate the probability that some process somewhere in the body could use the new protein. If the mutation is negative, the organism dies and nothing is passed on, so it doesn't accumulate. Only the positive or neutral mutations are passed on. The positive mutations accumulate, the negative mutations are removed

James
  (still traveling, so I am afraid I will remain slow to respond)

View Post

Hi James,

I hope your travels are going well and you that will have an excellent holiday season.

First off, it is important to remember that science almost never works by using "proofs". Science is a competition between theories. The best theory is the one that accounts for the most data without conflicting with accepted facts. The theory of gravity, molecular theory, gas theories etc are simply the best account of data.


(as a side note, the theories you described above have predictive powers. That is, given certain parameters we can predict what will happens. ToE is not a predictive theory. IMO, that is why it is hard to disprove)

I just want to step back and see the forest through the trees so to speak. Sometimes we get into the minutia and don’t see the big picture.

1. We are talking about one of the most important aspects of evolution: How do morphological changes happen.
2. The Primary Axiom of evolution: The information in DNA is accomplished by mutation plus natural selection.

If you notice our discussion, we are still talking about hypothesis rather than theories or laws. We think gene duplication may have the answer but we don’t know. The question I have for you is: Does this sound like settled science- that we have the answer? That Darwinism is settled science?

Or, are we still at stage 2 (out of 5)
1, alternative mechanisms are being proposed. random variation culled by natural selection and preliminary evidence in favor of the new hypothesis is gathered and systematized.
2. We have hypothesis warranting further development and investigation.
3. Design has not been negated or eliminated as a strong if not probable possibility.


Again, this is the most important question for evolution- How do morphological changes happen. We should not be talking about hypothesis at this point if it was a settled science.

Bruce

#33 jamesf

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Posted 18 December 2007 - 07:05 PM

Hi James,

I hope your travels are going well and you that will have an excellent holiday season.

View Post


Thanks Bruce!

... as a side note, the theories you described above have predictive powers.  That is, given certain parameters we can predict what will happens.  ToE is not a predictive theory.  IMO, that is why it is hard to disprove)

View Post


I will have to disagree with you here. Evolutionary theory has tremendous prediction power. The two big ones are

1. The location and depth of fossils.
You can point to any point on earth and I will be able to tell you what kinds of fossils are possible and what kinds will not be found. The accuracy is tremendous. Finding a fossil even slightly out of place is a million to one shot, and the goal of every paleontologist. I have unearthed thousands of fossils, from the Burgess shale in British Columbia, to trilobites in New York to very early dinosaurs in New Mexico. Fossils are virtually never found out of their places - never higher than predicted from evolutionary theory. As I stated before, the following predictions are true everywhere on earth.
What is the alternative theory for these facts?


If we go from the bottom of the geological column we get a very very very clear ordering. The ordering I describe here is found all over the earth. We get a few minor oddities where there are major geological folds, but the folds are quite clear geologically and they are quite rare. The ordering is

1. Bottom layers: No life. No algae, no plants, no complex life, no shells, no bones, no fish, no pollen, no seeds, no land animals, no dinosaurs, no modern mammals

2. Next layers (for many layers): single cell life (algae), no multicellular plants, no complex life, no shells, no bones, no fish, no pollen, no seeds, no land animals, no dinosaurs, no modern mammals.

3. Next layers (Pre-Cambrian), first multicellular life (odd Ediacaran life forms) and possible precursors to both vertebrates and trilobites. No shells, no bones, no fish, no land plants, no pollen, no seeds, no land animals, no dinosaurs, no modern mammals. See picture below.

4. Cambrian animals appears in many places across the planet. First shells, but no bones, no fish, no land plants, no pollen, no seeds, no land animals, no dinosaurs, no modern mammals.

5. First fish appear (extinct placoderms etc). Mostly cartiledge bones, so at first no bones in the fossil record but these appear later. But still no evidence of land plants. No pollen, no seeds, no land animals, no dinosaurs, no modern mammals.

6. First land plants in the fossil record, followed by the first seeds. First, gymnosperm pollen but no angiosperm (flowering plant) pollen. No land animals, no dinosaurs, no modern mammals.

