Darwin re-visited

[Biochemist]

..Say we have a genetic change in a bacteria, which is consistent with version 2.0. Next, we transcribe this to make new mRNA and then translate that into a new protein, which will be an enzyme. The next logical question is, how does the cell decide where to place this new protein? If this was random, like the mutation, even a good change can cause a problem. Or it can end in a place in the cell where it has no ability to function. For example, a new and improved ion pump protein won't work well in the middle of the Kreb's cycle if that happened to be the random placement. The cell deals with this in a more orderly fashion.

This phenomenon is one of the primary statistical critiques of natural selection as a primary vehicle for speciation. To an evolutionary biologist, a cell does not "decide" anything. The placement of a new enzyme would have to be a de facto resultant of local chemical factors.

 

If you compound this problem with the incredible sophistication (and efficacy) of the degradation pathways in cells (particularly lysosomes in eukaryotes) it drives the probability of mutative benefit to an incredibly small number. A number that, incidentally, has not been credibly addressed by evolutionary biologists.

 

Were you suggesting some sort of mechanism in your "Version 3.0" that does not require a brain? I understand your argument in higher mammals, but you lost me at the single cell level.

[Biochemist]

The DNA has the easy job in evolution. A mutation is essentially a mistake relative to perfect base pairing. Anyone can make a mistake. The hard part is turning that mistake into something useful. This is where the cell body has to use skill. An analogy is a mother (cell body) is making her favorite stew for supper that she always makes. Her child is analogous to DNA, who is trying to help randomly, and dumps the wrong ingredient in. The mother has to scramble to save supper. ....Nature has taking steps to keep junior out of the kitchen, without supervision, since not all mistakes can be saved this way. Nature developed proof reading enzymes to screen what is in junior's hand to make sure it is not putting crayons in the pot. ...Evolution 3.0 will address how mother keeps an eye on junior and helps to push junior into the direction so need for change is satisfied by a given bandwidth of mistakes.

It seems like you are anthropomorphizing genes. You seem to be granting higher-level services/characteristics to lower level entities. You are suggesting that "nature" took steps to "keep junior out of the kitchen". If we are talking about a single-celled organism, are you just inserting highly sophisticated processes into less sophisticated life forms? It sounds like you are giving each cell a brain, or giving all cells some coordination from "nature". Are you?

[Galapagos]

This phenomenon is one of the primary statistical critiques of natural selection as a primary vehicle for speciation. To an evolutionary biologist, a cell does not "decide" anything. The placement of a new enzyme would have to be a de facto resultant of local chemical factors.

 

If you compound this problem with the incredible sophistication (and efficacy) of the degradation pathways in cells (particularly lysosomes in eukaryotes) it drives the probability of mutative benefit to an incredibly small number. A number that, incidentally, has not been credibly addressed by evolutionary biologists.

 

Were you suggesting some sort of mechanism in your "Version 3.0" that does not require a brain? I understand your argument in higher mammals, but you lost me at the single cell level.

 

 

How is that a valid critique of natural selection? What was said seems to be completely ignoring what selection is. If the protein does not end up in the right place, than the mutation is deleterious. Deleterious mutations are subjected to natural selection and removed from the population.

[Biochemist]

How is that a valid critique of natural selection? ....If the protein does not end up in the right place, than the mutation is deleterious. Deleterious mutations are subjected to natural selection and removed from the population.

 

From a previous thread (slightly revised for errata), this is the statistical problem with a random alteration to DNA resulting in a viable enzyme (as part of an enzyme system) which could subsequently be "selected" for some advantage:

 

Pardon the biochemistry 101 preamble, but it is necessary for the statistical analysis.

 

 

1. DNA is a sequence of four nucleotides (guanine, cytosine, adenine, thymine)
   
2. Three nucleotides in a sequence form a codon. Each of the 64 possible codons "codes" for one of 20 amino acids.
   
3. There are an infinite number of amino acids possible in chemistry. Only 20 are used in living systems- pretty much the same 20 irrespective of the life system. Amino acid anomalies are extremely rare.
   
4. DNA only codes for proteins and RNA. Proteins are the little machines to do things. RNA pretty much only helps to "transcribe" the DNA to make the proteins. Everything that is done in the cell is either done by a protein, or done by something built by a protein.
   
