Darwin re-visited

[Turtle]

Now I think you are being absurd. You are suggesting that there is some "magical" mechanism that reduces the probability of 3 enzyme systems from 1 in 10^3000 to something reasonable, but (oddly) can't identify exactly what that is.

 

When I take one of several obvious possibilities:

 

1) this is not just much-less-than-random: (your argument)

2) it is likely, you call it absurd.

 

How much more absurd is mine that yours? Or even more critically, why would you rule out mine with evidence?

 

No; I'm not suggesting that. What I am saying is that probability plays no role here in how things happened or can happen in genetics, so when you introduce it as an argument (whether a premise or a conclusion) it is invalid, i.e. a mistake in logic. The reductio ad absurdum debate tactic, whether you know of it or not, is further amplified in your writing when you add capitals, or quotes, or big(ger) numbers as if it makes your argument better supported.

 

If you continue to use the tactic, I'll continue to call it out. :)

[Biochemist]

No; I'm not suggesting that. What I am saying is that probability plays no role here in how things happened or can happen in genetics,...

What?????? No role??????

 

What is a mutation???????? How likely is any individual mutation???

[Galapagos]

What?????? No role??????

 

What is a mutation???????? How likely is any individual mutation???

 

Mutation Rates

 

:)

[Turtle]

What?????? No role??????

 

What is a mutation???????? How likely is any individual mutation???

 

It doesn't matter how likely it is. The simple fact is, that it is, and it is what scientists have defined it as. A mutation by any other name....

[Galapagos]

Prepare to witness the impossible!!! :)

 

 

Copley, S. D. (2000). “Evolution of a metabolic pathway for degradation of a toxic xenobiotic: the patchwork approach.” Trends Biochem Sci 25(6): 261-265. PubMed

 

Harding, M. M., Anderberg, P. I. and Haymet, A. D. (2003). “‘Antifreeze’ glycoproteins from polar fish.” Eur J Biochem 270(7): 1381-1392. PubMed

 

Johnson, G. R., Jain, R. K. and Spain, J. C. (2002). “Origins of the 2,4-dinitrotoluene pathway.” J Bacteriol 184(15): 4219-4232. PubMed

 

Long, M., Betran, E., Thornton, K. and Wang, W. (2003). “The origin of new genes: glimpses from the young and old.” Nat Rev Genet 4(11): 865-875. PubMed

 

Nurminsky, D., Aguiar, D. D., Bustamante, C. D. and Hartl, D. L. (2001). “Chromosomal effects of rapid gene evolution in Drosophila melanogaster.” Science 291(5501): 128-130. PubMed

 

Patthy, L. (2003). “Modular assembly of genes and the evolution of new functions.” Genetica 118(2-3): 217-231. PubMed

 

Prijambada I. D., Negoro S., Yomo T., Urabe I. (1995). “Emergence of nylon oligomer degradation enzymes in Pseudomonas aeruginosa PAO through experimental evolution.” Appl Environ Microbiol. 61(5):2020-2. PubMed

 

Ranz, J. M., Ponce, A. R., Hartl, D. L. and Nurminsky, D. (2003). “Origin and evolution of a new gene expressed in the Drosophila sperm axoneme.” Genetica 118(2-3): 233-244. PubMed

 

Seffernick, J. L. and Wackett, L. P. (2001). “Rapid evolution of bacterial catabolic enzymes: a case study with atrazine chlorohydrolase.” Biochemistry 40(43): 12747-12753. PubMed

 

Source: The Panda's Thumb: Meyer's Hopeless Monster

[Galapagos]

Post # 463 was my first material post here.

 

Your calculations are nonsense. I now quote from John Wilkins' page on abiogenesis from TO:

Lies, Damned Lies, Statistics, and Probability of Abiogenesis Calculations

 

Every so often, someone comes up with the statement "the formation of any enzyme by chance is nearly impossible, therefore abiogenesis is impossible". Often they cite an impressive looking calculation from the astrophysicist Fred Hoyle, or trot out something called "Borel's Law" to prove that life is statistically impossible. These people, including Fred, have committed one or more of the following errors.

 

Problems with the creationists' "it's so improbable" calculations

 

1) They calculate the probability of the formation of a "modern" protein, or even a complete bacterium with all "modern" proteins, by random events. This is not the abiogenesis theory at all.

 

2) They assume that there is a fixed number of proteins, with fixed sequences for each protein, that are required for life.

 

3) They calculate the probability of sequential trials, rather than simultaneous trials.

 

4) They misunderstand what is meant by a probability calculation.