7. First transitional vertebrates between water and land. No angiosperm (flowering plants) pollen. No land animals, no dinosaurs, no modern mammals.
Here is a great link to this period in Pennsylvania
http://www.devoniant.../pages/who.html

8. First air breathing land animals (e.g., the Gorgons). No angiosperm (flowering plants) pollen, no dinosaurs, no modern mammals.

9. First dinosaurs, first evidence of flowering plants. No modern mammals have ever been found in these layers.

10. First modern mammals. Most all modern mammals appear only after dinosaurs go extinct.

11. First large primates

12. First evidence of humans

_____________________________________

2. In addition to fossil ordering, evolutionary theory has done a tremendously good job at predicting the genetic differences between animals based on the paleontological distances (although interesting differences have also been found in some cases). Scientists have recently been able to extract DNA from neanderthal skeletons. The current evolutionary theory based on fossil evidence suggests that they diverged from humans about 350,000 years ago. Creationists argue that neanderthals are humans that suffered from rickets or some disease.
So who do you think will provide a better prediction regarding the DNA when it is revealed next year? Will it have unique DNA or look like that of modern humans?

Hi James,

1. We are talking about one of the most important aspects of evolution: How do morphological changes happen.
2. The Primary Axiom of evolution: The information in DNA is accomplished by mutation plus natural selection.

If you notice our discussion, we are still talking about hypothesis rather than theories or laws.  We think gene duplication may have the answer but we don’t know.  The question I have for you is:  Does this sound like settled science- that we have the answer?  That Darwinism is settled science?

Or, are we still at stage 2 (out of 5)
1, alternative mechanisms are being proposed. random variation culled by natural selection and preliminary evidence in favor of the new hypothesis is gathered and systematized.
2. We have hypothesis warranting further development and investigation.
3.  Design has not been negated or eliminated as a strong if not probable possibility. 
Again, this is the most important question for evolution- How do morphological changes happen.  We should not be talking about hypothesis at this point if it was a settled science.

Bruce

View Post


All these issues will be debated for many years. In the last decade, we have learned a tremendous amount regarding how genes change over time, how they make backups, how switch on and off. There is even new evidence that Lamarckian evolution sometimes actually occurs (when some plants are stressed, they can pass down different genes).

Personally, I don't see how this in any way weakens the case for evolution. I don't see any other theory that even gets even close to explaining the fossil record or the variations we see in the animals around us. But if creationists want to try they should go for it and propose a detailed theory that makes predictions about the fossil record, DNA differences etc.

There are still lots of unanswered research questions in gravitational theory. The data that has led to theories of dark matter and dark energy has created a lot of excitement regarding what causes gravitational pull at large scales. But does such a debate make me question whether a rock will fall if I drop it? Of course not. The debate regarding a complete theory of gravity does not alter the fact that gravity happens.

James

It is fun debating with you Bruce. I always find it odd when such discussions get unnecessarily hostile. Here is a pretty extreme example...

http://www.theaustra...6-12377,00.html


Evolution vs creation row ends in stabbing
A FRUIT-picking trip to southern New South Wales ended in the death of a Scottish backpacker who became embroiled in a bizarre row about creationism and evolution.


#34 Bruce V.

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Posted 19 December 2007 - 08:38 AM

Thanks Bruce!
I will have to disagree with you here. Evolutionary theory has tremendous prediction power. The two big ones are

1. The location and depth of fossils.
    You can point to any point on earth and I will be able to tell you what kinds of fossils are possible and what kinds will not be found. The accuracy is tremendous. Finding a fossil even slightly out of place is a million to one shot, and the goal of every paleontologist. I have unearthed thousands of fossils, from the Burgess shale in British Columbia, to trilobites in New York to very early dinosaurs in New Mexico. Fossils are virtually never found out of their places - never higher than predicted from evolutionary theory. As I stated before, the following predictions are true everywhere on earth.
What is the alternative theory for these facts?
If we go from the bottom of the geological column we get a very very very clear ordering. The ordering I describe here is found all over the earth. We get a few minor oddities where there are major geological folds, but the folds are quite clear geologically and they are quite rare. The ordering is

1. Bottom layers: No life. No algae, no plants, no complex life, no shells, no bones, no fish, no pollen, no seeds, no land animals, no dinosaurs, no modern mammals

2. Next layers (for many layers): single cell life (algae), no multicellular plants, no complex life, no shells, no bones, no fish, no pollen, no seeds, no land animals, no dinosaurs, no modern mammals.