5. DNA is hence a little machine that builds machines (ribosomes) that build machines (proteins) that build machines (everything else). Since DNA builds itself, you could add at least one more generation on this sequence.
   
6. A typical protein is about 300-400 amino acids. They range from probably about 50 to over 10,000, but 300 is a good average. The set of codons that code for a protein is a gene. Ergo, a typical gene has 300x3 DNA bases in it, or about a thousand.
   
7. Most proteins are highly specific. In most proteins (that have been tested) most individual amino acid residues cannot be changed at all or the protein stops functioning. Most proteins have exactly one substrate, exactly one output, and several speed modulators that control the rate at which the protein functions. Proteins that are acting in this fashion are called enzymes. This is differentiated from proteins that are part of our mechanical structure.
   
8. Proteins are manufactured in a single-thread long string, but this 300 amino acid residue string "folds up" into a ball. It has to be in exactly one ball shape. Most proteins (all?) could fold up into different ball shapes which would be dysfunctional. They usually don't because other proteins ("chaperone proteins" ) manage the fold-up of the new protein to keep it the correct shape. Some diseases are thought to be errors in fold-up (e.g.,Alzheimers, cystic fibrosis) more about that issue at:http://www.faseb.org/opar/protfold/protein.html
   
9. Human DNA is about 3.6 billion nucleotide bases, but there are thought to be only 30,000-40,000 functional genes. Even if there were 100,000 functional genes, that would account for 100 million bases. The other 3.5 billion are just standing by. That is, the ratio of stand-by DNA to functional DNA is probably higher than 40:1. More on that here:http://www.biology.eku.edu/FARRAR/gen-prot.htm
   
10. Most proteins do not act alone. They act in a defined sequence of actions. Glycolysis, the Krebs cycle, the urea cycle, beta oxidation of fats: All of these are multi enzyme processes where the output of one enzyme is the input to the next. I will use the Krebs cycle as an 8-enzyme example (just because it it so famous). Picture here:http://www.bmb.leeds.ac.uk/illingwor...abol/krebs.htm
    
11. Most proteins systems need to be physically associated with each other to function. Hence, there are specific transport systems that transport proteins to their work site within the cell. These transport systems need to recognize the protein and "know" its appropriate location.
    
12. Enzymes occasionally break, or need to fluctuate in quantity. When they do, the DNA is triggered to produce more of the enzyme. A typical human chromosome is about 78 million bases, and is folded at least ten times (into at least a thousand parallel threads of DNA). The DNA is triggered to "unfurl" just a small portion of base pairs, "unzip", and let the ribosomes zip along it the make a new protein. The new protein is then chaperoned into a ball, transported into location, and usually inserted into a specific location in the target machinery.
    

Now the math:

 

Granted, the math I will present is related mostly to the human genome. Frankly, at the level of detail we are talking about, it would apply pretty well to bacteria as well. Bacteria don't have genomes quite so big, and have substantially less non-coding DNA (maybe 10% versus human 98%) but the numbers are still impressive.

 

1. 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.
   
2. Proteins do not work alone, so figuring 5 enzymes in a sequence (being conservative, typical is 6 to 8), this give us 1in 10^1000.
   
3. Keep in mind that there are thousands of separate interdependent enzyme systems and structural construction systems. I am not including the calculations for other logically required systems. Any additional required system would be a multiplier (yes, that would be 1 in 10^1,000,000). Sheesh.
   
4. I have no idea how to calculate the odds of a chaperone protein, since we would have to know the odds of a specific protein folding incorrectly without one. Let's give this one a pass.
   
5. I have no idea how to calculate the odds of recognition in the protein transport systems. We would have to know the requirment for transport, versus the degree of activity if the enzyme system was floating freely. Heck. Let's give this a pass too.
   