 

5) They seriously underestimate the number of functional enzymes/ribozymes present in a group of random sequences.

 

I will try and walk people through these various errors, and show why it is not possible to do a "probability of abiogenesis" calculation in any meaningful way.

 

You didn't address any of these problems with your model before.

Wilkins continues:

A primordial protoplasmic globule

 

So the calculation goes that the probability of forming a given 300 amino acid long protein (say an enzyme like carboxypeptidase) randomly is (1/20)300 or 1 chance in 2.04 x 10390, which is astoundingly, mind-beggaringly improbable. This is then cranked up by adding on the probabilities of generating 400 or so similar enzymes until a figure is reached that is so huge that merely contemplating it causes your brain to dribble out your ears. This gives the impression that the formation of even the smallest organism seems totally impossible. However, this is completely incorrect.

 

Compare this to your calculation:

To get a functional protein by mutation: you would need at least 200 specific amino acids in specific sequence out of 300 in the protein (it is actually more like 260 on average, but I am making it simpler). This would be randomly 1 in 20^200, or about 1 in 10^260. Heck. To be conservative, let's make it a couple of trillion trillion trillion trillion times more likely, and make it 1 in 10^200.

 

Wilkins continues:

Firstly, the formation of biological polymers from monomers is a function of the laws of chemistry and biochemistry, and these are decidedly not random.

 

Secondly, the entire premise is incorrect to start off with, because in modern abiogenesis theories the first "living things" would be much simpler, not even a protobacteria, or a preprotobacteria (what Oparin called a protobiont [8] and Woese calls a progenote [4]), but one or more simple molecules probably not more than 30-40 subunits long. These simple molecules then slowly evolved into more cooperative self-replicating systems, then finally into simple organisms [2, 5, 10, 15, 28]. An illustration comparing a hypothetical protobiont and a modern bacteria is given below.

 

Modern enyzyme systems did not spring into existence. Nobody is claiming this except for creationists:

 

This is as much of his paper I am going to directly quote here. If you really want to, you can address each of his points head on(I mean with scientific citation and a full response to it, do not just quote his five points above and spit out some more unsupported nonsense). If you want to discuss it further with him personally, I'm sure he'd love to hear from an ID advocate over on his blog(linked above).

[Biochemist]

Mutation Rates

Thanks, Gala. That attachment is a nice little monograph.

 

I assume you recognize that I was befuddled by T's assertion that genetics had nothing to to with probability.

 

I should also mention that the mutation rate discussion in your attachment supports my view that the vast majority of genomic changes should be spontaneous, rather than induced. The issue (as alluded to in your attachment) is that some genomic changes are much more likely than others (referred to as hot spot and cold spots).

 

I think these sorts of discussion would seem less biased to me if we referred to "genomic changes" as just that rather than "mutations". The higher the likelihood of a particular genomic change, the less applicable the notion of "mutation" applies.

 

"Mutation" certainly applies (for example) when we hit DNA with UV. But where spontaneous genomic change occurs at a fixed rate in a random population, we should not assume it is a mutation. It could well be a propensity.

[Galapagos]

Thanks, Gala. That attachment is a nice little monograph.

 

I assume you recognize that I was befuddled by T's assertion that genetics had nothing to to with probability.

 

I should also mention that the mutation rate discussion in your attachment supports my view that the vast majority of genomic changes should be spontaneous, rather than induced. The issue (as alluded to in your attachment) is that some genomic changes are much more likely than others (referred to as hot spot and cold spots).

 

I think these sorts of discussion would seem less biased to me if we referred to "genomic changes" as just that rather than "mutations". The higher the likelihood of a particular genomic change, the less applicable the notion of "mutation" applies.

 

"Mutation" certainly applies (for example) when we hit DNA with UV. But where spontaneous genomic change occurs at a fixed rate in a random population, we should not assume it is a mutation. It could well be a propensity.

 

No, I think that page shows you have no idea what you are talking about with your assertions and calculations(I mean beyond the fact that you are claiming something to be impossible that occurs regularly).

 

There are many kinds of mutations:

Mutation - Wikipedia, the free encyclopedia

 

See the section on causes of mutation:

Mutation - Causes - Wikipedia, the free encyclopedia

 

The burden of proof is on you if you want to rewrite the biology textbooks. What is wrong with any of the above on the wiki page(one issue at a time, be specific)?

[Biochemist]

Your calculations are nonsense. ...You didn't address any of these problems with your model before.