3. Next layers (Pre-Cambrian), first multicellular life (odd Ediacaran life forms) and possible precursors to both vertebrates and trilobites. No shells, no bones, no fish, no land plants, no pollen, no seeds, no land animals, no dinosaurs, no modern mammals. See picture below.

4. Cambrian animals appears in many places across the planet. First shells, but no bones, no fish, no land plants, no pollen, no seeds, no land animals, no dinosaurs, no modern mammals.

5. First fish appear (extinct placoderms etc). Mostly cartiledge bones, so at first no bones in the fossil record but these appear later. But still no evidence of land plants. No pollen, no seeds, no land animals, no dinosaurs, no modern mammals.

6. First land plants in the fossil record, followed by the first seeds. First, gymnosperm pollen but no angiosperm (flowering plant) pollen. No land animals, no dinosaurs, no modern mammals.

7. First transitional vertebrates between water and land. No angiosperm (flowering plants) pollen. No land animals, no dinosaurs, no modern mammals.
Here is a great link to this period in Pennsylvania
http://www.devoniant.../pages/who.html

8. First air breathing land animals (e.g., the Gorgons). No angiosperm (flowering plants) pollen, no dinosaurs, no modern mammals.

9. First dinosaurs, first evidence of flowering plants. No modern mammals have ever been found in these layers.

10. First modern mammals. Most all modern mammals appear only after dinosaurs go extinct.

11. First large primates

12. First evidence of humans

_____________________________________

2. In addition to fossil ordering, evolutionary theory has done a tremendously good job at predicting the genetic differences between animals based on the paleontological distances (although interesting differences have also been found in some cases). Scientists have recently been able to extract DNA from neanderthal skeletons. The current evolutionary theory based on fossil evidence suggests that they diverged from humans about 350,000 years ago. Creationists argue that neanderthals are humans that suffered from rickets or some disease.
So who do you think will provide a better prediction regarding the DNA when it is revealed next year? Will it have unique DNA or look like that of modern humans?
All these issues will be debated for many years. In the last decade, we have learned a tremendous amount regarding how genes change over time, how they make backups, how switch on and off. There is even new evidence that Lamarckian evolution sometimes actually occurs (when some plants are stressed, they can pass down different genes).

Personally, I don't see how this in any way weakens the case for evolution. I don't see any other theory that even gets even close to explaining the fossil record or the variations we see in the animals around us. But if creationists want to try they should go for it and propose a detailed theory that makes predictions about the fossil record, DNA differences etc.

There are still lots of unanswered research questions in gravitational theory. The data that has led to theories of dark matter and dark energy has created a lot of excitement regarding what causes gravitational pull at large scales. But does such a debate make me question whether a rock will fall if I drop it? Of course not. The debate regarding a complete theory of gravity does not alter the fact that gravity happens.

James

It is fun debating with you Bruce. I always find it odd when such discussions get unnecessarily hostile. Here is a pretty extreme example...

http://www.theaustra...6-12377,00.html
Evolution vs creation row ends in stabbing
A FRUIT-picking trip to southern New South Wales ended in the death of a Scottish backpacker who became embroiled in a bizarre row about creationism and evolution.

View Post


Hi James,

I am sorry you feel that I was getting hostile- that was not my intention. I have very much enjoyed our debate. As always, the information you provide has been very informative and interesting. I have great respect on how you present your facts and how you arrived at your world view. I would like to continue the debate and I will try and be more respectful- sometimes written information comes across harder than it was intended.

James do you have a link for the quote below. There are 2 things that I would like to further explore:

(1) Neanderthal fossils- I thought the fossil record was extremely limited, but you are much more current on fossils than I am.
(2) DNA- I thought that DNA was very unreliable after ~ 1,000 years or so.

