Random mutations

[Phred]

And modern fertility rate is relevant to this topic how?

Not all deleterious mutations are fatal. Actually, most are not.

Because creationists don't use relevant data... just data.

 

[Zaius137]

Have you ever heard of bacteria resisting to antibiotics? How do you think bacteria can do that?

While I agree the peppered moth example is controversial, there are many others that are not.

Yes bacteria by damaging there envelope can give resistance to specific antibiotics but overall fitness has never been increased. If you know of a study concerning fitness to improve overall? Please post it now, I am really trying to locate information for further study on this topic.

Also the molecular mechanism as “Mark Kennedy (poster)” mentioned does not exist for evolution. There are a couple of articles I have read that claim a mechanism but they are too complicated and must have evolved themselves so saying they are the mechanism is an equivocation.

 

[Zaius137]

Because creationists don't use relevant data... just data.

Well phred your right not all mutations are fatal and that is why they are excluded statistically from the deleterious mutations.

 

[Loudmouth]

Well phred your right not all mutations are fatal and that is why they are excluded statistically from the deleterious mutations.

No they aren't. They are included. U measures the non-conservative changes in amino acid sequence, not the fatal mutation rate.

 

[Loudmouth]

Yes bacteria by damaging there envelope can give resistance to specific antibiotics but overall fitness has never been increased.

They can also have mutations in their gyrase gene that has no effect on gyrase activity but it does stop binding of antibiotics. This is an overall increase in fitness in environments containing gyrase specific antibiotics (I think spectinomycin is an example).

Nonetheless, bacteria with these mutations outcompete bacteria without these mutations. This means that they are fitter overall.

Also the molecular mechanism as “Mark Kennedy (poster)” mentioned does not exist for evolution. There are a couple of articles I have read that claim a mechanism but they are too complicated and must have evolved themselves so saying they are the mechanism is an equivocation.

You mean changes in gene regulation in new environments expressing accumulated mutations in previously downregulated genes? I really don't see how this helps your argument.

 

[Zaius137]

phred...

“Eero Antero Mäntyranta - born 20 November 1937. He's passed on his genes already. So that's not an issue. He's 74 now. How old does he have to get before you accept that it's a beneficial mutation?

From The Economist: For instance, some people have innate genetic mutations which give them exactly the same sort of edge. Eero Mantyranta, a Finn, was a double Olympic champion in cross-country skiing. His body has a mutation that causes it to produce far more of a hormone called EPO than a normal person would. This hormone stimulates the production of red blood cells. A synthetic version of it is the (banned) drug of choice for endurance athletes.”

I am not saying that this gene variance does not exist. But what is to say that this gene was not already in the human genome but just concentrated in his genetic line. No empirical evidence exists to say otherwise. Adaptation is also central to a creationist’s explanation but not any case of supposed fitness gains by a single mutation.

 

[sfs]

Get a grip phred....

“Our estimate of U = 3 is slightly higher than another recent estimate in humans based on a similar approach (U = 1.6; EYRE-WALKER and KEIGHTLEY 1999 ). The difference between these estimates of U is due in part to the different estimates of constraint (1 - ). Eyre-Walker and Keightley's estimate of 1 - Ka/Ks = 0.38 is considerably lower than the value of 0.73 obtained by OHTA 1995 for a different set of genes. The genes analyzed by EYRE-WALKER and KEIGHTLEY 1999 appear to have an unusually low level of constraint and may not be representative of the genome as a whole. Our estimate of U = 3 is considerably higher than recent estimates from mutation accumulation experiments in Escherichia coli (U = 0.0002; KIBOTA and LYNCH 1996 ), Caenorhabditis elegans (U = 0.005; KEIGHTLEY and CABALLERO 1997 ), and Drosophila melanogaster (U = 0.02–1, MUKAIet al. 1972 ; KEIGHTLEY 1996 ; FRYet al. 1999 ). However, mutations of small effect may go undetected in these experiments. In general, organisms with larger genomes appear to have a greater number of deleterious mutations, although it does not appear that the deleterious mutation rate is constant per base pair across these organisms.”

These are eaileier estamats of th “U”. lets look at U= 3…

B=2e^3~ 40 births per female…
does this sound reasonable. Now look at the smallest U=1.6…
B=2e^1.6~ 10 births per female… well here are the actual birth rates today and you can see none of them approach an average of 10…

It's been explained to you repeatedly that that many births are only required under several conditions:
1) None of the deleterious mutations eliminate affected gametes or zygotes.
2) There is no synergistic epistasis between deleterious alleles.
3) All selection is hard.

(1) and (3) are known to be wrong, and (2) is very likely wrong as well. Therefore the number you are quoting is not the required number of offspring. So why do you keep quoting it?

