Chimp genome again

[shernren]

The genetics has been hashed out on this thread, so I'll completely derail it now.

Your analogy is weird ...

Tell us something new. When aren't my analogies weird? ^^

You'd be like arguing then that an answer is more correct if it's given as 0.00000230034031 instead of 0.00000230034. If you want to do that I might as well argue (as James Gleick does in Chaos) that you can't actually measure the surface area of a table.

Tell that to my honors friends doing various precision physics projects. One of them is dropping a Bose-Einstein condensate to measure the value of g to ten digits of accuracy.

 

[mark kennedy]

Don't know whether anyone's been keeping tabs on YECist Todd Wood's blog lately, but I thought this latest posting might be of interest:

Todd's Blog: Chimp genome again

• Single-nucleotide substitutions occur at a mean rate of 1.23% between copies of the human and chimpanzee genome, with 1.06% or less corresponding to fixed divergence between the species.
  
• On the basis of this analysis, we estimate that the human and chimpanzee genomes each contain 40–45 Mb of species-specific euchromatic sequence, and the indel differences between the genomes thus total 90 Mb. This difference corresponds to 3% of both genomes and dwarfs the 1.23% difference resulting from nucleotide substitutions; this confirms and extends several recent studies

Do the math...

 

[shernren]

• Single-nucleotide substitutions occur at a mean rate of 1.23% between copies of the human and chimpanzee genome, with 1.06% or less corresponding to fixed divergence between the species.
• On the basis of this analysis, we estimate that the human and chimpanzee genomes each contain 40–45 Mb of species-specific euchromatic sequence, and the indel differences between the genomes thus total 90 Mb. This difference corresponds to 3% of both genomes and dwarfs the 1.23% difference resulting from nucleotide substitutions; this confirms and extends several recent studies

Do the math...

But what about that paper by Britten? The one where he showed that the 99% identity figure had ignored important indel data and therefore should be revised down to 95% identity? Britten was wrong. His strategy of counting indels doesn't actually make any sense at all. Consider a simple example. Say you have two sequences, one 50,000 nucleotides long and the other 55,000 nucleotides long. The only difference between them is a single insertion of 5,000 nucleotides. Otherwise, the sequences are identical. What then should the percent identity be? Should it be 90%, counting the 5000 nucleotide difference as 10% of the smaller sequence? Or should it be 91%, counting the 5000 nucleotide difference as 9% of the total sequence in comparison (55,000)? Neither one makes any sense, since the reality is that there is only one difference between the sequences. It's a single insertion or deletion, representing one mutation. Why should we count that as 5000 differences when there's only one mutation?

Once you realize that we're only talking about one difference, then the problem becomes essentially intractable. If there's only one difference between the sequences, what is it a percent of? The total number of nucleotides? That doesn't make sense. It's apples and oranges. That's why you don't see actual genome researchers getting that excited about boiling down the similarity between two genomes to a single number. It's just not possible.
​

Do the reading.

 

[Smidlee]

I haven't been keeping up with Todd but I have been with the human Y-chromosome. I think the Y-chromosome is telling us something.

 

[sfs]

I haven't been keeping up with Todd but I have been with the human Y-chromosome. I think the Y-chromosome is telling us something.

What is it telling us?

 

[shernren]

 

[Assyrian]

I haven't been keeping up with Todd but I have been with the human Y-chromosome. I think the Y-chromosome is telling us something.

What is it telling us?

Do dangerous stuff... impress the girls...

 

[mark kennedy]

But what about that paper by Britten? The one where he showed that the 99% identity figure had ignored important indel data and therefore should be revised down to 95% identity? Britten was wrong. His strategy of counting indels doesn't actually make any sense at all. Consider a simple example. Say you have two sequences, one 50,000 nucleotides long and the other 55,000 nucleotides long. The only difference between them is a single insertion of 5,000 nucleotides. Otherwise, the sequences are identical. What then should the percent identity be? Should it be 90%, counting the 5000 nucleotide difference as 10% of the smaller sequence? Or should it be 91%, counting the 5000 nucleotide difference as 9% of the total sequence in comparison (55,000)? Neither one makes any sense, since the reality is that there is only one difference between the sequences. It's a single insertion or deletion, representing one mutation. Why should we count that as 5000 differences when there's only one mutation?

