How many mutations?

| 40 Comments

Tuuli Lappalainen tweeted a result presented by Daniel Wegmann:

Daniel Wegmann: Every non-lethal genome position is variable in the human population #bc2
– Tuuli Lappalainen (@tuuliel) July 4, 2013

Really?

There are 23 pairs of chromosomes in the human genome. If you counted the number of positions - A’s, T’s, G’s, and C’s - you would have approximately three billion positions across those 23 chromosomes. And because each chromosome is part of a pair, you can multiply that number by two, for a total of six billion places where a mutation can happen. Assuming there are not very many lethal positions, is it really possible to have a mutation at every site in at least one living human?


Yes!

In fact, we expect that across all humans, there are over 100 mutations at every single position in the human genome. And, here is the math to prove it:

The average mutation rate in the human genome is 1.2 x10^-8 mutations per site per generation. This is pretty small, so in each person, we only expect to observe a handful of new mutations relative to their parents. But, that handful of mutations adds up when you think of how many people are on the earth.

There are now 7.16 billion people on earth (at the time of this post the estimate was 7,165,212,612 ish).

If we let the birth of every person alive represent a single generation event, then we can estimate the average number of new mutations at each site across all 7.16 billion people by multiplying the mutation rate per generation, by the number of generations:

(1.2 x 10^-8) mutations/site/generation * 7,165,212,612 generations = 86 mutations/site

This says that if we could look at the genome of all 7 billion people, on average, we expect to observe 86 new mutations at each of the six billion individual positions across the genome. But we usually don’t talk about each copy of a chromosome individually (the one you got from your mother and the one you got from your father), we just talk about a single chromosome, like chromosome 1. That is, we think about the genome as folded in half (that three billion number I first mentioned).

So, the folded number (thinking about the number of differences across the three billion sites), suggests that there are about 172 mutations at each site of every chromosome across the whole human population.


That sounds like a lot of mutations, and it really is, but think about all of the people on the earth!

A beach in Sri Lanka, by Denish C


Taipei Rapid Transit on New Year’s Eve, by Changlc


School dedication ceremony, Pongwe, Tanzania, by Jesse Awalt


Urawa Reds vs Gamba Osaka in Tokyo, Japan, by Pocopen


When we consider all 7 billion of us together, a little math shows that, even though there are only a small number of new mutations in each individual, there really can be mutations at every single position in the genome. In fact, we expect hundreds of mutations at every single (non-lethal*) site!

Wow!!

*A mutation that results in death would not be tolerated, so we would not expect to observe mutations at a select set of very important sites. BUT, a mutation that is harmful in one tissue (like the brain) may not have any effect in a different tissue (say, the skin). That is a story for another day.

40 Comments

Interesting, but is the real variability not this simple. Is it not that there is potentially a one-bit to n-bit insertion at each site?

And that’s why it’s possible to detect the hallmarks of selection at different position in the human genome. When we do this we find that some regions are under strong selective constraint but most are not. Indeed most evolve as if the variation were neutral, thus providing evidence for the “junk DNA” hypothesis. But that’s the story of another thread.

DS said:

And that’s why it’s possible to detect the hallmarks of selection at different position in the human genome. When we do this we find that some regions are under strong selective constraint but most are not. Indeed most evolve as if the variation were neutral, thus providing evidence for the “junk DNA” hypothesis. But that’s the story of another thread.

More specifically, selective constraint is usually studied by comparing the frequencies of alleles in different regions (or better, different classes of regions). The reason this isn’t a knockdown argument for junk DNA is that it really only tells you the relative degree of constraint; unless you have some region that you know has no constraint, you really can’t determine that parts of the genome are neutrally evolving. (Unless you know the demographic history of the population in detail, that is, but we never know that for real populations.)

This calculation is of the number of mutations that will have occurred in the current generation. It does not take into account mutant alleles that occurred in an earlier generation and were then inherited in the present generation.

To know of that you need to take into account the total branch length of the coalescent tree connecting all present individuals. This is a little bit different than when the coalescent shows the ancestry of just a modest-sized sample of gene copies from a population.

Anyway, the probability of seeing almost all possible single-base mutations, each at least once, is fairly high.

And don’t forget that you *can* carry a non-functional mutation in a gene that is essential for life if (i) the gene is recessive, or (ii) the gene has multiple copies in the genome. I remember reading that every human carries around 6 lethal mutations (too long ago for me to recall the reference now).

Chris Lawson said:

And don’t forget that you *can* carry a non-functional mutation in a gene that is essential for life if (i) the gene is recessive, or (ii) the gene has multiple copies in the genome. I remember reading that every human carries around 6 lethal mutations (too long ago for me to recall the reference now).

The estimate is that you have from 1 to 3 lethal equivalents in your genome. It isn’t the fully recessive lethals that you have that are most of the problem. There are a lot of genes with problems as indicated in the second paper.

http://www.plosgenetics.org/article[…]pgen.1003484

http://www.ncbi.nlm.nih.gov/pmc/art[…]/PMC3299548/

Please excuse a dumb question: How can you get 86 mutations per site, when there are only 4 possible values at each site, and one should be the expected one? I’d say you can only have 3 possible mutations at each site if A, T, G, and C are the only possible values, and one of them is the “non-mutated” value.

I think the 86 was across the population, not within one individual organism.

Henry

Cl, As Henry J says, this was a back-of-the-envelope calculation of the number of people with a mutation at any given base pair. Not the number of possible variations at each base pair (which as you say maxes out at 4). Sayres is calculating the expected number of humans alive today with a single-point mutation at any given point.

This is obviously a rough calculation only – it does’t account for the fact that some parts of the genome have higher mutation rates, it doesn’t account for evolutionary pressure, and it doesn’t count frame-shift mutations, gene duplications, or other mutations…but it still makes the point that, contra the usual creationist rhetoric, even extremely rare events in an individual become common to the point of virtual certainty when applied to populations.

And if one applies the same logic to bacterial populations…well, the entire population of humans today (~7 billion) can be matched by an E. coli population in less than 100 ml of culture broth and E. coli can reproduce about every 20 minutes in good conditions…

Chris Lawson said:

Cl, As Henry J says, this was a back-of-the-envelope calculation of the number of people with a mutation at any given base pair. Not the number of possible variations at each base pair (which as you say maxes out at 4). Sayres is calculating the expected number of humans alive today with a single-point mutation at any given point.

This is obviously a rough calculation only – it does’t account for the fact that some parts of the genome have higher mutation rates, it doesn’t account for evolutionary pressure, and it doesn’t count frame-shift mutations, gene duplications, or other mutations…but it still makes the point that, contra the usual creationist rhetoric, even extremely rare events in an individual become common to the point of virtual certainty when applied to populations.

And if one applies the same logic to bacterial populations…well, the entire population of humans today (~7 billion) can be matched by an E. coli population in less than 100 ml of culture broth and E. coli can reproduce about every 20 minutes in good conditions…

So if “Darwinism” were true, those E. coli should be at least monkeys by now. ;-)

The unfortunate thing that this exercise tell us is that we - anyone who supports real science - must be absolutely clear what we mean by each word we use. And that anyone peddling doubt can afford to be very sloppy with terminology and definitions. In fact their strategy requires defining terms to suit the argument, and using multiple definitions whenever necessary. But that “requirement” is orders of magnitude easier than ours. Possibly the most fascinating thing I learned from 16 years of reading the antics of anti-evolution activists is how “naturally” those word games come to them. I remember falling for a few baits-and-switch myself early on.