Really interesting. Given that I did not discuss abiogenesis at all, or that i did not make any of the above mistakes, it is odd that you would include it. This is also that vague "oh those guys underestimate..." argument, and yet there is no counterpoint that is quantitative. The author gives the point that many protein sequences are viable, not just a specific one, and "we" underestimate that. But that number is actually reasonably small compard to the problem. If we assume that a 100 billion different species each have 100,000 uniquely different proteins (which pretty high, given the acceptance of common descent) that only gives us 10^16 total unique proteins. This barely scratches the surface of the probabilities, when we are discussing likelihoods on the order of 1 in 10^1000. Nice to get down to 1 in 10^984, but I don't feel a lot better.

Modern enyzyme systems did not spring into existence.

Never said they did. In fact, i started my analysis assuming that DNA and the related replication machinery was already in place. The largest problems occur once the lysosomes arrive. These little machines are highly effective at eradicating cytoplasmic protiens that are foreign. The moment that the evolutionary tree gave lysosomes to eukaryotes, it significantly cranked up the inhibitor to expressing a genomic change unless it was recognized as non-foreign by the lysosomes.

If you want to discuss it further with him personally, I'm sure he'd love to hear from an ID advocate over on his blog(linked above).

I wish you guys would get off this horse.

 

Maybe we should discuss a narrower problem: How does any "mutation" that involves more than a single protein get past a lysosome?

[Biochemist]

What is wrong with any of the above on the wiki page(one issue at a time, be specific)?

Nothing, but it might help describe (what might be) a semantic problem I am having.

 

In biology, mutations are changes to the nucleotide sequence of the genetic material of an organism. Mutations can be caused by copying errors in the genetic material during cell division, by exposure to ultraviolet or ionizing radiation, chemical mutagens, or viruses, or can be induced by the organism, itself, by cellular processes such as hypermutation. In multicellular organisms with dedicated reproductive cells, mutations can be subdivided into germ line mutations, which can be passed on to descendants through the reproductive cells, and somatic mutations, which involve cells outside the dedicated reproductive group and which are not usually transmitted to descendants.

 

In this definition, any change to a nucleotide sequence is a mutation. By this definition, all changes to species are due to mutation.

 

You have defined away the problem, not solved it.

 

My suggestion is that some genomic changes (e.g., UV light damage to DNA) truly are mutations. Other genomic changes that are highly likely based on the extant state of the genome should not be called mutations. They a code-based changes.

[Turtle]

.. If we assume that a 100 billion different species each have 100,000 uniquely different proteins (which pretty high, given the acceptance of common descent) that only gives us 10^16 total unique proteins. This barely scratches the surface of the probabilities, when we are discussing likelihoods on the order of 1 in 10^1000. Nice to get down to 1 in 10^984, but I don't feel a lot better. Never said they did. In fact, i started my analysis assuming that DNA and the related replication machinery was already in place.

...

Maybe we should discuss a narrower problem: How does any "mutation" that involves more than a single protein get past a lysosome?

 

No; we are not changing the topic yet again. Your assumptions, your "pretty highs", your "barely", your yada, yada, yada, probability ad nauseum is invalid. Period.

[Biochemist]

No; we are not changing the topic yet again. Your assumptions, your "pretty highs", your "barely", your yada, yada, yada, probability ad nauseum is invalid. Period.

This is a narrower slice of the same problem. Since you seem to want to accept by faith that this "just happened somehow", let's focus on the lysosome problem.

 

Bio

[Galapagos]

Your claims about mutations are untrue and misleading:

Evolutionary Genetics - Mutation - Learn At Scitable

 

Genetic Mutation

 

By: Dr. Laurence Loewe (School of Biological Sciences, University of Edinburgh, Scotland, UK.) © 2008 Nature Education

Citation: Loewe, L. Genetic mutation. Nature Education 1(1), (2008)

 

Are Mutations Random?

 

The statement that mutations are random is both profoundly true and profoundly untrue at the same time. The true aspect of this statement stems from the fact that, to the best of our knowledge, the consequences of a mutation have no influence whatsoever on the probability that this mutation will or will not occur. In other words, mutations occur randomly with respect to whether their effects are useful. Thus, beneficial DNA changes do not happen more often simply because an organism could benefit from them. Moreover, even if an organism has acquired a beneficial mutation during its lifetime, the corresponding information will not flow back into the DNA in the organism's germline. This is a fundamental insight that Jean-Baptiste Lamarck got wrong and Charles Darwin got right.