Once you realize that we're only talking about one difference, then the problem becomes essentially intractable. If there's only one difference between the sequences, what is it a percent of? The total number of nucleotides? That doesn't make sense. It's apples and oranges. That's why you don't see actual genome researchers getting that excited about boiling down the similarity between two genomes to a single number. It's just not possible.
​

Do the reading.

Grow up.

The fact is that the indels represent a comparative difference that can be represented by a percentage should be regarded as a vast difference because it is. The sheer size of these insertions and deletions are staggering and with research discovering that the so called junk DNA actually has a funtion. Saying that the two genomes are 98% identical is not only wrong, it's been definitively proven to be false. That does not take into consideration differences that would have had to result from huge chromosomal rearrangements, gross structural differences in protein coding genes and that enigmatic HAR 1F regulatory gene. More to the point, counting an indel of 8 bases long the same as one a million bases wrong is not only wrong headed, it's absurd.

I've done the reading champ, it's the same tired old rationalizations that do a diservice to the actual facts.

The Intial Sequence of the Chimpanzee Genome paper said the same thing, in fact, cited other examples of studies that came to the same conclusion with the Britten paper included:

• Fortna, A. et al. Lineage-specific gene duplication and loss in human and great ape evolution. PLoS Biol. 2, E207 (2004)
• Britten, R. J. Divergence between samples of chimpanzee and human DNA sequences is 5%, counting indels. Proc. Natl Acad. Sci. USA 99, 13633–13635 (2002)
• Frazer, K. A. et al. Genomic DNA insertions and deletions occur frequently between humans and nonhuman primates. Genome Res. 13, 341–346 (2003)
• Locke, D. P. et al. Large-scale variation among human and great ape genomes determined by array comparative genomic hybridization. Genome Res. 13, 347–357 (2003)

He should know this...

What is more, the actual divergence has got to be higher, there are just too many differences. Even though I don't spend a lot of time in these debates anymore I still browse the topic from time to time:

Now, Anzai et al. have published a new report in the Proceedings of the National Academy of Sciences that confirms this statement. In the study, nearly one-half of the MHC (major histocompatibility complex) region was sequenced, ‘which to date represents the longest continuous sequence within this species [chimps], our closest evolutionary relative’, and has been described as a ‘rapidly evolving’ part of the genome. Although it has been held that human/chimp similarity in the MHC is ‘so great that the alleles must have originated before the supposed chimp/human evolutionary divergence’, the sequence results actually dropped the DNA similarity estimate down to 86.7%!​

Human/chimp DNA similarity continues to decrease: counting indels

The indels are not big news, researchers have known about them for years. The fact that they are trying to hedge the facts by rationalizing away the differences is telling me something and the message gets louder all the time.

Have a nice day
Mark

 

[mark kennedy]

That's really impressive. He knows what he's talking about, and says it clearly. Now if he could just manage to get Mark Kennedy to understand it . . .

I think you mean accept it. At any rate, making a million dollars the same as one dollar because they are both only spent once makes no sense. if only I could get you to understand that, or do I mean admit that?

Have a nice day Steve
Mark

 

[shernren]

More to the point, counting an indel of 8 bases long the same as one a million bases wrong is not only wrong headed, it's absurd.

Then let me ask you a simple question. How often does a 47 million nucleotide indel occur?