We may have the evidence and some major court victories, but in the “court of public opinion” that is painfully not enough. They (anti-evolution activists) have the majority - roughly 1/4 each of (1) those who won’t accept evolution under any circumstances, (2) those with doubts due to poor understanding and/or interest, (3) those who accept it (usually for the wrong reason) but think it’s fair to “teach both sides” in science class.

One advantage that we have that is not exploited nearly enough in my opinion, is that we have the numbers. Everything from number of mutations to ages of fossils. Sure, the scam artists take numbers out of context too to spin their web of half-truths. But it’s harder for them than with words. For geologic time alone I never miss an opportunity to say how many millions (or billions) of years ago X happened. And most scam artists have learned not to call attention to the fatal differences between YEC and OEC, so they rarely deny those ages, especially if an audience is present. Even if one finds oneself in the presence of a number-manipulator like Dembski, just ask what their numbers are. When they pretend that the mutation rate is too low for speciation, ask them how many “kinds” there are, and when those “kinds” first appeared. And don’t let them drag the “debate” back to “Darwinism.”

Henry J said:

I think the 86 was across the population, not within one individual organism.

Henry

At any one site. Using the same rate, an individual has (on average) roughly the same number of mutations across all sites from the previous generation.

Chris Lawson said:

And if one applies the same logic to bacterial populations…well, the entire population of humans today (~7 billion) can be matched by an E. coli population in less than 100 ml of culture broth and E. coli can reproduce about every 20 minutes in good conditions…

I recently did a similar back-of-the-envelop calculation starting with these numbers, using the “worst case” creationist assumptions about mutation rates (those really big scary the-odds-make-it-impossible numbers and all), and came up with the conclusion that in the population of bacteria on Earth there is about 1 beneficial mutation every 20 minutes. Taking it one step further, again assuming the “worst case” creationist assumptions including requiring a strictly linear sequence of beneficial mutations, the numbers came out to something like 10,000 years to create a new feature in a bacterium. Not just a slight variation on a theme, like the creation of nylonase, but a de novo Irreducibly Complex feature.

Cl said:

Please excuse a dumb question: How can you get 86 mutations per site, when there are only 4 possible values at each site, and one should be the expected one? I’d say you can only have 3 possible mutations at each site if A, T, G, and C are the only possible values, and one of them is the “non-mutated” value.

The direct part of your question has been answered. Within the human population, if we define one base pair as the normal one at a given site, we should, on average, expect 86 individuals to have one of the other base pairs at that site. (Actually, 86 genomes, but for this purpose, genome and individual are the same thing.)

This is a very crude but very valuable calculation.

First of all, it’s interesting to note that the number 86 can be perceived as unexpectedly “large” or unexpectedly “small” (out of more than 7 billion).

However, while noting the value of the calculation, it’s still important to note its limitations. “The human genome” is an imaginary “typical” haploid germline genome that models real human genomes. In reality, every nucleated cell in every human body that exists has its own unique genome, and there are trillions of cells in an adult human body. And for normal nucleated cells that aren’t sperm or ovum, actually, that’s usually two genomes, since normal human cells other than germ cells are usually diploid. Some normal polyploid nuclei and numerous multinucleated cells also exist within human bodies.

Individual human genomes don’t have exactly three billion base pairs, and any two are likely to have somewhat different base pair number.

Furthermore, above, we have implicitly been talking about point mutations. A point mutation merely changes a base at a site to a different base. E.g. AC to AG. However, there are also “indels” - insertions and deletions of one or more bases, e.g. AC to ATC. There are gene duplications and other events that generate or delete many base pairs in one mutation event.

Of course, I’ve barely touched the surface here. Many of the pro-science people could expand all day on what I’ve started.

Scott F said:

Chris Lawson said:

And if one applies the same logic to bacterial populations…well, the entire population of humans today (~7 billion) can be matched by an E. coli population in less than 100 ml of culture broth and E. coli can reproduce about every 20 minutes in good conditions…

I recently did a similar back-of-the-envelop calculation starting with these numbers, using the “worst case” creationist assumptions about mutation rates (those really big scary the-odds-make-it-impossible numbers and all), and came up with the conclusion that in the population of bacteria on Earth there is about 1 beneficial mutation every 20 minutes. Taking it one step further, again assuming the “worst case” creationist assumptions including requiring a strictly linear sequence of beneficial mutations, the numbers came out to something like 10,000 years to create a new feature in a bacterium. Not just a slight variation on a theme, like the creation of nylonase, but a de novo Irreducibly Complex feature.

Anyone who knows anything about basic molecular biology knows that life has to evolve.

It was amazing that Darwin (and Wallace) deduced a basic mechanism of biological evolution without knowing about molecular genetics, or even classical Mendelian genetics. To deduce that from the “top down” was remarkable.

However, once you know how DNA replicates, it becomes instantly obvious that life must evolve.

Thanks to all for the clarification. Seems obvious I guess, but for some reason I was not reading it as 86 individuals having a mutation at the given site.

Ron Okimoto said:

Chris Lawson said:

And don’t forget that you *can* carry a non-functional mutation in a gene that is essential for life if (i) the gene is recessive, or (ii) the gene has multiple copies in the genome. I remember reading that every human carries around 6 lethal mutations (too long ago for me to recall the reference now).

The estimate is that you have from 1 to 3 lethal equivalents in your genome. It isn’t the fully recessive lethals that you have that are most of the problem. There are a lot of genes with problems as indicated in the second paper.

http://www.plosgenetics.org/article[…]pgen.1003484

http://www.ncbi.nlm.nih.gov/pmc/art[…]/PMC3299548/

This is supremely awesome. I really am looking forward to the day when I get a high coverage version of my genome.

But what’s the deal with this finding? The vast majority of mutations degrade reproductive fitness and so natural selection will weed them out. There are only 3 million base pair differences between any two humans, and most of these are found in non-essential regions of the genome (formerly called “junk DNA” by the Darwinists).

https://me.yahoo.com/a/RdfV1YQJ1oSF[…]6ZE0XxwYlRtQ–#ad533 said:

But what’s the deal with this finding? The vast majority of mutations degrade reproductive fitness and so natural selection will weed them out. There are only 3 million base pair differences between any two humans, and most of these are found in non-essential regions of the genome (formerly called “junk DNA” by the Darwinists).

This is again Atheistoclast, who’s been banned. His statement “The vast majority of mutations degrade reproductive fitness” is bullshit.

What’s the vast majority? In complex organisms, most mutations are neutral. Because they’re in Junk DNA, which is still called Junk because there’s positive evidence most of the genome cannot suffer a deleterious mutation. So it’s still Junk– because we’ve got positive evidence, and you don’t.

Among the subset of mutations that affect function, maybe 90-94% are deleterious and 6-10% are beneficial; sometimes more. For a discussion with references, see Scott Buchanan’s discussion of beneficial vs. deleterious mutations.

diogeneslamp0 said: What’s the vast majority? In complex organisms, most mutations are neutral. Because they’re in Junk DNA, which is still called Junk because there’s positive evidence most of the genome cannot suffer a deleterious mutation. So it’s still Junk– because we’ve got positive evidence, and you don’t.

http://www.ncbi.nlm.nih.gov/pubmed/22661327

The vast majority of mutations are deleterious and are eliminated by purifying selection.