In addition to fossil ordering, evolutionary theory has done a tremendously good job at predicting the genetic differences between animals based on the paleontological distances (although interesting differences have also been found in some cases). Scientists have recently been able to extract DNA from neanderthal skeletons. The current evolutionary theory based on fossil evidence suggests that they diverged from humans about 350,000 years ago. Creationists argue that neanderthals are humans that suffered from rickets or some disease.
So who do you think will provide a better prediction regarding the DNA when it is revealed next year? Will it have unique DNA or look like that of modern humans?


Empirical equations can have predictive power as well. I work with catalyst and we have a black box. We have complicated equations that explain how it should and does work. But in the field we use empirical equations: Equations build from experience and not theory. I may be wrong but the fossil records predictive power looks empirical to me. Can ToE look at a new fossil and predict what the next fossil will look like based on ToE?

Say we are looking at the transition from water breathing animals to land air breathing animals. Some say that would take a large number of morphological evolutionarily steps: I have heard that the number ~ 5,000 or ~50,000 (not sure of the decimal point) in any case it is a large number. The fossil record has a limited number of transition fossils from sea to land animals. The problem is that with ~ 5,000 morphological changes required for that transition we should many fossil examples. I understand that these limited fossils have competing theories, like they were composite species similar to the duck bill platypuses.


Bruce

#35 jamesf

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Posted 19 December 2007 - 09:15 AM

Hi James,

I am sorry you feel that I was getting hostile- that was not my intention.  I have very much enjoyed our debate.  As always, the information you provide has been very informative and interesting. I have great respect on how you present your facts and how you arrived at your world view.  I would like to continue the debate and I will try and be more respectful- sometimes written information comes across harder than it was intended.

James do you have a link for the quote below.  There are 2 things that I would like to further explore:

(1) Neanderthal fossils- I thought the fossil record was extremely limited, but you are much more current on fossils than I am.
(2)  DNA-  I thought that DNA was very unreliable after ~ 1,000 years or so. 
Empirical equations can have predictive power as well.  I work with catalyst and we have a black box.  We have complicated equations that explain how it should and does work.  But in the field we use empirical equations:  Equations build from experience and not theory.  I may be wrong but the fossil records predictive power looks empirical to me.  Can ToE look at a new fossil and predict what the next fossil will look like based on ToE?
Bruce

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Hi Bruce,
I did not at all mean to suggest you have been hostile. Quite the opposite. You have been the most amiable person I have met on this blog. I just saw that story and thought how strange it was - and unnecessary for people to get so angry.
I will do a bit more work later, but here is a starting link. From what I understand, they have a lot more DNA from a recent neanderthal find in Israel which will provide a much more detailed insight into neanderthal DNA.
http://news.bbc.co.u...ure/4986668.stm

Can scientists predict fossils? Sure! Most of the search for human fossils skulls is directed towards the layers and locations of older and younger fossils in lower and higher layers and locations. And yes, they make pretty good predictions regarding skull size etc.
Also this transitional fossil was predicted to be in a particular layer and location in the Canadian artic. They predicted it would be there and they found it.
http://news.bbc.co.u...ure/4879672.stm
James

#36 Bruce V.

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Posted 19 December 2007 - 09:40 AM

Hi Bruce,
    I did not at all mean to suggest you have been hostile. Quite the opposite. You have been the most amiable person I have met on this blog. I just saw that story and thought how strange it was - and unnecessary for people to get so angry.
    I will do a bit more work later, but here is a starting link. From what I understand, they have a lot more DNA from a recent neanderthal find in Israel which will provide a much more detailed insight into neanderthal DNA.
  http://news.bbc.co.u...ure/4986668.stm

    Can scientists predict fossils? Sure! Most of the search for human fossils skulls is directed towards the layers and locations of older and younger fossils in lower and higher layers and locations. And yes, they make pretty good predictions regarding skull size etc.
  Also this transitional fossil was predicted to be in a particular layer and location in the Canadian artic. They predicted it would be there and they found it.
  http://news.bbc.co.u...ure/4879672.stm
    James

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Hi James,

I thought this paper was interesting.