Also:

Now, Anzai et al. have published a new report in the Proceedings of the National Academy of Sciences that confirms this statement. In the study, nearly one-half of the MHC (major histocompatibility complex) region was sequenced, ‘which to date represents the longest continuous sequence within this species [chimps], our closest evolutionary relative’, and has been described as a ‘rapidly evolving’ part of the genome. Although it has been held that human/chimp similarity in the MHC is ‘so great that the alleles must have originated before the supposed chimp/human evolutionary divergence’, the sequence results actually dropped the DNA similarity estimate down to 86.7%!​

Human/chimp DNA similarity continues to decrease: counting indels

The major histocompatibility complex plays a big role in the immune response of the human body. Do you want to know how unique we are? Unlike gorillas and chimpanzees, we get malaria and AIDS. That's what those massive indels do for us. Isn't it wonderful to be created in the image of God?

 

[sfs]

I think you mean accept it.

No, I meant understand it, since the last 20 or 30 times you posted on the subject you didn't understand what was being discussed. For example, you were unable to understand what the mutation rate meant -- what "base-pair" means in the expression 2x10[sup]-8[/sup] mutations/base-pair/generation -- and this despite being corrected by half a dozen people on multiple forums. Has that changed?

At any rate, making a million dollars the same as one dollar because they are both only spent once makes no sense. if only I could get you to understand that, or do I mean admit that?

It makes sense when what you're doing is counting the number of transactions; it all depends on what question you're asking. When we're asking how genetically diverged humans and chimpanzees are, we're almost always asking how many mutations have occurred, not how functional the differences are. The great majority of both single-base substitutions and indels have no functional effects at all. (Which is why your money analogy is not a good one: every dollar is worth the same amount, while mutations have vastly different effects.)

 

[mark kennedy]

No, I meant understand it, since the last 20 or 30 times you posted on the subject you didn't understand what was being discussed. For example, you were unable to understand what the mutation rate meant -- what "base-pair" means in the expression 2x10[sup]-8[/sup] mutations/base-pair/generation -- and this despite being corrected by half a dozen people on multiple forums. Has that changed?

Its not what I don't understand that is telling, it what is obvious that is at issue here. We are not 98% the same in our DNA, that is a simple fact that evolutionists are trying to dodge. Lets cut to the chase Steve:

As a biostatistician with a long standing interest in human origins, I was to line up the human DNA sequences next to that of or closest living relative and take stock. A humbling truth emerged: our DNA blueprints are nearly 99 percent identical to theirs. That is, of the three billion letters that make up the human genome, only 15 million of them-less then 1 percent-have changed in the six million years or so since the human and chimp lineages diverged. (Scientific American, by Katharine S. Pollard. May 2009)​

Is this a true and factual statement?

Or is this one?

On the basis of this analysis, we estimate that the human and chimpanzee genomes each contain 40–45 Mb of species-specific euchromatic sequence, and the indel differences between the genomes thus total ~90 Mb. This difference corresponds to ~3% of both genomes and dwarfs the 1.23% difference resulting from nucleotide substitutions; this confirms and extends several recent studies...(Nature, Sept 2005)​

Because it can't be 15 million and less then 1% and 90 million that 'corresponds to ~3%'. It doesn't add up and the analogy of the big difference between a large amount of money and a small amount still stands.

This is where the statistics become interesting:

Using conservative calculations of the proportion of the genome subject to purifying selection, we estimate that the genomic deleterious mutation rate (U) is at least 3. This high rate is difficult to reconcile with multiplicative fitness effects of individual mutations and suggests that synergistic epistasis among harmful mutations may be common. Estimate of the Mutation Rate per Nucleotide in Humans​

Now if this seemed a little high at 1.33% why does it cause no problem with it's 4%? The truth is that it does which is why the blog article in the OP and various other sources are still saying 1% when they know better.

It makes sense when what you're doing is counting the number of transactions; it all depends on what question you're asking. When we're asking how genetically diverged humans and chimpanzees are, we're almost always asking how many mutations have occurred, not how functional the differences are. The great majority of both single-base substitutions and indels have no functional effects at all. (Which is why your money analogy is not a good one: every dollar is worth the same amount, while mutations have vastly different effects.)