TOWARD A REALISTIC MODEL OF MUTATIONS AFFECTING FITNESS

http://www.bioone.org/doi/abs/10.15[…]5D2.0.CO%3B2

Analysis of a recent mutation accumulation (MA) experiment has led to the suggestion that as many as one-half of spontaneous mutations in Arabidopsis are advantageous for fitness. We evaluate this in the light of data from other MA experiments, along with molecular evidence, that suggest the vast majority of new mutations are deleterious.

Thanks for playing.

Scott F said:

Chris Lawson said:

And if one applies the same logic to bacterial populations…well, the entire population of humans today (~7 billion) can be matched by an E. coli population in less than 100 ml of culture broth and E. coli can reproduce about every 20 minutes in good conditions…

I recently did a similar back-of-the-envelop calculation starting with these numbers, using the “worst case” creationist assumptions about mutation rates (those really big scary the-odds-make-it-impossible numbers and all), and came up with the conclusion that in the population of bacteria on Earth there is about 1 beneficial mutation every 20 minutes. Taking it one step further, again assuming the “worst case” creationist assumptions including requiring a strictly linear sequence of beneficial mutations, the numbers came out to something like 10,000 years to create a new feature in a bacterium. Not just a slight variation on a theme, like the creation of nylonase, but a de novo Irreducibly Complex feature.

Well, go ahead and show us your back of the envelope calculations. Let’s try to calculate the odds of a trilobyte eye arising due to random mutation during the Cambrian. There is no evidence of an intermediate Trilobyte eye, they appear fully formed in the fossil record. But let’s just use the standard Darwinist trick of helping ourselves to imaginary evidence. Even the simple eye spot is composed of roughly 900 genes and genes have roughly 200 to 1200 amino acids, let’s say 300 on average, so that’s about 810,000 dna mutations. So given that the mutation rate among trilobytes is probably around 1 * 10^-7 and let’s say that the trilobyte genome was around a billion dna. So we’re talking about a 1000 mutations per generation even though that is probably too generous. There’s no way that you can go from no eye to even simple eye-spot in one generation.

https://me.yahoo.com/a/UIFqpY46nexU[…]agSA6W#dd2ba said:

diogeneslamp0 said: What’s the vast majority? In complex organisms, most mutations are neutral. Because they’re in Junk DNA, which is still called Junk because there’s positive evidence most of the genome cannot suffer a deleterious mutation. So it’s still Junk– because we’ve got positive evidence, and you don’t.

http://www.ncbi.nlm.nih.gov/pubmed/22661327

The vast majority of mutations are deleterious and are eliminated by purifying selection.

TOWARD A REALISTIC MODEL OF MUTATIONS AFFECTING FITNESS

http://www.bioone.org/doi/abs/10.15[…]5D2.0.CO%3B2

Analysis of a recent mutation accumulation (MA) experiment has led to the suggestion that as many as one-half of spontaneous mutations in Arabidopsis are advantageous for fitness. We evaluate this in the light of data from other MA experiments, along with molecular evidence, that suggest the vast majority of new mutations are deleterious.

Thanks for playing.

Is the want-wit above once again the banned Atheistoclast? Can you fingerprint stupidity?

Can someone please check the IP address of this want-wit?

The want-wit just cited a couple of theoretical papers to try to refute EXPERIMENTAL results.

Even in the paper cited by this blithering toff, the authors mention the EXPERIMENTAL result from MA experiments that half of all non-neutral mutations in Arabidopsis are beneficial.

You have to be a real IDiot to cite a defeater like that.

There’s a whole bunch of EXPERIMENTAL papers measuring the ratio of beneficial to deleterious mutations. It’s 5-10% depending on species, environment, etc.

In Perfeito et al. 2002, in E. coli, they saw 10%. So eat shit, want-wit, that’s EXPERIMENTAL.

The dumb fuck who wrote that comment has ~130 more novel random point mutations than his parents; twice that many relative to his grandparents; etc. If “the vast majority of mutations are deleterious” as he thinks, he’d have 65+ MORE deleterious mutations than his parents; twice that relative to his grandparents; etc. All of his organs would be dead, instead of just his brain.

There’s a whole bunch of EXPERIMENTAL papers measuring the ratio of beneficial to deleterious mutations. It’s 5-10% depending on species, environment, etc.

If there are so many beneficial mutations and if a human has between 30 and 90 mutations per person then go ahead and name for me some beneficial mutations that eventually built a new gene. I’m not talking about breaking preexisting genes, I’m talking about building new genes. There aren’t any. That’s why the theory of NS acting on RM has NO evidence in its favor. Most of your post by the way was just argumentum ad ridiculum.

https://me.yahoo.com/a/iS9p19oQ3c6V[…]01EUrz#3f071 said:

There’s a whole bunch of EXPERIMENTAL papers measuring the ratio of beneficial to deleterious mutations. It’s 5-10% depending on species, environment, etc.

If there are so many beneficial mutations and if a human has between 30 and 90 mutations per person then go ahead and name for me some beneficial mutations that eventually built a new gene. I’m not talking about breaking preexisting genes, I’m talking about building new genes. There aren’t any.

Bullshit. How the hell would you know? Your post showed you have no clue how how proteins evolve. You think they evolve by random scrambling of parts, like a tornado. No, the simultaneous random scrambling of all parts does not model evolution– it models your mental processes.

Every creationist asks where are the new genes? Asked and answered a thousand times. We can start with T-urf13 in maize and Finnegan in drosophila and go on from there. There are genes that encode unstructured proteins that are functional, so structure is not necessary for function. New genes can also be produced by shuffling exons of other genes.

But because it only takes a few mutations in some existing proteins to evolve a novel function, it is NOT necessary to create a gene de novo in order to gain complexity or a beneficial mutation.

What evidence is there that ANY new genes were involved in the evolution of apes to humans? (Actually there is ONE, exactly one known, but it’s a very small RNA gene, not highly improbable.)

There are numerous examples of proteins evolving novel enzymatic functions, like the nylonase bug and others that degrade or consume xenobiotics.

Gene duplication is common and has happened recently in the human race– e.g. humans differ in their copy numbers of alpha amylase.

Given that gene duplication, neo-functionalization and beneficial mutations happen everywhere we look, what mechanism do you imagine could TURN THAT OFF and magically stop it from happening?

Do you admit that gains in complexity do not require de novo gene creation, but can (and usually do) occur more commonly via other OBSERVED processes?

If 1. Humans really are much more complex than apes, and 2. de novo gene creation were the only way to gain complexity, then why do you suppose NO de novo new protein-coding genes were needed to turn an ape into a human? Why? Why? Why? 1 or 2 must be wrong, or both.

Bullshit. How the hell would you know? Your post showed you have no clue how how proteins evolve. You think they evolve by random scrambling of parts, like a tornado. No, the simultaneous random scrambling of all parts does not model evolution– it models your mental processes. Every creationist asks where are the new genes?

None of that is an argument.

Asked and answered a thousand times. We can start with T-urf13 in maize

That’s the breaking of preexisting genes. We are talking about building new genes not breaking preexisting ones.

There are genes that encode unstructured proteins that are functional, so structure is not necessary for function.

True, but that does not prove that NS acting on RM is responsible for all the diversity of life.