 

[sfs]

Well phred your right not all mutations are fatal and that is why they are excluded statistically from the deleterious mutations.

Most deleterious mutations are not fatal.

 

[CabVet]

Copying and pasting to make it perfectly clear once more:

No they aren't. They are included. U measures the non-conservative changes in amino acid sequence, not the fatal mutation rate.

So, your other claim is that antibiotic resistance is not an example of overall improved fitness. 50 years ago an antibiotic dose would kill almost every bacteria on someone's body (keyword almost). Today, [FONT=verdana, geneva, arial, helvetica]about 70 percent of the bacteria that cause infections in hospitals are resistant to at least one of the drugs most commonly used for treatment. Some organisms are resistant to all approved antibiotics and can only be treated with experimental and potentially toxic drugs. [/FONT][FONT=verdana, geneva, arial, helvetica] Wound infections, gonorrhea, tuberculosis, pneumonia, septicemia and childhood ear infections are just a few of the diseases that have become hard to treat with antibiotics.

The biological definition of fitness is: [/FONT]The extent to which an organism is adapted to or able to produce offspring in a particular environment.
[FONT=verdana, geneva, arial, helvetica]
So, the bacteria's environment changed with the introduction of antibiotics 50 years ago. Today they survive much better in an environment full of antibiotics than they did back when treatments started. Are you saying this is not improvement in overall fitness?
[/FONT]

 

[Loudmouth]

I am not saying that this gene variance does not exist. But what is to say that this gene was not already in the human genome but just concentrated in his genetic line. No empirical evidence exists to say otherwise. Adaptation is also central to a creationist’s explanation but not any case of supposed fitness gains by a single mutation.

So all of those differences between the human and chimp genomes do not benefit humans in any way?

 

[Zaius137]

(phred)…

Adaptation is real… speciation by adaptation is not. A moth never changes to a butterfly and monkey hominid can never change into humans (U-paradox). Anatomically a species stays a species this is observed to be true for retroviruses to whales.


So what is going on here?

Well, the best way to put it is that what we are seeing is the scientific process at its best. Majerus and other ecologists have carefully examined the details of Kettlewell's work and found them to be lacking. As Majerus explains, to be absolutely certain of exactly how natural selection produced the rise and fall of the carbonaria form, we need better experiments to show that birds (in a natural environment) really do respond to camouflage in the ways we have presumed, that the primary reason the dark moths did better in polluted areas was because of camouflage (and not other factors like behavior), and that migration rates of moths from the surrounding countryside are not so great that they overwhelm the influence of selection in local regions by birds. Until these studies are done, the peppered moth story will be incomplete. Not wrong, but incomplete.

 

[Zaius137]

(sfs)

Good to see you again… I see your still trying to invoke a reprieve from reality.
Did you get to look at any new research about silent mutations? Maybe the Scientific American article?

It's been explained to you repeatedly that that many births are only required under several conditions:
1) None of the deleterious mutations eliminate affected gametes or zygotes.
2) There is no synergistic epistasis between deleterious alleles.
3) All selection is hard.

(1) and (3) are known to be wrong, and (2) is very likely wrong as well. Therefore the number you are quoting is not the required number of offspring. So why do you keep quoting it?

You keep thinking I came up with this calculation… I did not. This is simply the same calculations evolutionists use to calculate birth rates. You repeatedly argue against scientists that came up with the birth rate paradox.

“The high deleterious mutation rate in humans presents a paradox. If mutations interact multiplicatively, the genetic load associated with such a high U would be intolerable in species with a low rate of reproduction (MULLER 1950 http://www.genetics.org/content/156/1/297.full#R45#R45; WALLACE 1981 http://www.genetics.org/content/156/1/297.full#R46#R46; CROW 1993 http://www.genetics.org/content/156/1/297.full#R47#R47; KONDRASHOV 1995 http://www.genetics.org/content/156/1/297.full#R48#R48; EYRE-WALKER and KEIGHTLEY 1999 http://www.genetics.org/content/156/1/297.full#R16#R16). The reduction in fitness (i.e., the genetic load) due to deleterious mutations with multiplicative effects is given by 1 - e-U (KIMURA and MORUYAMA 1966 http://www.genetics.org/content/156/1/297.full#R49#R49). For U = 3, the average fitness is reduced to 0.05, or put differently, each female would need to produce 40 offspring for 2 to survive and maintain the population at constant size.”

http://www.genetics.org/content/156/1/297.full

Your argument is with Nachman…

 

[CabVet]

Adaptation is real… speciation by adaptation is not. A moth never changes to a butterfly and monkey hominid can never change into humans (U-paradox). Anatomically a species stays a species this is observed to be true for retroviruses to whales.