 

However, the idea that mutations are random can be regarded as untrue if one considers the fact that not all types of mutations occur with equal probability. Rather, some occur more frequently than others because they are favored by low-level biochemical reactions. These reactions are also the main reason why mutations are an inescapable property of any system that is capable of reproduction in the real world. Mutation rates are usually very low, and biological systems go to extraordinary lengths to keep them as low as possible, mostly because many mutational effects are harmful. Nonetheless, mutation rates never reach zero, even despite both low-level protective mechanisms, like DNA repair or proofreading during DNA replication, and high-level mechanisms, like melanin deposition in skin cells to reduce radiation damage. Beyond a certain point, avoiding mutation simply becomes too costly to cells. Thus, mutation will always be present as a powerful force in evolution.

Read the whole thing, I have only quoted a small portion.

 

And here, direct estimation of mutation rates:

PLoS Biology - Direct Estimation of the Mitochondrial DNA Mutation Rate in Drosophila melanogaster

 

 

Mitochondrial DNA (mtDNA) variants are widely used in evolutionary genetics as markers for population history and to estimate divergence times among taxa. Inferences of species history are generally based on phylogenetic comparisons, which assume that molecular evolution is clock-like. Between-species comparisons have also been used to estimate the mutation rate, using sites that are thought to evolve neutrally. We directly estimated the mtDNA mutation rate by scanning the mitochondrial genome of Drosophila melanogaster lines that had undergone approximately 200 generations of spontaneous mutation accumulation (MA). We detected a total of 28 point mutations and eight insertion-deletion (indel) mutations, yielding an estimate for the single-nucleotide mutation rate of 6.2 × 10−8 per site per fly generation. Most mutations were heteroplasmic within a line, and their frequency distribution suggests that the effective number of mitochondrial genomes transmitted per female per generation is about 30. We observed repeated occurrences of some indel mutations, suggesting that indel mutational hotspots are common. Among the point mutations, there is a large excess of G→A mutations on the major strand (the sense strand for the majority of mitochondrial genes). These mutations tend to occur at nonsynonymous sites of protein-coding genes, and they are expected to be deleterious, so do not become fixed between species. The overall mtDNA mutation rate per base pair per fly generation in Drosophila is estimated to be about 10× higher than the nuclear mutation rate, but the mitochondrial major strand G→A mutation rate is about 70× higher than the nuclear rate. Silent sites are substantially more strongly biased towards A and T than nonsynonymous sites, consistent with the extreme mutation bias towards A+T. Strand-asymmetric mutation bias, coupled with selection to maintain specific nonsynonymous bases, therefore provides an explanation for the extreme base composition of the mitochondrial genome of Drosophila.

[Galapagos]

This is a narrower slice of the same problem. Since you seem to want to accept by faith that this "just happened somehow", let's focus on the lysosome problem.

 

Bio

 

I say it isn't a problem. Got any citation?

[freeztar]

In this definition, any change to a nucleotide sequence is a mutation. By this definition, all changes to species are due to mutation.

 

You have defined away the problem, not solved it.

 

My suggestion is that some genomic changes (e.g., UV light damage to DNA) truly are mutations. Other genomic changes that are highly likely based on the extant state of the genome should not be called mutations. They a code-based changes.

 

In biology, mutations are changes to the nucleotide sequence of the genetic material of an organism.

 

Mutation - Wikipedia, the free encyclopedia

 

It's important to know your definitions!

[Turtle]

This is a narrower slice of the same problem. Since you seem to want to accept by faith that this "just happened somehow", let's focus on the lysosome problem.

 

Bio

 

:hyper: You crack me up Bio. :lol: The probability that life, moreover intelligent life, occured on Earth is exactly 1. Ergo, it did "just happen."

 

Now each & every time you invoke the probability argument, no matter if applied to lysosomes or mutations or what-have-you, I intend to interject a reminder that it is a logical fallicy of the reductio ad absurdum kind. I will also be adding to that, the fact you also employ the debate tactic called argumentum ad ignorantiam, which is also a logical fallicy. :)

 

Argument from ignorance - Wikipedia, the free encyclopedia

...The argument from personal incredulity, also known as argument from personal belief or argument from personal conviction, refers to an assertion that because one personally finds a premise unlikely or unbelievable, the premise can be assumed to be false, or alternatively that another preferred but unproven premise is true instead. ...

[Biochemist]

Your claims about mutations are untrue and misleading:

 

Read the whole thing, I have only quoted a small portion.

I give up. You are now trying to correct me for things that I agree with. I must be unable to make my point.

 

But thanks, sincerely, for trying to respond.

 

Bio