New genes can also be produced by shuffling exons of other genes.

You’re just assuming that there is no mind that is doing the shuffling.

But because it only takes a few mutations in some existing proteins to evolve a novel function, it is NOT necessary to create a gene de novo in order to gain complexity or a beneficial mutation.

But it is necessary if you believe that NS acting on RM is responsible for all the diversity of life.

What evidence is there that ANY new genes were involved in the evolution of apes to humans? (Actually there is ONE, exactly one known, but it’s a very small RNA gene, not highly improbable.)

Are you crazy we are on track to discover at least 50 to 100 and this is not counting the genes that apes have that we do not have. We’re not arguing about common ancestry which I accept, we’re arguing about NS.

The Journal of Biological Chemistry writes:

Among the approximately 23,000 genes found in human DNA, scientists currently estimate that there may be as few as 50 to 100 that have no counterparts in other species. Expand that comparison to include the primate family known as hominoids, and there may be several hundred unique genes. http://news.wustl.edu/news/Pages/11349.aspx

Besides, it’s not quantity of genes that counts but how we use them. Genes are alternatively spliced by a consciousness and put back together.

There are numerous examples of proteins evolving novel enzymatic functions, like the nylonase bug and others that degrade or consume xenobiotics.

Again, this is the breaking of preexisting genes not building new genes.

Gene duplication is common and has happened recently in the human race– e.g. humans differ in their copy numbers of alpha amylase. Given that gene duplication, neo-functionalization and beneficial mutations happen everywhere we look, what mechanism do you imagine could TURN THAT OFF and magically stop it from happening?

Intelligence.

Do you admit that gains in complexity do not require de novo gene creation, but can (and usually do) occur more commonly via other OBSERVED processes?

There’s not such thing as an observed process. When you observe something move you don’t observe the thing that moves it. For every observed effect there is an unobserved caused.

If 1. Humans really are much more complex than apes, and 2. de novo gene creation were the only way to gain complexity, then why do you suppose NO de novo new protein-coding genes were needed to turn an ape into a human? Why? Why? Why? 1 or 2 must be wrong, or both.

Let’s just say that there are no de nove genes between humans and apes which there are not. That would not prove that all mutations are random which is what we’re arguing about.

https://me.yahoo.com/a/iS9p19oQ3c6V[…]01EUrz#3f071 said:

Let’s just say that there are no de nove genes between humans and apes which there are not. That would not prove that all mutations are random which is what we’re arguing about.

Well Joe, let’s just say there is something we can not observe making the occaisional intelligently directed tweak to DNA using forces we can not measure, but which neccesarily violate the known Laws of Physics. How does that add anything to our understanding of the world around us? Come back once you can tell us something more specific about its motives and methods.

diogeneslamp0 said: In Perfeito et al. 2002, in E. coli, they saw 10%. So eat shit, want-wit, that’s EXPERIMENTAL.

The dumb fuck who wrote that comment has ~130 more novel random point mutations than his parents; twice that many relative to his grandparents; etc. If “the vast majority of mutations are deleterious” as he thinks, he’d have 65+ MORE deleterious mutations than his parents; twice that relative to his grandparents; etc. All of his organs would be dead, instead of just his brain.

I don’t care much for your personal and disgusting attacks directed at me. There is a wealth of evidence that virtually all mutations are deleterious, although most are only very slightly harmful - so we are not in danger of an imminent mutational meltdown and extinction as a species. The effect of mutations is mitgated by the fact that there exists much redundancy in the genome which can compensate for this. However, falling fecundity rates in humans may be attributed to the accumulation of harmful mutations.

1) How can no mutations be positive? Positive means results in a change in phenotype, relative to the parent, that confers a statsitical reproductive advantage, within tht environment. What magic prevents this circumstance, which would be expected, from ever happening?

2) Bacteria are prokaryotes and have very little junk DNA. However, even in bacteria, numerous mutations are possible that are neutral, due to having essentially no impact on amino acid coding or anything else. What prevents these mutations from occurring.

3) In eukaryotes, large sequences of the genome appear to be under no selective pressure. One explanation would be that mutations in these areas tend to have little impact on the phenotype, and that thus, mutations in these areas tend to be neutral with regard to fitness. If they were negative, they would be selected against. How do advocates of “virtually no neutral mutations” deal with the fact that many mutations are not selected against?

Dave Lovell said:

https://me.yahoo.com/a/iS9p19oQ3c6V[…]01EUrz#3f071 said:

Let’s just say that there are no de nove genes between humans and apes which there are not. That would not prove that all mutations are random which is what we’re arguing about.

Well Joe, let’s just say there is something we can not observe making the occaisional intelligently directed tweak to DNA using forces we can not measure, but which neccesarily violate the known Laws of Physics. How does that add anything to our understanding of the world around us? Come back once you can tell us something more specific about its motives and methods.

I see that Dave Lovell is asking a question very similar to the ones I am asking, so I’ve included it here.

https://me.yahoo.com/a/UIFqpY46nexU[…]agSA6W#dd2ba said:

diogeneslamp0 said: In Perfeito et al. 2002, in E. coli, they saw 10%. So eat shit, want-wit, that’s EXPERIMENTAL.

The dumb fuck who wrote that comment has ~130 more novel random point mutations than his parents; twice that many relative to his grandparents; etc. If “the vast majority of mutations are deleterious” as he thinks, he’d have 65+ MORE deleterious mutations than his parents; twice that relative to his grandparents; etc. All of his organs would be dead, instead of just his brain.

I don’t care much for your personal and disgusting attacks directed at me. There is a wealth of evidence that virtually all mutations are deleterious

No there isn’t– we’ve heard creationists say this 1000 times, but they never cite experimental papers, so this is evidence of nothing but creationist dishonesty. If there were experimental evidence, you would have cited it– but you didn’t because there is no experimental evidence.

I cited Perfeito et al. Your response: crickets. I linked to Scott Buchanan’s page which cites about 10 experimental papers. Your response: crickets.

You’re a product of a creationist culture built on lying. We know that culture and its disgusting mythologies better than you do. We’ve seen your bullshit 1000 times and we know you will NEVER cite an experimental paper. NEVER. EVER.

Because you didn’t get it from published experiments, you copied and pasted from lying creationist websites. You’re not honest enough to admit that’s where you got your assertions. You’ll dissemble and lie and evade and PRETEND you got it from an experimental paper – a paper you will NEVER name. Never. Ever. Go on lying: we will expose you.

You call my insults disgusting, but your allegations about science are egregiously false, and lying is disgusting to scientists. Lying creationists have no moral standing from which to call anyone else disgusting.

Atheistoclast writes:

What evidence is there that ANY new genes were involved in the evolution of apes to humans? (Actually there is ONE, exactly one known, but it’s a very small RNA gene, not highly improbable.)

Are you crazy we are on track to discover at least 50 to 100

Who the hell are WE, Joe!? And “on track” only means that you’re anticipating results before they’ve come in. And how many of those proteins are NOT DE NOVO? I talked specifically about DE NOVO genes, not duplicates or things with close homologs. You’re comparing apples and oranges: de novo and close homologs.

The Journal of Biological Chemistry writes:

Among the approximately 23,000 genes found in human DNA, scientists currently estimate that there may be as few as 50 to 100 that have no counterparts in other species.