What should this one have cost?

The 118-bp HAR1 region showed the most dramatically accelerated change (FDR-adjusted P < 0.0005), with an estimated 18 substitutions in the human lineage since the human&#8211;chimpanzee ancestor, compared with the expected 0.27 substitutions on the basis of the slow rate of change in this region in other amniotes (Supplementary Notes S3). Only two bases (out of 118) are changed between chimpanzee and chicken, indicating that the region was present and functional in our ancestor at least 310 million years (Myr) ago. No orthologue of HAR1 was detected in the frog (Xenopus tropicalis), any of the available fish genomes (zebrafish, Takifugu and Tetraodon), or in any invertebrate lineage, indicating that it originated no more than about 400 Myr ago. (An RNA gene expressed during cortical development evolved rapidly in humans)​

Grace and peace,
Mark

 

[sfs]

Its not what I don't understand that is telling, it what is obvious that is at issue here.

But Mark, the problem is that you really don't understand, with the result that you think things are obvious that are actually wrong. That's why I wished you would understand this stuff. And based on this post, you still don't. Until you do, you will continue to make meaningless challenges to evolution.

We are not 98% the same in our DNA, that is a simple fact that evolutionists are trying to dodge. Lets cut to the chase Steve:

As a biostatistician with a long standing interest in human origins, I was to line up the human DNA sequences next to that of or closest living relative and take stock. A humbling truth emerged: our DNA blueprints are nearly 99 percent identical to theirs. That is, of the three billion letters that make up the human genome, only 15 million of them-less then 1 percent-have changed in the six million years or so since the human and chimp lineages diverged. (Scientific American, by Katharine S. Pollard. May 2009)​

Is this a true and factual statement?

No, it's not accurate. I understand what she's trying to say, but it's not an accurate statement of the differences between humans and chimpanzees.

Or is this one?

On the basis of this analysis, we estimate that the human and chimpanzee genomes each contain 40–45 Mb of species-specific euchromatic sequence, and the indel differences between the genomes thus total ~90 Mb. This difference corresponds to ~3% of both genomes and dwarfs the 1.23% difference resulting from nucleotide substitutions; this confirms and extends several recent studies...(Nature, Sept 2005)​

Because it can't be 15 million and less then 1% and 90 million that 'corresponds to ~3%'. It doesn't add up and the analogy of the big difference between a large amount of money and a small amount still stands.

Yes, that one's accurate (to the best of current knowledge, ignoring some trifling changes since then).

This is where the statistics become interesting:

Using conservative calculations of the proportion of the genome subject to purifying selection, we estimate that the genomic deleterious mutation rate (U) is at least 3. This high rate is difficult to reconcile with multiplicative fitness effects of individual mutations and suggests that synergistic epistasis among harmful mutations may be common. Estimate of the Mutation Rate per Nucleotide in Humans​

Now if this seemed a little high at 1.33% why does it cause no problem with it's 4%?

It causes no problem when the difference is 4% because the issue with the deleterious mutation rate (if there is one) is that might be too many deleterious mutations per generation, counting just single-base substitutions. But adding indel mutations to the single-base rate does not increase the deleterious mutation rate by 300%; it increases it by 20% or 30%. That's because the problem with deleterious mutations is the number of bad mutations that occur per person, while the 4% measures the number of bases that have been changed by mutation (between humans and chimps, in this case). Since indel mutations can change many bases in a single mutation, you can have a large number of bases changed by mutation that contribute very little to the deleterious mutation rate.

This is precisely the issue you have never understood, and the one that I was wishing you would get.

 

[mark kennedy]

But Mark, the problem is that you really don't understand, with the result that you think things are obvious that are actually wrong. That's why I wished you would understand this stuff. And based on this post, you still don't. Until you do, you will continue to make meaningless challenges to evolution.