6. I have no idea how to calculate the feedback loop for production of additional protein from DNA, but this one probably dwarfs all of the previous numbers. Remember that we have to expose the specific thread of DNA to let the mRNA zip along it so that it can be transcribed form the gene, and transported outside of the nucleus so that the ribosomes can zip along it. The DNA unfurls on signal, and this means that one single loop of perhaps 1000-2000 codons out of maybe 70-80 million bases in a chromosome is exposed. I didn't mention that related enzymes are often associated in adjacent genes (called an "operon") and are transcribed as a set, rather than as a single enzyme. I already accidentally gave us a pass for the probability of 5 or 6 adjacent genes of 1000 codons being arranged together on a string of 80 million bases (about 25 million codons). But the real problem is that ANY mutation to the chromosome would tend to mess up this complex unfurling arrangement. So we have to allow for not just the 1 in 10^1000 problem of a mutation to create the enzyme system, but we have to make sure any of the series of mutations to establish the enzyme system does not mess up the feedback unfurling of several thousand OTHER genes on the same chromosome. No guess for the odds here.
   
7. We have not yet discussed the "lysosome problem". Cells are remarkably efficient scavengers, in that they destroy useless junk routinely. This means that the lysosomes (or other scavenger pathways in lower lifeforms) recognize foreign from non-foreign chemicals. This means that a new random protein would likely get scavenged. If it didn't, the cell would be swamped in non-functional proteins. I can't find any information on the efficiency of the cell scavenger process, but certainly a minority of proteins in the cell is non-functional. Otherwise, an organism would spend most of its energy (and food consumption) on production of non-functional material. Clearly not the case. Even if we assume that every 1 in 10^6 mutations was functional (a ludicrously positive assumption) we have to assume that lysosomes destroy the vast majority of these. The lysosome has to recognize these as non-foreign to let them remain. For each enzyme in the sequence. This would be mandatory, or the house of cards falls apart.
   
8. I brought up bacteria above, and that they have perhaps 10% non-functional DNA. Using them as examples of prokaryotes, it sure is odd that these archaic, simplistic systems are so efficient. Is it odd that the progenitors are so genomically efficient and yet the sophisticated, higher systems are not? If we have systems to reverse mutations in DNA (we do) and to eradicate foreign proteins (we do), why don't we have systems to eradicate nonfunctional DNA? My suggestion is that we probably do. I suggest this "non-coding" DNA is not nonfunctional. It is required.
   

Anyone who wants to advocate improved morphology by mutation has to get the 1 in 10^1000 number (not to mention the 1 in 10^1,000,000 number) down to something like 1 in 10^6 to 1 in 10^8 to make it have any chance of playing a role in speciation. As a biochemist, I have no idea how do do that intelligently.

 

Do keep in mind the magnitude of the problem. For comparison, there have been less than 5 * 10^17 seconds since the big bang. And we are trying to improve on the probability of at LEAST one in 10^1000.

 

This is the statistical problem with natural selection as a resultant of random mutation at the DNA level.

[Buffy]

I have no idea how to calculate the odds of a chaperone protein...

I have no idea how to calculate the odds of recognition in the protein transport systems...

I have no idea how to calculate the feedback loop for production of additional protein from DNA...

Do keep in mind the magnitude of the problem. For comparison, there have been less than 5 * 10^17 seconds since the big bang. And we are trying to improve on the probability of at LEAST one in 10^1000.

 

This is the statistical problem with natural selection as a resultant of random mutation at the DNA level.

Well, no, it is a problem of someone having an intention of manipulating probabilities without knowing the specific data and not knowing how to combine it into odds given that the individual sub-probabilities are "not independent." (Yes, you should look up the meaning of that phrase as it refers to probability... :rolleyes: )

 

This is simply a restatement of the "tornado hits junkyard producing 747" problem, which is a gross fallacy....

 

One needs to be slow to form convictions, but once formed they must be defended against the heaviest odds, :phones:

Buffy

[Biochemist]

This is simply a restatement of the "tornado hits junkyard producing 747" problem, which is a gross fallacy....

I am a little disappointed in your usual keen insight, Buff.

 

The examples you extracted above are the elements that I chose not to include in the calculations. If they were included, it would only make the probability far less likely. The fact that some items are unknown (undeniably true) does not offset the miniscule probability of the items that are known. We still have the problem of getting the probability from upwards of 1 in 10^1000 down toward something nearer 1 in 10^10 to have any real probability of speciation-by-mutation occurring.