[http://news.wustl.edu/news/Pages/11349.aspx]

Oh. “Scientists estimate”. That count includes genes that are NOT DE NOVO. I talked specifically about DE NOVO genes. This estimate clearly includes or things with close homologs, NOT DE NOVO, as we will see below.

Joe’s source [http://news.wustl.edu/news/Pages/11349.aspx] demolishes his argument! Pathetic. Although Joe’s source speaks of an “estimate” of 50 to 100 “new” genes, it turns out that that article defines a gene as “new” when it is obviously not DE NOVO, but has close homologs in other species, including apes.

That article focuses on one gene in particular, TBC1D3, which is shared by humans and apes [hominoids]. I asked Joe for an example of a DE NOVO protein in humans and NOT in apes, and he gives me a gene that is NOT DE NOVO and IS PRESENT IN APES!!

The very name TBC is an abbreviation for Tre-2/Bub2/Cdc16 domain, and Bub2 is a yeast gene. So this domain has homologs in YEAST and is NOT DE NOVO.

I asked Joe for an example of a DE NOVO protein in humans and NOT in apes, and he gives me a gene that is NOT DE NOVO and has homologs in YEAST!!

We can start with T-urf13 in maize

That’s the breaking of preexisting genes. We are talking about building new genes not breaking preexisting ones.

Here Joe invokes the Fundamental Fraud of Intelligent Design (FFID): Joe dismisses DE NOVO, FUNCTIONAL GENES and calls them “broken” when they’re functional, because he knows their origin was natural.

But ID is sold as allowing us to infer the origin of “patterns” merely by looking at the pattern, without knowing its origin. In reality, ID really operates like this: “I’ll tell you how this gene originated… Step One: tell me how this gene originated.”

There are numerous examples of proteins evolving novel enzymatic functions, like the nylonase bug and others that degrade or consume xenobiotics.

Again, this is the breaking of preexisting genes not building new genes.

Joe, like all IDiots, can only call a gene “broken” after he’s been told it originated by natural processes. ID is sold as telling us something about how biological structures originate, but in fact it demands as INPUT, not output, knowledge of how biological structures originate, so that IDiots can shift their goal posts as needed to defraud their audience.

It’s fraud. No ID version of arglebargle– “specified complexity” or “irreducible complexity” or Behe’s definition of “blunted” genes– has ever been subjected to a double-blind test, in which the IDiots have NO prior knowledge of the origin of a sequence, and must distinguish the random ones or natural ones from the intelligently designed ones. IDiots adamantly refuse to do double blind tests. No double blind tests means ID is a fraud.

Atheistoclast writes: Genes are alternatively spliced by a consciousness and put back together.

This is definitely Atheistoclast– only he would write such tripe.

If you believe God causes gene splicing, then God kills a lot of babies, because gene splicing can be lethal. Your God kills babies every day by “intelligently designing” lethal mutations.

I’m not invoking invisible spooks like you do for everything because no invisible spook has ever been observed to produce any genetic change, of any size, ever, never.

New genes can also be produced by shuffling exons of other genes.

You’re just assuming that there is no mind that is doing the shuffling.

AGAIN: If you believe God causes exon shuffling, then God kills a lot of babies, because those genetic changes are often lethal. Your God kills babies every day by “intelligently designing” lethal mutations.

If you believe a spook causes gene splicing and exon shuffling, seen IN THE LAB!!, you might as well believe spooks cause every observable, reproducible process– spooks causes hydrogen to burn and make H20, spooks causes electricity to flow in wires, blah blah. Ug kemosabe, telegraph wire full of talking spirits. Camera photo take my soul. Ug.

I’m not invoking invisible spooks like you do for everything because no invisible spook has ever been observed to produce any genetic change, of any size, ever, never.

Gene duplication is common and has happened recently in the human race… Given that gene duplication, neo-functionalization and beneficial mutations happen everywhere we look, what mechanism do you imagine could TURN THAT OFF and magically stop it from happening?

Intelligence.

Caspar the Friendly Ghost STOPS beneficial mutations!? A ghost STOPS gene duplication!? IDiot, these are observed processes.

Atheistoclast writes:

There’s not such thing as an observed process.

And that tells us all we need to know about Joe: another science-hater. You spout bullshit– that we have observed.

Atheistoclast writes:

But because it only takes a few mutations in some existing proteins to evolve a novel function, it is NOT necessary to create a gene de novo in order to gain complexity or a beneficial mutation.

But it is necessary if you believe that NS acting on RM is responsible for all the diversity of life.

So what? De novo gene evolution has been observed. I already listed T-urf13, and Jack Szostak got a de novo RNA-binding protein from a library of random sequences [Nature. 2001 Apr 5;410(6829):715-8. Functional proteins from a random-sequence library. Keefe AD, Szostak JW] and Seelig’s lab found a de novo RNA ligase by in vitro evolution.

Your post showed you have no clue how how proteins evolve. You think they evolve by random scrambling of parts, like a tornado. No, the simultaneous random scrambling of all parts does not model evolution– it models your mental processes.

None of that is an argument.

Wrong. In your post you showed how ignorant you are by counting up the number of amino acids in a set of proteins and then saying that each one had to be mutated individually. Do you call that a measure of information? If merely counting amino acids is your measure of information, then OBSERVED processes of gene duplication created vast increases of “information” by your measure.

No ID creationist has ever written down any definition of “information” which has the three necessary properties at once: 1. found in biological systems; 2. not produced by natural processes; 3. observed to be produced by invisible spooks.

In your post your definition of information required that it be proportional to the number of amino acids, so gene duplication increases it, thus violating requirement 2.

That would not prove that all mutations are random which is what we’re arguing about.

NO. That is NOT what we are arguing about. You have no proof any spook ever produced ANY genetic changes, large or small. This is what we are arguing about: No ID creationist has ever written down any definition of “information” which has the three necessary properties at once: 1. found in biological systems; 2. not produced by natural processes; 3. observed to be produced by invisible spooks. The end.

And how many of those proteins are NOT DE NOVO? I talked specifically about DE NOVO genes, not duplicates or things with close homologs. You’re comparing apples and oranges: de novo and close homologs.

Dong-Dong Wu writes: The de novo origin of a new protein-coding gene from non-coding DNA is considered to be a very rare occurrence in genomes. Here we identify 60 new protein-coding genes that originated de novo on the human lineage since divergence from the chimpanzee. http://www.plosgenetics.org/article[…]pgen.1002379

Here Joe invokes the Fundamental Fraud of Intelligent Design (FFID): Joe dismisses DE NOVO, FUNCTIONAL GENES and calls them “broken” when they’re functional, because he knows their origin was natural.