I'm not challenging evolution, I'm challenging the a priori assumption of universal common ancestry that's what you need to understand. Until you do you will continue to make these fallacious ad hominems that dodge the real challenges to chimpanzee/human common ancestry particularly with regard to the three-fold expansion of the human brain from that of apes.

No, it's not accurate. I understand what she's trying to say, but it's not an accurate statement of the differences between humans and chimpanzees.

Yet this statement is being made regularly and no one challenges the people who make them.

Yes, that one's accurate (to the best of current knowledge, ignoring some trifling changes since then).

Ok, lets move on.

It causes no problem when the difference is 4% because the issue with the deleterious mutation rate (if there is one) is that might be too many deleterious mutations per generation, counting just single-base substitutions. But adding indel mutations to the single-base rate does not increase the deleterious mutation rate by 300%; it increases it by 20% or 30%. That's because the problem with deleterious mutations is the number of bad mutations that occur per person, while the 4% measures the number of bases that have been changed by mutation (between humans and chimps, in this case). Since indel mutations can change many bases in a single mutation, you can have a large number of bases changed by mutation that contribute very little to the deleterious mutation rate.

Unless one of the most accelerated regions has a vital RNA sequence that allows 18 substitutions after only allowing only 2 in 400 million years. What is more, just because there is no know function of a DNA sequence in the genome does not mean it doesn't actually do something. What is more the indels could and do represent a dramatic difference between the respective genomes leave plenty of room for skepticism:

Comparing 231 orthologous genes on the chromosomes, (Watanabe et al. DNA sequence and comparative analysis of chimpanzee chromosome 22. Nature 2004) found 179 cases in which the human and chimpanzee protein-coding sequences were of equal lengths. Of these, approximately 80% have at least one amino-acid difference between the two species, leading to an average amino-acid divergence of 0.82%. Interestingly, of the remaining 52 orthologs, 15 were found to have indels within their coding sequences and 32 were found to have changes in the first ATG (start codon) or the stop codon, changes that would potentially lead to gross structural differences between the human and chimpanzee protein products. Given that fewer than 54% of human-mouse orthologs have coding sequences of different lengths (Initial sequencing and comparative analysis of the mouse genome.) , it seems rather surprising that as many as 20% have changed between humans and chimpanzees, despite the significantly shorter time since their divergence.(Watanabe et al. DNA sequence and comparative analysis of chimpanzee chromosome 22. Nature 2004) hypothesized that indels and structural changes may represent one of the major mechanisms of proteome evolution in the higher primates. What makes us human?​

This is precisely the issue you have never understood, and the one that I was wishing you would get.

I have often wondered about why you are pushing this aspect but I think I understand more then you are comfortable with. The odds against getting past the struggle for credulity are almost zip. I used to think that genetics would decide this issue but that was just me being overly optimistic.

The mutation rate does increase when the known divergence grows by orders of magnitude, that's a given. To make an indel a million bases long the same as one, say, less then 300 bases is shallow logic. I honestly am not all that worried about the actual mutation rate, that was never the point. What I'm most interested in is the ability of evolutionists to cling to homology arguments regardless of the actual level of commonality. There are huge differences and if evolutionists had the courage of their beliefs they would openly admit that the known divergence, too often they simply don't.

Always a pleasure Steve.

Grace and peace,
Mark

 

[sfs]

I'm not challenging evolution, I'm challenging the a priori assumption of universal common ancestry that's what you need to understand.

Of course you're challenging evolution, since the conclusion of universal common descent is a key part of evolutionary biology, and that's what you're challenging.

Yet this statement is being made regularly and no one challenges the people who make them.

If I heard someone say that in conversation, I'd challenge it. I wouldn't make a big deal out of it, since the specific number in her statement makes almost no practical biological difference.

I have often wondered about why you are pushing this aspect but I think I understand more then you are comfortable with. The odds against getting past the struggle for credulity are almost zip. I used to think that genetics would decide this issue but that was just me being overly optimistic.

Wrong. I'm not "pushing this aspect"; I'm simply responding to you making the same mistake over and over. Stop making the mistake and I'll stop responding to it.