 

I only selected the elements that probably are reasonably close to being truly random events (some are not). But I entirely skipped some other VERY highly unlikely events in the calculations.

 

For example, the probability of the very first life form selecting the exact, correct 20 amino acids (out of, essentially, an infinite field) that would work in all subsequent life forms is a pretty tough statistical problem. But it would probably make the 1 in 10^1000 probability look large in comparison.

[Galapagos]

From a previous thread (slightly revised for errata), this is the statistical problem with a random alteration to DNA resulting in a viable enzyme (as part of an enzyme system) which could subsequently be "selected" for some advantage:

 

Pardon the biochemistry 101 preamble, but it is necessary for the statistical analysis.

 

 

 

Do keep in mind the magnitude of the problem. For comparison, there have been less than 5 * 10^17 seconds since the big bang. And we are trying to improve on the probability of at LEAST one in 10^1000.

 

This is the statistical problem with natural selection as a resultant of random mutation at the DNA level.

This is a common creationist argument, the same mistakes are often made in creationist arguments about "improbability of abiogenesis", "improbability of functioning genetic sequences ", and "improbability in functional change of protein sequence".

I would review this page on "the improbability of abiogensis", as the argument is very similar to the one you are making:

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

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.

 

 

Beyond this, there are plenty of observed, published, and peer reviewed examples of novel genes arising and beneficial changes in phenotype evolving:

Related Articles for PubMed (Select 11682312) - PubMed Results

 

Richard Lenski's page has a few good examples:

Richard Lenski's Web Page

Evolution of Penicillin-Binding Protein 2 Concentration and Cell Shape during a Long-term Experiment with Escherichia coli -- Philippe et al., 10.1128/JB.01419-08 -- The Journal of Bacteriology

Peptidoglycan is the major component of the bacterial cell wall, and is involved in osmotic protection and determining cell shape. Cell shape potentially influences many processes including nutrient uptake as well as cell survival and growth. Peptidoglycan is a dynamic structure that changes during the growth cycle. Penicillin-binding proteins (PBPs) catalyze the final stages of peptidoglycan synthesis. Although PBPs are biochemically and physiologically well characterized, their broader effects, especially on organismal fitness, are not well understood. In a long-term experiment, 12 populations of Escherichia coli were founded from a common ancestor and evolved for more than 40,000 generations in a defined environment. We previously identified mutations that were substituted in half of these populations in the pbpA operon, which encodes proteins PBP2 and RodA that are involved in cell-wall elongation. In this study, we characterized the effects of two of these mutations on competitive fitness and other phenotypes. By constructing and competing strains that are isogenic except for the pbpA alleles, we show that both evolved mutations are beneficial in the environment of the long-term experiment, and that these mutations cause parallel phenotypic changes. In particular, they reduce the cellular concentration of PBP2, thereby generating spherical cells with an increased volume. By contrast to their fitness-enhancing effect in the environment where they evolved, both mutations decrease cellular resistance to osmotic stress. Moreover, one mutation reduces fitness during prolonged stationary phase. Alteration of the PBP2 concentration therefore contributes to physiological trade-offs and ecological specialization during 40,000 generations of experimental evolution.

 

Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli ? PNAS

The role of historical contingency in evolution has been much debated, but rarely tested. Twelve initially identical populations of Escherichia coli were founded in 1988 to investigate this issue. They have since evolved in a glucose-limited medium that also contains citrate, which E. coli cannot use as a carbon source under oxic conditions. No population evolved the capacity to exploit citrate for >30,000 generations, although each population tested billions of mutations. A citrate-using (Cit+) variant finally evolved in one population by 31,500 generations, causing an increase in population size and diversity. The long-delayed and unique evolution of this function might indicate the involvement of some extremely rare mutation. Alternately, it may involve an ordinary mutation, but one whose physical occurrence or phenotypic expression is contingent on prior mutations in that population. We tested these hypotheses in experiments that “replayed” evolution from different points in that population's history. We observed no Cit+ mutants among 8.4 × 1012 ancestral cells, nor among 9 × 1012 cells from 60 clones sampled in the first 15,000 generations. However, we observed a significantly greater tendency for later clones to evolve Cit+, indicating that some potentiating mutation arose by 20,000 generations. This potentiating change increased the mutation rate to Cit+ but did not cause generalized hypermutability. Thus, the evolution of this phenotype was contingent on the particular history of that population. More generally, we suggest that historical contingency is especially important when it facilitates the evolution of key innovations that are not easily evolved by gradual, cumulative selection.