You’re just assuming a cause is natural. You can’t even observe a cause so how do you know what is causing the cause? You also don’t even have a definition for natural. Most likely you believe that motion is natural if motion is random. You have to prove motion is random through an analysis of probability. If dna mutatations are all random then why are there so many repeat sequences in the genome? As for the T-urf13, William Dembski refutes this just fine:

The counterexample concerns the gene T-urfl3 and its protein product URF13. The two are found in the mitochondria of Texas cytoplasmic-male-sterile maize (cms-T). URF13 is a protein 113 amino acids long. It forms three membrane-spanning alpha helices and a channel in the mitochondrial membrane. The problem is that T-urfl3, the gene that encodes URF13, was produced by recombining non-protein-coding gene segments only. What’s more, most of the sequence is homologous to a nearby ribosomal RNA gene (rrn26). It therefore appears that a biologically functional 113-amino acid protein formed de novo, and thus that biological specified complexity can arise purely by natural causes after all. But let us consider this claim more closely. First off, T-urfl3 appears not to be doing Texas cytoplasmic male-sterile maize any good—its protein product URF13 renders the plant sterile and increases its susceptibility to fungal toxins. What’s more, any time one strings together a sequence of amino acids, one is likely to obtain some three-dimensional structure that includes alpha helices since these are easy to form. URF13’s function is therefore deleterious and not all that well defined. Also its form does not appear carefully adapted to its function. URF13 has 113 amino acids. It is therefore one of 20^113 possible proteins sequences of length 113. Since 20^113 is approximately 10^147, URF13’s improbability of 1 in 10^147 does not fall below the universal probability bound of 10^-150. What’s more, the minimal functional size of URF13 is 83 amino acids since the last 30 are not needed for function. Since 2083 is approximately 10107, the improbability of URF13 is now at 1 in 10107. This is still uncomfortably small, but well above the universal probability bound. We can increase this probability still further by considering the mutational stability of these 83 amino acids. Some swapping of amino acids retains function, thereby increasing the probability of proteins performing the same function as URF13. At issue is not the individual improbability of URF13 but the improbability of getting it or some homologous sequence that performs the same function It seems then that we have averted the challenge of t-URF13 to the naturalistic generation of complex specified information, though just barely. But what if we came upon a longer protein that was more specific and did its host organism some evident good? What if that protein resulted from a gene that in turn resulted from recombining portions of DNA all of which were non-protein-coding gene segments? What if any way we sliced it, the improbabilities computed turned out to be less than the universal probability bound? Would that demonstrate that CSI had been naturalistically generated? No. First off, there is no reason to think that non-protein-coding gene segments themselves are truly random—as noted above, T-urfl3, which is composed of such segments, is homologous to ribosomal RNA. So it is not as though these segments were produced by sampling an urn filled with loosely mixed nucleic acids. What’s more, it is not clear that recombination is itself truly random. All recombinations that are supposed to confirm the naturalistic generation of CSI do, after all, occur within a cellular context. The CSI—if indeed it is CSI—that we see in genes produced from recombining non-protein-coding gene segments could just be CSI that had gone underground and now has been reconstituted. Unlike computer simulations, following the information trail for actual biological systems in the wild is rarely possible and depends on contingencies that may forever lie beyond the veil of history. Nonetheless, the mathematics underlying CSI is clear—you cannot get it via chance and necessity.

But ID is sold as allowing us to infer the origin of “patterns” merely by looking at the pattern, without knowing its origin. In reality, ID really operates like this: “I’ll tell you how this gene originated… Step One: tell me how this gene originated.”

No, it’s not. Darwinism is step one: all mutations are random. ID says: show me your math. Dembski just showed you his math above, now let’s see yours. Darwinsim replies: No.

Joe, like all IDiots, can only call a gene “broken” after he’s been told it originated by natural processes. ID is sold as telling us something about how biological structures originate, but in fact it demands as INPUT, not output, knowledge of how biological structures originate, so that IDiots can shift their goal posts as needed to defraud their audience.

This is false. Darwinism asserts that DE NOVO genes arise at random. Let’s see some math.

It’s fraud. No ID version of arglebargle– “specified complexity” or “irreducible complexity” or Behe’s definition of “blunted” genes– has ever been subjected to a double-blind test, in which the IDiots have NO prior knowledge of the origin of a sequence, and must distinguish the random ones or natural ones from the intelligently designed ones. IDiots adamantly refuse to do double blind tests. No double blind tests means ID is a fraud.

This is false. Doug Axe has more than demonstrated that the odds of a functioning protein arising spontaneously is well beyond 1 in 10^-75

Atheistoclast writes: Genes are alternatively spliced by a consciousness and put back together.

This is definitely Atheistoclast– only he would write such tripe.

That is an argument from ridicule and hence a fallacy.

If you believe God causes gene splicing, then God kills a lot of babies, because gene splicing can be lethal. Your God kills babies every day by “intelligently designing” lethal mutations.

I don’t speak for atheistoclast but I subscribe to the Shapiro brand of intelligent design: organisms design themselves. God sets the limits within which mind can move matter.

New genes can also be produced by shuffling exons of other genes.

You’re just assuming that there is no mind that is doing the shuffling.

If you believe a spook causes gene splicing and exon shuffling, seen IN THE LAB!!, you might as well believe spooks cause every observable, reproducible process– spooks causes hydrogen to burn and make H20, spooks causes electricity to flow in wires, blah blah. Ug kemosabe, telegraph wire full of talking spirits. Camera photo take my soul. Ug.

You don’t understand what panpsychism is all about. Panpsychism is the belief that all matter is conscious but not all minds are able to communicate with other minds. Minds move matter within the limits determined by God. Since you’re someone who does not understand that the argumentum ad ridiculum is a fallacy I won’t waste my time trying to enlighten you. I’m not invoking invisible spooks like you do for everything because no invisible spook has ever been observed to produce any genetic change, of any size, ever, never.

Gene duplication is common and has happened recently in the human race… Given that gene duplication, neo-functionalization and beneficial mutations happen everywhere we look, what mechanism do you imagine could TURN THAT OFF and magically stop it from happening?

Intelligence.

Caspar the Friendly Ghost STOPS beneficial mutations!? A ghost STOPS gene duplication!? IDiot, these are observed processes.

Like I said, consciousness designs its own body so of course there are smart minds and dumb binds. Some minds don’t understand how to design their body effectively.

Atheistoclast writes:

There’s not such thing as an observed process.

And that tells us all we need to know about Joe: another science-hater. You spout bullshit– that we have observed.

One, this is an argument from ridicule and hence a fallacy. Two, you can’t even define science so your statement is meaningless.

Atheistoclast: You scored one in your own goal. Your post proved my point about the Fundamental Fraud of Intelligent Design (FFID). You quote Dembski, but Dembski invokes FFID.

The Fundamental Fraud of Intelligent Design is the claim that ID can tell us about how patterns originated, but Step One is always “First, tell me exactly how the pattern originated.” If the IDer knows the pattern originated from a natural process, then he shifts the goal posts and redefines his definitions of “information”, “novel gene”, “irreducible” etc. etc. and your quote from Dembski proves it.

Thus, ID claims to tell us about how patterns came about as OUTPUT, but actually they require it as INPUT!

Compare these two passages: here Dembski 2005 “sells” Intelligent Design by claiming that it can tell us how patterns came about, without prior knowledge of their origin.

Can objects, even if nothing is known about how they arose, exhibit features that reliably signal the action of an intelligent cause?

[William Dembski, “Specification: The Pattern That Signifies Intelligence”, 2005]

In the passage you cited, which I presume is from “No Free Lunch” although you did not cite it, Dembski needs to explain away the de novo origination of a new gene, T-urf13.

Step One: Tell me exactly how it originated!

Dembski wrote:

…what if we came upon a longer protein that was more specific and did its host organism some evident good? What if that protein resulted from a gene that in turn resulted from recombining portions of DNA all of which were non-protein-coding gene segments? What if any way we sliced it, the improbabilities computed turned out to be less than the universal probability bound? Would that demonstrate that CSI had been naturalistically generated? No. First off, there is no reason to think that non-protein-coding gene segments themselves are truly random—as noted above, T-urfl3, which is composed of such segments, is homologous to ribosomal RNA.