The mutation rate does increase when the known divergence grows by orders of magnitude, that's a given.

And it's wrong. Still wrong. Still the thing you don't understand, which I wish you did.

 

[mark kennedy]

Of course you're challenging evolution, since the conclusion of universal common descent is a key part of evolutionary biology, and that's what you're challenging.

Evolution has been loosely defined as the change of alleles in populations over time, no where have I seen it defined as the assumption of universal common descent by exclusively naturalistic mechanisms. I refuse to make that assumption you consider a 'key part' of evolution and reserve the right to 'challenge' aspects that are neither directly observed nor demonstrated.

Most of all I refuse to accept naturalistic assumptions, that exclude God categorically, as the very definition of evolution. What I am challenging is a false assumption since I do know that God acts in time and space. What is more I trust the explicit testimony of Moses and Paul far more then the transcendental generalities of what you are calling 'evolution'.

If I heard someone say that in conversation, I'd challenge it. I wouldn't make a big deal out of it, since the specific number in her statement makes almost no practical biological difference.

If we were just talking about the frequency of indels I don't think I would care. What I'm really trying to focus on are differences and large scale change assumed, but more importantly, it's about getting the facts straight. I'm told that there is a gradual progression in the cranial capacity in our supposed assent from apes over 6 million years. I now know this to be false, in fact, it would have had to be 2 mya that it doubled. What is more there would be no evidence that our closest relative even existed if chimpanzees were not alive today.

It makes a big biological difference if genome sequences are changing on a large scale given the affect of mutations. You might think that because they don't happen in protein coding genes that they are meaningless, perhaps given to relaxed functional constraint due to the fact that nothing vital is affected. This goes out the window when an RNA sequence like HARf gets 18 substitutions in a regulatory gene that has allowed only 2 in 400 million years.There are others:

These structural variants encompass at least 24 Mb of DNA and overlap with >245 genes. Seventeen of these genes contain exons missing in the chimpanzee genomic sequence and also show a significant reduction in gene expression in chimpanzee. Compared with the pioneering work of Yunis, Prakash, Dutrillaux, and Lejeune, this analysis expands the number of potential rearrangements between chimpanzees and humans 50-fold. A genome-wide survey of structural variation between human and chimpanzee​

There are whole genes that are human specific that simply don't exist in the Chimpanzee genome:

This region contains four human genes (POM121, WBSCR20C, TRIM50C, and FKBP6) that are not found at this location in chimpanzee.​

The differences are on a far larger scale then we are being told.

Wrong. I'm not "pushing this aspect"; I'm simply responding to you making the same mistake over and over. Stop making the mistake and I'll stop responding to it.

No I think you are just trying to make the fact that indels and other differences seem meaningless. I think you want to make spending or depositing 1 dollar the same as thousands or millions since they are all one time events. It's not that I don't understand what you are saying, I just don't agree with it.

And it's wrong. Still wrong. Still the thing you don't understand, which I wish you did.

What I understand is that the differences dispel homology arguments. I also understand that evolutionists love to tell people that we are 99% the same as chimpanzees in our DNA. What I understand is that our cranial capacity is three times that of and the genetic basis for such a major morphological change is largely, if not completely, unknown.

I also understand that these debates will never be settled based on the facts. It really doesn't matter if I make mistakes because the central focus will always be on credulity whether the 'mistakes' I make or real or exaggerated. Should we be experimenting with areas of the genome known as 'gene deserts' because there is no known function? I think not, because what we will find is that the differences between chimpanzees and humans involve far more then 'junk DNA'. How can we say, at this stage of the game, that these differences don't represent improbable giant leaps of adaptive evolution?

The important thing here is not to rush to judgment since the truth is slowly coming out, the differences are far larger then we have been told. This undermines credulity for the scientist and look around, there aren't that many creationists on here. Who are you trying to convince?

Grace and peace,
Mark

 

[shernren]

You haven't answered me mark.