http://www.scienceda...20219075535.htm

University of Toronto anthropologist David Begun and his European colleagues are re-writing the book on the history of great apes and humans, arguing that most of their evolutionary development took place in Eurasia, not Africa. In back-to-back issues of the Journal of Human Evolution, Begun and his collaborators describe two fossils, both discovered in Europe. One comes from the oldest relative of all living great apes (orangutans and African apes) and humans; the other is the most complete skull ever found of a close relative of the African apes and humans. In the November 2001 issue, Begun and colleague Elmar Heizmann of the Natural History Museum of Stuttgart discuss the earliest-known great ape fossil, broadly ancestral to all living great apes and humans. "Found in Germany 20 years ago, this specimen is about 16.5 million years old, some 1.5 million years older than similar species from East Africa," Begun says. "It suggests that the great ape and human lineage first appeared in Eurasia and not Africa." In the December 2001 paper, Begun and colleague L•szl€ Kordos of the Geological Museum of Hungary describe the skull of Dryopithecus, discovered in Hungary by their team a couple of years ago. The fossil is identical to living great apes in brain size and very similar to African apes in the shape of the skull and face and in details of the teeth, the researchers say.



Someone should start a thread on this. I think this would could lead to an interesting discussion. I don't have much to say other than ask questions.

#37 jamesf

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Posted 20 December 2007 - 08:38 PM

(1) Neanderthal fossils- I thought the fossil record was extremely limited, but you are much more current on fossils than I am.
(2)  DNA-  I thought that DNA was very unreliable after ~ 1,000 years or so. 
Empirical equations can have predictive power as well.  I work with catalyst and we have a black box.  We have complicated equations that explain how it should and does work.  But in the field we use empirical equations:  Equations build from experience and not theory.  I may be wrong but the fossil records predictive power looks empirical to me.  Can ToE look at a new fossil and predict what the next fossil will look like based on ToE?

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Hi Bruce,
I am in the midst of a great little book called The Jesuit and the Skull. It is about a French Jesuit priest by the name of Teilhard de Chardin. He was part of the group that discovered Peking Man - a collection of Homo Erectus skulls found near Beijing dating from around 400,000 years ago. Chardin saw no conflict between science and Christianity and was an avid student of evolution near the beginning of the last century. However, his papers on evolution made the Vatican uneasy and he was sent off to China in the hope that the problem would go away. But that didn't work out very well. The fossil animals that were found in caves in China (along with some primitive stone tools) suggested to Chardin and his Chinese colleagues that a "missing link" could possibly be found in the area. In 1929, after several years, they found the first skull and in the years that followed they found a number of others. All the skulls were much larger than chimps and significantly smaller than humans. Home Erectus also had no chin.
The Vatican and Jesuits made several attempts to ban some of Chardin's books and publications. However today, some of his work and ideas form the basis of many of the Vatican's current notions of evolution (e.g., that although evolution happened, it was guided by God and God gave man a devine soul).
In any case, the theory predicted that early homo fossils might be found there, so they searched and they found them. The theory makes a lot of such predictions. The current theory predicts that no human fossils before homo sapians will be found in the Americas, and none has been found.

Not sure we will ever get DNA from a Homo Erectus, but they are getting DNA from Neanderthal skeletons dating back from 50,000 years. Most of the DNA was mitochondrial but one of the recent finds is expected to reveal much more. Here is a picture of the locations of Neanderthal skeletons. In some of these locations, they have found whole families. I think they have almost 300 individuals now.
Posted Image

As I understand it, Mitochondrial DNA is much more repetitive (each mitochondrial cell has many copies) so the redundancy gives you a better chance to reconstruct degraded DNA. When the mtDNA is measured one finds that Neanderthal DNA is unique. The graph shows the differences between human and human DNA, human versus Neanderthal DNA and human versus chimp DNA.
Posted Image

Again, I can see how this sort of difference is predicted from evolutionary theory. I don't see how it is predicted by anything proposed by 'answers in genesis'. But always happy to learn.

James

#38 Bruce V.