Fundamental Fraud of ID. Dembski is using his knowledge of the origin of T-urf13 as INPUT so that he can change the rules– change his probability calculations– change his method of calculating “specified complexity”! NOW you see why ID is fraud– because it REFUSES to take a double-blind test, in which the ID algorithm has NO knowledge of how patterns originated. That knowledge is necessary so the IDer can shift his goal posts, change his definitions, and reject everything produced by natural causes.

Notice how, using his knowledge of how T-urf13 originated as INPUT to his method, he now changes his probability calculation:

Dembski wrote:

So it is not as though these segments were produced by sampling an urn filled with loosely mixed nucleic acids. What’s more, it is not clear that recombination is itself truly random.

See what he did there? He’s saying he will NOT (in this case, because knows its origin) compute how T-urf13 originated with a probability equal to the random scrambling of all parts. He will NOT (in this case) set p = 1/K^L, where K is the number of kinds of “letters” and L is sequence length.

However, in every other case, Dembski DOES compute specified complexity by setting probability equal to the random scrambling of all parts, that is, p = 1/K^L. That is how Dembski computed the probabilities for the Caputo case and the flagellum in “No Free Lunch.”

ID will NEVER submit a double-blind test, in which the ID algorithm has NO knowledge of how patterns originated. That knowledge is necessary so the IDer can shift his goal posts, change his definitions, and reject everything produced by natural causes.

No double-blind test means Intelligent Design is a fraud.

You convict yourself.

Atheistoclast says:

Doug Axe has more than demonstrated that the odds of a functioning protein arising spontaneously is well beyond 1 in 10^-75

Bullshit, he asserted that many times, but it was never true. The fact that IDiots say it over and over does not make it true. Amongst other problems, Axe 2004 screened for one protein function, not all possible protein functions.

Moreover, in Jack Szostak’s experiment with random strings of amino acids, he found an RNA-binding protein in 1*10^12 sequences. They were about 80 amino acids long, so IDiot math would say each sequence had improbability 20^80. So IDiot math is off by 92 orders of magnitude. [Nature. 2001 Apr 5;410(6829):715-8. Functional proteins from a random-sequence library. Keefe AD, Szostak JW.]

You’re just assuming a cause is natural. You can’t even observe a cause so how do you know what is causing the cause?

Your assumption that invisible spooks are behind natural processes observed in the lab or in the wild– like the evolution of new complexity– means that ID is non-falsifiable (like we didn’t know that already.)

ID begins by asserting:

1. Certain kinds of ooga booga (irreducible complexity or whatever) cannot be produced by natural processes, but only by humans or invisible spooks.

Then when we observe these kinds of ooga booga (irreducible complexity or whatever) actually being produced by natural processes, then ID asserts:

2. If certain kinds of ooga booga (irreducible complexity or whatever) are observed to be produced ANYWHERE in ANY observation or ANY experiment, and a human didn’t cause it, then a spook caused it, but it was invisible.

When you combine 1 and 2, your logic is perfectly circular and can never be experimentally falsified.

We could equally well assert that observed phenomena are caused by an infinite number of invisible entities.

Water evaporation is caused by an invisible carrot. What is my proof? Wherever we see water evaporating, we know a carrot caused it, but it was invisible.

Then you demand I prove no spooks were present, when you say they’re invisible! I could as easily ask you to disprove my invisible carrot.

I asked before: why should we assume Casper the Friendly Ghost or other invisible entities are behind natural processes, like hydrogen burning or electricity running in wires. Gene duplication, point mutations, hydrogen burning etc. do not need to be directed by humans and occur with humans watching and without humans watching.

If you assume spooks are behind all chemical reactions, you’re invoking circular logic and ID is non-falsifiable.

Bullshit, he asserted that many times, but it was never true. The fact that IDiots say it over and over does not make it true.

And you’re denying it does not make it false.

Amongst other problems, Axe 2004 screened for one protein function, not all possible protein functions.

Moreover, in Jack Szostak’s experiment with random strings of amino acids, he found an RNA-binding protein in 1*10^12 sequences. They were about 80 amino acids long, so IDiot math would say each sequence had improbability 20^80. So IDiot math is off by 92 orders of magnitude. [Nature. 2001 Apr 5;410(6829):715-8. Functional proteins from a random-sequence library. Keefe AD, Szostak JW.]

Then go ahead and crunch the numbers and try to come up with the odds of the Cambrian Explosion happening.

You’re just assuming a cause is natural. You can’t even observe a cause so how do you know what is causing the cause?

Your assumption that invisible spooks are behind natural processes observed in the lab or in the wild– like the evolution of new complexity– means that ID is non-falsifiable (like we didn’t know that already.)

Number one, calling something a spook is an argumentum ad ridiculum and it demonstrates your inability to understand reason. Two, you already believe that there are invisible spooks behind “natural processes.” Is there something invisible causing your mother to move or is she just a swarm of random atoms moving around getting lucky? You already believe that there is something invisible which makes people different from just a collection of random atoms. Three, ID is falsifiable. Darwinism, among other things, is the belief that ALL mutations are random. We can falsify that statement through statistics.

ID begins by asserting:

1. Certain kinds of ooga booga (irreducible complexity or whatever) cannot be produced by natural processes, but only by humans or invisible spooks.

Then when we observe these kinds of ooga booga (irreducible complexity or whatever) actually being produced by natural processes,

This is false. You’re just assuming that randomness causes movement. You need to prove that movement is random through statistics. Since the Darwinists either do not put forth math or they put forth bogus math, they have nothing to support their assertions.

then ID asserts: 2. If certain kinds of ooga booga (irreducible complexity or whatever) are observed to be produced ANYWHERE in ANY observation or ANY experiment, and a human didn’t cause it, then a spook caused it, but it was invisible. When you combine 1 and 2, your logic is perfectly circular and can never be experimentally falsified.

You don’t understand. If you assert that movements on the roulette wheel are random then that statement would be verified if we found that all 36 slots were normally distributed. If instead the ball keeps going in one slot then the null-hypothesis is falsified. It’s the same with the genome. In order to build an organism each cell needs to become the right cell of a number different cell types at the right time. The only thing that is conscious of cell time and time is consciousness itself. Darwinism has no explanation how you one cell knows what type of cell it has to be.

We could equally well assert that observed phenomena are caused by an infinite number of invisible entities. Water evaporation is caused by an invisible carrot. What is my proof? Wherever we see water evaporating, we know a carrot caused it, but it was invisible.

This is false. There are only two types of causation: either two different particles agree to coordinate or they do not. All particle movements are caused by consciousness but not all particle movements are coordinated with other particle movements. We do not need to posit a carrot to explain the movement of particle x because a carrot is an observed effect of some other cause and effects by definition are not causes. The fact that you would even suggest something so crazy leads me to not even take you seriously as a rational agent.

Then you demand I prove no spooks were present, when you say they’re invisible! I could as easily ask you to disprove my invisible carrot. I asked before: why should we assume Casper the Friendly Ghost or other invisible entities are behind natural processes, like hydrogen burning or electricity running in wires. Gene duplication, point mutations, hydrogen burning etc. do not need to be directed by humans and occur with humans watching and without humans watching.