Wow, a whole new discussion, now adaptation is real... Even with such an incomplete fossil record we can hypothesize, with very high confidence, that species do change.

 

[Phred]

Adaptation is real… speciation by adaptation is not. A moth never changes to a butterfly and monkey hominid can never change into humans (U-paradox). Anatomically a species stays a species this is observed to be true for retroviruses to whales.

Strawman Zaius. Moths don't change to Butterflies and nobody ever claimed that they did.

On the other hand, hominids of some sort did indeed change into humans. What never happened is we never had people just suddenly, magically appear on the planet. No species just "poofed" into existence. Your U-paradox has been explained and dealt with. I believe you just don't get the answers so... I have to just dismiss your constant use of the item.

Anatomically a species stays a species. This is false. However, it's also slightly true. In terms of immediate time parents never give birth to children they don't recognize as their own. But take say, 10,000 generations and have that 10K Great Grandmother look at her 10K great grandchild... would someone from her generation be able to breed with someone 10,000 generations later? What about 100,000 generations? We see speciation where part of a population can no longer breed with another part. This is observed FACT. If this can happen then any further changes in one group no longer can be transferred back to the other group. So they can only grow further and further apart.

What is your magic wall that stops them from growing anatomically different? What invisible magic thing that we don't know about stops species from becoming different from other species? You make claims and you throw them out. But in the end... in the end there is only one answer.

You're wrong.

 

[sfs]

(sfs)

It's been explained to you repeatedly that that many births are only required under several conditions:
1) None of the deleterious mutations eliminate affected gametes or zygotes.
2) There is no synergistic epistasis between deleterious alleles.
3) All selection is hard.

(1) and (3) are known to be wrong, and (2) is very likely wrong as well. Therefore the number you are quoting is not the required number of offspring. So why do you keep quoting it?

You keep thinking I came up with this calculation… I did not. This is simply the same calculations evolutionists use to calculate birth rates.

And the same scientists then go on to say why the calculation isn't right -- in the same papers you're quoting. Which have been quoted back to you, even in this thread. So it's simply not true that biologists actually think this is the genetic load imposed by this number of deleterious mutations.

You repeatedly argue against scientists that came up with the birth rate paradox.

“The high deleterious mutation rate in humans presents a paradox. If mutations interact multiplicatively, the genetic load associated with such a high U would be intolerable in species with a low rate of reproduction (MULLER 1950 ; WALLACE 1981 ; CROW 1993 ; KONDRASHOV 1995 ; EYRE-WALKER and KEIGHTLEY 1999 ). The reduction in fitness (i.e., the genetic load) due to deleterious mutations with multiplicative effects is given by 1 - e-U (KIMURA and MORUYAMA 1966 ). For U = 3, the average fitness is reduced to 0.05, or put differently, each female would need to produce 40 offspring for 2 to survive and maintain the population at constant size.”

http://www.genetics.org/content/156/1/297.full

Your argument is with Nachman…

You mean the Nachman who then wrote this?

This assumes that all mortality is due to selection and so the actual number of offspring required to maintain a constant population size is probably higher. The problem can be mitigated somewhat by soft selection (WALLACE 1991 ) or by selection early in development (e.g., in utero). However, many mutations are unconditionally deleterious and it is improbable that the reproductive potential on average for human females can approach 40 zygotes. This problem can be overcome if most deleterious mutations exhibit synergistic epistasis; that is, if each additional mutation leads to a larger decrease in relative fitness (KONDRASHOV 1995 ; CROW 1997 ; EYRE-WALKER and KEIGHTLEY 1999 ). In the extreme, this gives rise to truncation selection in which all individuals carrying more than a threshold number of mutations are eliminated from the population. While extreme truncation selection seems unrealistic, the results presented here indicate that some form of positive epistasis among deleterious mutations is likely.

The scientist you're quoting doesn't think this is likely to actually be a problem. So no, it's not the scientists I'm arguing with, it's you.

So I'll ask you again: why do you keep quoting this calculation? Does your brain turn off when you read that paragraph? Do you not understand what it means? Do you think we don't know about it? What's the deal?

 

[CabVet]

(sfs)

Good to see you again… I see your still trying to invoke a reprieve from reality.
Did you get to look at any new research about silent mutations? Maybe the Scientific American article?


You keep thinking I came up with this calculation… I did not. This is simply the same calculations evolutionists use to calculate birth rates. You repeatedly argue against scientists that came up with the birth rate paradox.