 

Also, recently published on changes in Lizard morphology:

Rapid large-scale evolutionary divergence in morphology and performance associated with exploitation of a different dietary resource ? PNAS

Although rapid adaptive changes in morphology on ecological time scales are now well documented in natural populations, the effects of such changes on whole-organism performance capacity and the consequences on ecological dynamics at the population level are often unclear. Here we show how lizards have rapidly evolved differences in head morphology, bite strength, and digestive tract structure after experimental introduction into a novel environment. Despite the short time scale (≈36 years) since this introduction, these changes in morphology and performance parallel those typically documented among species and even families of lizards in both the type and extent of their specialization. Moreover, these changes have occurred side-by-side with dramatic changes in population density and social structure, providing a compelling example of how the invasion of a novel habitat can evolutionarily drive multiple aspects of the phenotype.

Lizards Undergo Rapid Evolution After Introduction To A New Home

Lizards Undergo Rapid Evolution After Introduction To A New Home

 

ScienceDaily (Apr. 18, 2008) — In 1971, biologists moved five adult pairs of Italian wall lizards from their home island of Pod Kopiste, in the South Adriatic Sea, to the neighboring island of Pod Mrcaru. Now, an international team of researchers has shown that introducing these small, green-backed lizards, Podarcis sicula, to a new environment caused them to undergo rapid and large-scale evolutionary changes.

[...]

Observed changes in head morphology were caused by adaptation to a different food source. According to Irschick, lizards on the barren island of Pod Kopiste were well-suited to catching mobile prey, feasting mainly on insects. Life on Pod Mrcaru, where they had never lived before, offered them an abundant supply of plant foods, including the leaves and stems from native shrubs. Analysis of the stomach contents of lizards on Pod Mrcaru showed that their diet included up to two-thirds plants, depending on the season, a large increase over the population of Pod Kopiste.

[...]

Examination of the lizard’s digestive tracts revealed something even more surprising. Eating more plants caused the development of new structures called cecal valves, designed to slow the passage of food by creating fermentation chambers in the gut, where microbes can break down the difficult to digest portion of plants. Cecal valves, which were found in hatchlings, juveniles and adults on Pod Mrcaru, have never been reported for this species, including the source population on Pod Kopiste.

 

There seems to be quite a bit of data demonstrating what you have predicted to be impossible.

Is there any peer-reviewed work-- by actual evolutionary biologists supporting your contention?

[Biochemist]

This is a common creationist argument, the same mistakes are often made in creationist arguments about...

Thanks for the thoughtful response, but again we are attacking the source (or in this instance, making a false association in an attempt to discredit the argument). I don't think I mentioned anything above about divine intervention. And I was also not discussing abiogenesis. I was doing a statistical assessment of the probability of an enzyme system arising denovo, given that the DNA structure was already in place.

 

In the original thread, the narrow issue under discussion was whether it was possible or reasonable for a new enzyme system to arise by "natural" phenomenon in the 250 million years between the preCambrian period and the Cambrian explosion. We made the (reasonable) assumption that we would have had to see the expression of at least one new enzyme system in the 250 million year period. This has nothing to do with abiogenesis.

 

I have not had a chance to read your references in the post yet, but I would be highly surprised if anyone has demonstrated anything related to this since I last researched this in detail a year or two ago.

 

There are not "plenty" of examples. There are a number of instances where biochemical machinery (or substrates) are reused for starkly different purposes. This is indeed interesting, but does not avoid the problem of the remarkable efficiency of lysosomes (in all eukaryotes) degrading foreign or abberant proteins. There are almost NO extra proteins floating around in cells. We have found and named most of them. Intracellular trash is FAR less than 1% of intracellular protein volume. This means there are VERY few chances for multiple, functional enzymes to be formed, survive and associate. If a new enzyme system (of at least 6 enzymes) were to be expressed through a set of random natural events (e.g., UV damage to DNA), each of the 6 functional enzymes would have to survive in some sort of presursor form, survive degradation by lysosomes, and end up being physically associated with each other at a particular intracellular locus.