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Posted 21 December 2007 - 02:32 PM

http://www.clarifyin...m/ape_men.shtml

Circular Reasoning

Most rock layers are “dated” by the fossils they contain. Scientists will then choose a special reference fossil called an “index fossil.” Then they assume (based on the phylogenetic tree) that the “simple” index fossils were the oldest. Finding one of these “oldest” index fossils in a layer identifies that layer as the “oldest.” They then assign a date to that rock layer (based on the theory of evolution) and record that date on their geologic time scale. They continue this process with the “more complex” index fossils—assigning each increase in “complexity” to a younger rock layer until they complete filling out the geologic time scale. (A complete geologic time scale is also referred to as a “geologic column.”)

Notice that although the layers of the earth were dated using index fossils, the index fossils were dated by guessing their age based on the theory of evolution. This is not science nor a valid application of the scientific method. Suggesting a hypothetical age for a fossil (based on a theory) and then telling everyone it is an established fact is not the way to apply the scientific method. If you quiz paleontologists about this, many will assure you that their techniques are indeed scientific. They will tell you they accurately date the fossil using the date of the rock layer in which they found it.

Did you notice what just happened? They assigned a date to the fossil, then dated the layer of earth which contained that fossil. Then they turned around and told you they knew the age of the fossil, because they knew the date of that layer of earth. This is called “circular reasoning.”



Problems with missing links

Investigating the scientific literature reveals that all these proposed ”missing links” are either very humanlike with a trace of some apelike characteristic, or very apelike with a trace of some human characteristic. There is nothing really in between (where you would expect a “real” transitional species). One example of a change seen by scientists would be in the shape of a jaw. The jaws in some apes are almost rectangular and others are more curved. Since the human jaw is roughly parabolic (a rounded “V”), those apes possessing a more curved jaw are claimed to be “more human.” Similarly, a human skull that had a slightly squared jaw would be considered “more apelike.” Therefore, please keep in mind that the tiny variations seen by scientists may actually be variations in normal ape and human populations that are incorrectly labeled as missing links.


Which came first man, or its transitional links?

One of the biggest stumbling blocks to this theory is the discovery by scientists of modern human (Homo Sapiens) fossils in Pliocene layers—geologic layers so “early” that none of the proposed “missing links” could have possibly been ancestors. However, since these discoveries fly so strongly in the face of the currently popular evolutionary theory, these discoveries are ignored.


Neanderthal Man

The earliest examples of “mainstream” Neanderthal findings were discovered at Saccopastore, Ehringsdorf, and Krapina and dated in the Riss-Wurm Interglacial period. Interestingly, scientists found fully “modern” human fossil (Homo Sapiens) remains of the same geologic age at Fontechevade. One of the earliest (if not the earliest) “Neanderthal” fossils was discovered at Steinheim, and dated in the Riss-Mindel Interglacial period. However, again they discovered a fully modern human fossil of the same age at Swanscombe. Again, we have evidence that modern humans existed at the same time, and Neanderthal man could not possibly be a missing link to modern men. Although beyond the scope of this message, many scientists now believe that the “Neanderthal” fossils were modern men that suffered from rickets, arthritis, and other diseases that alter bone structure.

There are additional problems with Neanderthal man as a possible “ancestor” of modern humans. The Neanderthal fossil skulls are typically as large as a modern man’s skull. Some are slightly larger—an indication of “greater brain capacity.” Since the brain capacity of Neanderthal is the same as or larger than modern man, it is unreasonable to assume that this is an ancestor of modern man. After all, if the theory of evolution is correct, why should brain capacities (which presumably get larger as humans “evolve”), suddenly become smaller after Neanderthal? The reality is that the scientific community is trying to force the actual evidence to agree with an incorrect theory and has to contradict itself occasionally to make the theory of evolution seem rational.


James if you want to continue talking about fossils we should start a new thread. I am hoping you will take the lead because that is one of your strengths.

Bruce

#39 Bruce V.

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Posted 21 December 2007 - 07:22 PM

Hi James,

Hope your vacation is going well. If you are like me, I just purchased my wife a present. Men are notorious late shoppers. I will be gone for a week, so this is my last posting for a while.