“The high deleterious mutation rate in humans presents a paradox. If mutations interact multiplicatively, the genetic load associated with such a high U would be intolerable in species with a low rate of reproduction (MULLER 1950 ; WALLACE 1981 ; CROW 1993 ; KONDRASHOV 1995 ; EYRE-WALKER and KEIGHTLEY 1999 ). The reduction in fitness (i.e., the genetic load) due to deleterious mutations with multiplicative effects is given by 1 - e-U (KIMURA and MORUYAMA 1966 ). For U = 3, the average fitness is reduced to 0.05, or put differently, each female would need to produce 40 offspring for 2 to survive and maintain the population at constant size.”

http://www.genetics.org/content/156/1/297.full

Your argument is with Nachman…

Cherry picking again? I think somebody already pasted this quote here, but I will do it again (and state that I see you are still trying to invoke a reprieve from reality.

Here is how the very article that you quote continues after the word "size" where you finish your quote:

"This assumes that all mortality is due to selection and so the actual number of offspring required to maintain a constant population size is probably higher. The problem can be mitigated somewhat by soft selection (WALLACE 1991 ) or by selection early in development (e.g., in utero). However, many mutations are unconditionally deleterious and it is improbable that the reproductive potential on average for human females can approach 40 zygotes. This problem can be overcome if most deleterious mutations exhibit synergistic epistasis; that is, if each additional mutation leads to a larger decrease in relative fitness (KONDRASHOV 1995 ; CROW 1997 ; EYRE-WALKER and KEIGHTLEY 1999 ). In the extreme, this gives rise to truncation selection in which all individuals carrying more than a threshold number of mutations are eliminated from the population. While extreme truncation selection seems unrealistic, the results presented here indicate that some form of positive epistasis among deleterious mutations is likely."

 

[Split Rock]

Mutations are always genetic damage.[/FONT][/SIZE]

What does this even mean?

 

[Zaius137]

Death is the champion of evolution but you would reduce it. An evolutionist can not have his cake and eat it too.

"This assumes that all mortality is due to selection and so the actual number of offspring required to maintain a constant population size is probably higher. The problem can be mitigated somewhat by soft selection (WALLACE 1991 http://www.genetics.org/content/156/1/297.full#R50) or by selection early in development (e.g., in utero). However, many mutations are unconditionally deleterious and it is improbable that the reproductive potential on average for human females can approach 40 zygotes. This problem can be overcome if most deleterious mutations exhibit synergistic epistasis; that is, if each additional mutation leads to a larger decrease in relative fitness (KONDRASHOV 1995 http://www.genetics.org/content/156/1/297.full#R48; CROW 1997 http://www.genetics.org/content/156/1/297.full#R51; EYRE-WALKER and KEIGHTLEY 1999 http://www.genetics.org/content/156/1/297.full#R16). In the extreme, this gives rise to truncation selection in which all individuals carrying more than a threshold number of mutations are eliminated from the population. While extreme truncation selection seems unrealistic, the results presented here indicate that some form of positive epistasis among deleterious mutations is likely."

The problem is that this is just hand waiving and those things like synergistic epistasis is not widely observed in nature but may be very rare. There has never been any research done with synergistic epistasis on apes or humans so that the science can not support such a suggestion. Science is observable and reproducible so bring up wild hypotheses if you want but it would just be for curiosity sake.

Death is the champion of evolution but you would reduce it. If you can think critically and scientifically such reduction in deaths defeat the entire premise of evaluative adaptation. An evolutionist can not have his cake and eat it too.

 

[CabVet]

The problem is that this is just hand waiving

No, the problem is that the part of the paper that you agree with is treated by you as evidence, and the part that you don't agree with is considered hand waving. On the very same paper. The evidence they have for the first part of the paragraph is about the same as the second, and epistasis is not the only explanation they give for explaining their data.

 

[Zaius137]

(sfs)…

“And the same scientists then go on to say why the calculation isn't right -- in the same papers you're quoting. Which have been quoted back to you, even in this thread. So it's simply not true that biologists actually think this is the genetic load imposed by this number of deleterious mutations.”

The problem is that the calculation is right but the science is not pointing to common decent. Some scientists not just creationist object to such hand waiving and recognize that such a practice has no place in the science.

“Sanford vigorously objected to the hand-waving in Nachman’s paper and Nachman’s appeals to “synergistic epistasis” to kluge away the problems. “Synergistic epistasis” was essentially a phrase to cover up a serious problem [for example, the Darwinists concocted "abiogenesis" and compartmentalized away a major problem for their theory]. There may be isolated examples of “Synergistic epistasis”, but as a generalized principle and cure-all for the U-paradox, Sanford is highly skeptical.”


http://www.uncommondescent.com/intelligent-design/other-problems-for-human-evolution-nachmans-u-paradox/

Mutation is not the savior of evolution but is the downfall of it.