Then let me ask you a simple question. How often does a 47 million nucleotide indel occur?

 

[Schroeder]

Well genes, but are we talking about 100% copies, or their gene for hemoglobin is simular to ours giving room for genetic drift? Lets not forget that that the most basic microbe shares 50% or something like that of it's genetic material with us, *or was it higher it's been a while* but thats due to the fact that there are many genes and such that are universally used.

ALso in one of the books I read, think it was a Dawkins one on evolution, it was pointed out that while only 99% of our encoding DNA is different, easily majority of our genes are different from chimps and such by one or more basepairs, wich is where the differences add up. A single deletion or insertion can change a gene.

and this single deletion or insertion causes what to happen. most theory evolution is based on accidental or mutations of genes from conception to birth. only so much in conception is passed on and then it depends on dominance genes between the two. if a mutation happens it has to be helpful. Of course that percent is very very small. It then has to survive to pas it on. it has to find a mate etc etc thiss till reduces the chance of theory evolution. the earth would have to be multi multi billions of years old. much old then what is mentioned. the odds are way way out there. And our genes would be similiar seeing how our bodies work similiarly. everything on earth should and will share similiar genes creation would suppose this just as easy as the theory.

The gene that gives us our brain size and such was just 13 base pair difference out of 152 or some odd.

And not sure if this was confused here, but the 99 or so % identical to chimps and the 95% are two different comparisons. One is of encoding DNA AKA our genes, the other is our entire DNA junk, encoding, pseudogenes and so on.

Just 13 well that proves it. so how many mutations in just the right place and time and parents and domination of parents genes etc would this take. what would the odds be for this evolution to slowly take us to humans. YOur good at giveing overall links but not so good at details of how it is even possible to bring us to human. the brain size would have to have what mutations when that would not kill the species of monkey. do we have a mutation in skeletol structure to accomadate the later random mutation of the brain to grow. but if the skull is to big the brain bounces around. if the brain grows and skull doesnt we have problems. If we have the brain telling the body to do things it isnt designed to do problems. see how are the problem dealt with besides just saying time heals all wounds or problems. Or the time tested populations change. except mutations happen in individuals which then need to pass it on.

 

[gluadys]

and this single deletion or insertion causes what to happen. most theory evolution is based on accidental or mutations of genes from conception to birth.

Actually, mutations which occur from conception to birth, like those that occur after birth, are generally irrelevant to evolution, as they are not passed on to the next generation unless they occur in a germ cell.

The mutations that are most relevant to evolution are those that occur during the production of germ cell due to uncorrected miscopying of DNA or to the recombination of DNA as the chromosomes re-form and cross-over. By the time you get to fertilization, all the mutations that apply to this generation have basically occurred, and the next round happens when the adult organism generates its germ cells.

if a mutation happens it has to be helpful.

Not true. Most mutations are neither helpful nor harmful. In some cases, even a slightly harmful mutation will persist over many generations, and definitely will persist if it is recessive.

When a mutation is helpful it will spread through the population faster and occur more frequently in following generations. But some mutations spread even without being helpful (genetic drift).

Of course that percent is very very small. It then has to survive to pas it on. it has to find a mate etc etc thiss till reduces the chance of theory evolution.

Since one mutation doesn't make a new species, it has no problem finding a mate among the rest of the population it is part of. Remember, evolution is a change in the species, not a change in the organism. By passing on its mutation to its offspring, it ensures that it will be preserved in the species. If it is a helpful mutation, it will become more common in the species. When the mutant version of the gene has become the most common in the species, the species has evolved a little bit.

Just 13 well that proves it. so how many mutations in just the right place and time and parents and domination of parents genes etc would this take. what would the odds be for this evolution to slowly take us to humans.