Polyploidy is when all the chromosomes are doubled. If I repeat this sentence, does it tell you more? If I repeat my sentence, does it tell you more? If every page of a book was written twice we obviously are not increasing information. The point is that coping information does not increase information. In fact it can be harmful, it takes you twice as long to read, in this case, and in a living cell it takes twice as much to energy to support that cell.

Aneoploidy (when a chromosome is doubled) – is entirely lethal for larger chromosomes. For smaller chromosomes an extra copy is not always lethal. Tragically the individuals have the extra information display severe abnormalities. The most common example of this is Down’s syndrome—resulting from an extra copy of chromosome 21. There are countless smaller duplications and insertions which also have been shown to cause genetic disease.

http://www.ces.ncsu..../polyploidy.htm

As you can read, in the 1930s some plant breeders learned how to help produce these polyploidal plants (with duplicate genes and chromosomes). Yes, the duplicate genes can be harmful, but they can also be quite beneficial. Here is a quote from the above link.

[i]Plants with increased ploidy levels are often apparent by their distinct morphology. Increasing ploidy often results in increased cell size that in turn results in thicker, broader leaves and larger flowers and fruit. Shoots are often thicker and can have shortened internodes and wider crotch angles. Plants with high ploidy levels (e.g. octaploids) can have distorted growth and reduced growth rates.

James

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Most plants with most plants that result polyploidy are almost always very stunted morphologically distorted and generally sterile. The reason for this should be obvious – the plants must waste twice as much energy to make twice as much DNA, but with no new genetic information!

The nucleus is roughly twice as large, disrupting proper cell size and shape In fact, the plant actually have less information than before because a great deal of information which controls gene regulation depends on gene dosage (copy number). Loss of regulatory control is loss of information. This is really the same reason why an extra chromosome causes Down’s syndrome. Thousands of genes become improperly regulated, because of the extra genetic copies.

Also, the extra DNA created by polyploidy causes other problems as well. The DNA’s are very susceptible to horizontal gene transfer and gene insertion with each other. This is almost always deleterious.

Almost all mutations that have some beneficial effects loose genetics information in the process. For mutations to create morphological changes we have to see a real increase in information: Information that is building toward creating new systems.

Pilpel and colleagues mined the wealth of available yeast data for viable mutants lacking one of the members of duplicate gene pairs and examined the expression profiles of the paralogs. The more dispensable genes, that is, those with better backup, differ from their paralogs in their expression. When both are present, they tend not to be coexpressed. When one is absent, the other is up-regulated to back up the missing

This coexpression of DNA is usually deleterious in plants because its architecture is very specific and exacting. Any cross function of genes between the two DNA’s will generally disrupt the finely tuned architecture: If you look at DNA like a computer code, adding new lines of code in random locations wil disrupt the codes original function. This is exactly what plant geneticists have been seeing when we there is polyploidy duplication.


Cheers,

Bruce

#40 jamesf

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Posted 29 December 2007 - 01:16 PM

Hi James,

Hope your vacation is going well.  If you are like me, I just purchased my wife a present.  Men are notorious late shoppers.  I will be gone for a week, so this is my last posting for a while.

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Hi Bruce,
Hope you had a great Christmas. Yes, always last minute shopping for the wife. Found out this is very dangerous online - arrived in the mail Christmas eve - much too close.

Polyploidy is when all the chromosomes are doubled.  If I repeat this sentence, does it tell you more?  If I repeat my sentence, does it tell you more? If every page of a book was written twice we obviously are not increasing information. 

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Gene doubling and chromosome doubling can change the organism. Sometimes the increased number can increase the number of proteins which can be either harmful or beneficial. However, as we discussed earlier, what is interesting is when the duplicated gene mutates, then there is a backup gene to perform the original function while the new gene can produce a possible new function. As I stated before...

From Behe...
"Gene duplication is thought to be a major source of evolutionary innovation because it allows one copy of a gene to mutate and explore genetic space while the other copy continues to fulfill the original function."

So lets go through this. First a gene duplicates. The mutation is neutral because both genes continue to produce the same protein.