Because the alternative is implausible and the alternative is luck. It’s the same with your mother. It could be the case that your mother does not really exist. She could just be getting lucky all the time. She could really not speak English and she could just be a lucky poser. If we believe that then we have to destroy logic and reason. Logic and reason are founded on the belief that you know that A causes B. If you bring luck into your ontology to explain coordination and design then you have no principle way of distinguishing between coordination and luck. If you assert that luck explains coordination A but luck does not explain coordination B then you have contradicted yourself.

In this debate you have demonstrated that you do not have a pure desire for truth. You’re willing to use ridicule to pose an argument. I have asked you questions and you have refused to answer them. I asked you to present to me mathematics to prove that ALL mutations are random and you have not done that. I’m not going to waste my time with someone who is more interested in looking good than truth.

Atheistoclast: You scored one in your own goal. Your post proved my point about the Fundamental Fraud of Intelligent Design (FFID). You quote Dembski, but Dembski invokes FFID.

You’re a fraud and you’ve been exposed. You have no evidence spooks do shit.

No ID creationist has ever written down any definition of “information” which has the three necessary properties at once: 1. found in biological systems; 2. not produced by natural processes; 3. observed to be produced by invisible spooks.

In your post your definition of information required that it be proportional to the number of amino acids, so gene duplication increases it, thus violating requirement 2.

In your citation to Dembski he switched his method of computing probability, to exclude products of natural processes. That definition of information excludes biological structures as having information, violating principle 1.

No ID creationist ever wrote down an equation for any ooga booga information that has 1, 2 and 3. So there can be no inference to any biological structures created by spooks.

Did I hurt your feelings by calling your spooks spooks? You pull your hair and shriek and cry “Waah!! don’t call my spooks spooks! It’s argumentum ad riduculum and it’s a fallacy when you call my fraud a fraud!”

It’s not a fallacy to expose your fraud as fraud. You wish it was. If you had evidence your spooks do shit, it wouldn’t matter what word we use for spooks. It matters to you what we call your spooks only because you know you have ZERO evidence any spook ever made any genetic changes to anything. Not even one nucleotide. Not one nucleotide. Never. Not one. Ever.

Your understanding of statistics is infantile as well. In statistics the null hypothesis is always that X and Y are uncorrelated.

If you assert that movements on the roulette wheel are random then that statement would be verified if we found that all 36 slots were normally distributed. If instead the ball keeps going in one slot then the null-hypothesis is falsified. It’s the same with the genome.

No, the slots are not normally distributed on a roulette wheel. The null hypothesis in statistics is that X and Y are uncorrelated. If X are mutations and Y is fitness, the null hypothesis is that they’re uncorrelated.

Any fraud who says spooks made a correlation between mutation and fitness has the burden of proof ON HIM to prove a correlation exists. That’s how real statistics work. The fraud must define a TESTABLE hypothesis, define a rejection region, and tot up the probability mass function over it.

Easy to do for real scientists. NEVER been done by IDers because ID is scientific fraud.

ID will NEVER submit a double-blind test, in which the ID algorithm has NO knowledge of how patterns originated. That knowledge is necessary so the IDer can shift his goal posts, change his definitions, and reject everything produced by natural causes.

No double-blind test means Intelligent Design is a fraud.

No ID creationist has ever written down any definition of “information” which has the three necessary properties at once: 1. found in biological systems; 2. not produced by natural processes; 3. observed to be produced by invisible spooks.

Write down an equation with properties 1, 2 and 3 NOW. Not 10 comments from now. NOW.

You never will, because ID is a fraud.

This was my favorite:

If dna mutatations are all random then why are there so many repeat sequences in the genome?

It’s hard to find a more succinct example of cluelessness on multiple levels. Congratulations.

John Harshman said:

This was my favorite:

If dna mutatations are all random then why are there so many repeat sequences in the genome?

It’s hard to find a more succinct example of cluelessness on multiple levels. Congratulations.

It’s true. I too felt hat was Atheistoclast at his very dumbest. I wrote a rebuttal explaining what transposons are and… deleted it.

They want to change the subject because we’ve got them nailed. I didn’t want to lose focus.

/delurk

Masked Panda: If dna mutatations are all random then why are there so many repeat sequences in the genome? John Harshman: It’s hard to find a more succinct example of cluelessness on multiple levels. Congratulations.

For the benifit of lurkers (like me) its good to elaborate why this statement is clueless.

In statistics, when one variable is described as random, its always a desicrption of its corelation to some other variable. If two variables change in lockstep to each other, they are strongly corelated. The opposite relation, where there is no effect of change in one variable on the other the two are said to be random in respect to each other.

When biologist say that mutation is random it is with respect to fitness i.e. mutations happen weather or not they actually result in the organsim having more or fewer children and grand children.

The actual physical process of replication(which includes mutation) is very non-random with respect to DNA sequence. Indeed, if the final sequence after mutation was random with respect to the sequence being replicated, inheritance would be impossible.

This is a very basic mistake which brings into question if the poster understands any of the papers he keeps quoting.

/relurk

One type of mutation is duplication of existing sequences. Point mutations (changing of individual locations) are more common, but duplications happen sometimes, and can cause repeats of stuff.

(Somebody who knows more than me can elaborate on that.)

https://me.yahoo.com/a/iS9p19oQ3c6V[…]01EUrz#3f071 said:

Darwinism has no explanation how you [sic] one cell knows what type of cell it has to be.

First, I will assume that by “Darwinism” you mean, “The knowledge that Charles Darwin had about how species evolve.” If that’s what you mean, they yes, Darwin did not know how cells differentiate.

But fortunately for Science, and Humanity in general, people have learned quite a lot about how the world works in the last 150 years. In fact, we’ve learned quite a lot about how cells work, and in particular, how they differentiate. We know quite a bit about how one stem cell differentiates into many different cells, what the difference is between different cells types, and how those cells end up in just the right spot in a developing organism. It’s called the study of Evolutionary Development, or Evo-Devo for short. It’s PZ Myers’ area of specialty, and he posts here at Panda’s on an irregular basis. Perhaps you’ve missed his posts? It’s all about chemical gradients, and the intersection of different types of chemical gradients. And we know what causes the chemical gradients too.

So, unlike Darwin, today modern science has a very precise and detailed explanation for how “one cell knows what type of cell it has to be.” It really isn’t a mystery at all, any more. In fact, Evo-Devo can be used to make predictions about how other cells in other organisms will respond to certain stimuli. And when scientists make those predictions, and do experiments to confirm or deny those predictions, guess what? More often than not, those predictions are often correct. And when the predictions turn out to be wrong, we either learn more about how the world works, or we at least learn new questions to ask. It’s how science works.

On the other hand, perhaps your explanation for how a fertilized egg develops into a mature organism requires supernatural conscience intervention at every cell division? Is that perhaps what you’re saying? Are you saying that “Darwin” didn’t know how “one cell knows what type of cell it has to be”, or are you saying that it is fundamentally unknowable because of that supernatural cause?

About this Entry

This page contains a single entry by M. Wilson Sayres published on July 16, 2013 9:07 AM.

The lying liars of the Disco ‘Tute was the previous entry in this blog.

Orthonevra nitida is the next entry in this blog.

Find recent content on the main index or look in the archives to find all content.

Categories

Archives

Author Archives

Powered by Movable Type 4.38

Site Meter