Same as the odds of anything that has taken place: 1

Note that the 13 mutations did not all have to occur in the same generation. They just each had to persist in and spread through the population. Each would provide some benefit of some kind, and as each became more common, it would also become more common for some individuals to have 3 or 7 or 10 of the 13 mutations instead of just one or two of them. There could be a positive epistasis (two or more mutations together being even more helpful than a simple addition of their benefits would produce) to spread the relevant genes even faster.

 

[matthewgar]

and this single deletion or insertion causes what to happen. most theory evolution is based on accidental or mutations of genes from conception to birth. only so much in conception is passed on and then it depends on dominance genes between the two. if a mutation happens it has to be helpful. Of course that percent is very very small. It then has to survive to pas it on. it has to find a mate etc etc thiss till reduces the chance of theory evolution. the earth would have to be multi multi billions of years old. much old then what is mentioned. the odds are way way out there. And our genes would be similiar seeing how our bodies work similiarly. everything on earth should and will share similiar genes creation would suppose this just as easy as the theory.

Just 13 well that proves it. so how many mutations in just the right place and time and parents and domination of parents genes etc would this take. what would the odds be for this evolution to slowly take us to humans. YOur good at giveing overall links but not so good at details of how it is even possible to bring us to human. the brain size would have to have what mutations when that would not kill the species of monkey. do we have a mutation in skeletol structure to accomadate the later random mutation of the brain to grow. but if the skull is to big the brain bounces around. if the brain grows and skull doesnt we have problems. If we have the brain telling the body to do things it isnt designed to do problems. see how are the problem dealt with besides just saying time heals all wounds or problems. Or the time tested populations change. except mutations happen in individuals which then need to pass it on.

Actually one of the thing that allows for humans to have bigger brain size from what I understand has 0 to do with the brain or the skull, what actually happened was one of the major muscles linked to the jaw bone, that in apes gives them their extreme jaw strength was weakened, this weakening allowed the muscle to be loser, allowing dun dun dun, for the brain case to continue to grow bigger during development, this is partly believed to be why we have the soft spot as babies, because in chimps the skull would fit the way it normally did. Also conicidently, this muscle is also whatallows us speach *and some humans have it where th protein is returned partly and they have limited speach* by being weaker our jaws can move more. The gene removed a protein that made this muscle stronger by breaking it.

And as for mate and survive, your guys understanding of biology is kind bizzare...are you picturing it a single zebra with the great mutation and if he dies thats it? Every young has mutations, it doesn't have to be every single beneficial mutation to pass on, yes many things might cause that great mutation to not be passed on, but were talking in many species, thousands of individuals every year, many that do survive.

Not to mention in many species like herd/pack and such a mutation that allows 1 zebra to move 1% faster then the others, has the entire herd behind it. It's the old joke I have told here many times before.

A Safari guide is traveling with a american, and he's telling him what to do in the jungle if he sees a lion, and he tells him, "What ever you do don't run, it will catch you, you have to climb a tree or try to scare it." a bit later on they a lion jumps out of the bushes, the american starts looking for a tree when he spots the guide running off, he takes off after the guide yelling, "I thought you said we couldn't outrun the lion." to wich the guide yes, "Yes, but I only have to outrun you."

Nature isn't just one individual with one predator thats it, it's everything in between, and it's not all or nothing with gene mutations, nor is it okay that one had the beneficial mutation...oops he's dead. Many of these mutations are multistage. Maybe it takes 2-3 mutations for something to happen, if the son dies, the rest of the fathers offspring and descendants still have the chance for that mutation. Or even if it's a single stage mutation, it's still possible to come back around, it's been shown in the Ecoli experiment that some mutations take 2 or more mutations to have a effect, but can happen multiple times.

The creationist simplistic view of evolution and mutations doesn't really begin to address the nature of it all.

And on the 13 mutations, who says they all effect it, it's just saying there were 13 changes, this usually shows heavy genetic pressure for change. And not all at once, maybe each one makes small adjustments to improve, or were starter points for bigger changes. No one thinks BAM all 13 changes miraculously appeared at once. Were talking 7 million yeras or so time here.