Second, another mutation changes the amino acids in one of the two genes. Four things can happen.
1. The new gene fails to produce a protein (no problem here since you have the other protein)
2. The new gene produces a new protein that is useless (again, no problem)
3. The new gene produces a protein that interferes with some other process
4. The new gene produces a protein that assists some other process

As long as 3 does not occur, then the animal continues to produce viable offspring. If 1,2 or 4 occur then to use Behe's phrase, the gene can continue to "explore genetic space while the other copy continues to fulfill the original function."


Aneoploidy (when a chromosome is doubled) – is entirely lethal for larger chromosomes. For smaller chromosomes an extra copy is not always lethal.  Tragically the individuals have the extra information display severe abnormalities.  The most common example of this is Down’s syndrome—resulting from an extra copy of chromosome 21.  There are countless smaller duplications and insertions which also have been shown to cause genetic disease.
Most plants with most plants that result polyploidy are almost always very stunted morphologically distorted and generally sterile.  The reason for this should be obvious – the plants must waste twice as much energy to make twice as much DNA, but with no new genetic information!

The nucleus is roughly twice as large, disrupting proper cell size and shape  In fact, the plant actually have less information than before because a great deal of information which controls gene regulation depends on gene dosage (copy number).  Loss of regulatory control is loss of information.  This is really the same reason why an extra chromosome causes Down’s syndrome. Thousands of genes become improperly regulated, because of the extra genetic copies.

Also, the extra DNA created by polyploidy causes other problems as well.  The DNA’s are very susceptible to horizontal gene transfer and gene insertion with each other.  This is almost always deleterious.

Almost all mutations that have some beneficial effects loose genetics information in the process. For mutations to create morphological changes we have to see a real increase in information:  Information that is building toward creating new systems. 
This coexpression of DNA is usually deleterious in plants because its architecture is very specific and exacting.  Any cross function of genes between the two DNA’s will generally disrupt the finely tuned architecture:  If you look at DNA like a computer code, adding new lines of code in random locations wil disrupt the codes original function.  This is exactly what plant geneticists have been seeing when we there is polyploidy duplication. 
Cheers,

Bruce

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I think we are talking across each other here. Yes, I agree that mutations, gene doubling, chromosome doubling etc CAN and usually IS harmful and often lethal.

However, when they are lethal, they are instantly removed from the gene pool. The rare beneficial one multiplies through the gene pool. Plant breeder have created a whole host of useful plants by using polyploidy. I am sure that the vast majority of attempts by plant breeders were failures. But the rare successful ones became extremely popular.

This artificial form of selection is typically much faster than natural selection, but the basic idea is the same. Harmful, mutations are removed. The rare beneficial mutation multiplies.

From wikepedia
http://en.wikipedia....wiki/Polyploidy

Polyploid crops

Polyploid plants tend to be larger and better at flourishing in early succession habitats such as farm fields. In the breeding of crops, the tallest and best thriving plants are selected for. Thus, many crops (and agricultural weeds) may have unintentionally been bred to a higher level of ploidy.

The induction of polyploids is a common technique to overcome the sterility of a hybrid species during plant breeding. For example, Triticale is the hybrid of wheat (Triticum turgidum) and rye (Secale cereale). It combines sought-after characteristics of the parents, but the initial hybrids are sterile. After polyploidization, the hybrid becomes fertile and can thus be further propagated to become triticale.

In some situations polyploid crops are preferred because they are sterile. For example many seedless fruit varieties are seedless as a result of polyploidy. Such crops are propagated using asexual techniques such as grafting.

Polyploidy in crop plants is most commonly induced by treating seeds with the chemical colchicine.

Examples of Polyploid Crops

    * Triploid crops: banana, apple, ginger, watermelon, citrus [8]
    * Tetraploid crops: durum or macaroni wheat, maize, cotton, potato, cabbage, leek, tobacco, peanut, kinnow, Pelargonium
    * Hexaploid crops: chrysanthemum, bread wheat, triticale, oat
    * Octaploid crops: strawberry, dahlia, pansies, sugar cane

Some crops are found in a variety of ploidy. Apples, tulips and lilies are commonly found as both diploid and as triploid. Daylilies (Hemerocallis) cultivars are available as either diploid or tetraploid. Kinnows can be tetraploid, diploid, or triploid.


Best, James




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