 

Then, the feedback mechanism to maintain the quantity of the enzyme (based, presumably, on metabolic requirements) by the DNA feedback loop described above would have to be live as well to maintain the new enzyme system.

 

Associating this problem with "creationists" is a false argument.

[Biochemist]

There seems to be quite a bit of data demonstrating what you have predicted to be impossible.

Is there any peer-reviewed work-- by actual evolutionary biologists supporting your contention?

I read through your examples, and they seem to be irrelevant, although the E Coli instance is the most interesting.

 

That lizards (for example) can rapidly change morphology argues strongly AGAINST a genetic alteration driven by selection. Rather, it argues that the species has a precoded adaptive mechanism (e.g., mammals grow more hair in cold climates, and less in warm climates). These examples are typically reversible when the environment reverts (as with Darwin's famous finch examples). Ergo, they are extremely unlikely to be driven by genomic change. Rather, there are pre-existing adaptive mechanisms (i.e., both morphologies exist in the genome) and the preferential expression is expressed when keyed by an environmental challenge.

 

This bolsters my case, not yours. These are examples of adaptation that is very probably NOT due to genomic change.

[Moontanman]

In the original thread, the narrow issue under discussion was whether it was possible or reasonable for a new enzyme system to arise by "natural" phenomenon in the 250 million years between the preCambrian period and the Cambrian explosion. We made the (reasonable) assumption that we would have had to see the expression of at least one new enzyme system in the 250 million year period. This has nothing to do with abiogenesis.

 

.

 

I am curious, why is this a problem? Or is it a problem? If indeed recycling the old enzymes works and is easier than making totally new ones why would you expect to see new ones evolve in the past 250,000,000 years? I don't see why this is a reasonable assumption.

[Galapagos]

Thanks for the thoughtful response, but again we are attacking the source (or in this instance, making a false association in an attempt to discredit the argument). I don't think I mentioned anything above about divine intervention.

I'm not here to play games, and what you are doing is transparent. I've read your post history, you are one of the only proponents on hypography of the religious pseudoscience Intelligent Design, and as recently as yesterday you were posting links to the religious propaganda machine The Discovery Institute.

Intelligent design is the assertion that "certain features of the universe and of living things are best explained by an intelligent cause, not an undirected process such as natural selection."[1][2] It is a modern form of the traditional teleological argument for the existence of God that avoids specifying the nature or identity of the designer.[3] The idea was developed by a group of American creationists who reformulated their argument in the creation-evolution controversy to circumvent court rulings that prohibit the teaching of creationism as science.[4][5][6] Intelligent design's leading proponents, all of whom are associated with the Discovery Institute, a politically conservative think tank,[7][8] believe the designer to be the God of Christianity.[9][10] Advocates of intelligent design argue that it is a scientific theory,[11] and seek to fundamentally redefine science to accept supernatural explanations.[12]

 

The consensus in the scientific community is that intelligent design is not science.[13][14][15][16] The U.S. National Academy of Sciences has stated that "creationism, intelligent design, and other claims of supernatural intervention in the origin of life or of species are not science because they are not testable by the methods of science."[17] The US National Science Teachers Association and the American Association for the Advancement of Science have termed it pseudoscience.[18] Others in the scientific community have concurred, and some have called it junk science.[19][20]

 

So continue to deny that this is about religion, but all ID proponents do it, so keep in mind that it is very obvious what you are attempting.

 

And I was also not discussing abiogenesis. I was doing a statistical assessment of the probability of an enzyme system arising denovo, given that the DNA structure was already in place.

 

Which biologist studying the origin of life has stated that DNA would arise before any metabolic systems? Quite a different picture is painted in "The Major Transitions In Evolution" by world-class evolutionary biologists John Maynard Smith and Eors Szmarthy, which is supported by the extensive academic bibliography:

The Major Transitions in Evolution - Google Book Search

You simply do not know enough about the state of the art in order for your comments to be fruitful. Many of your assumptions are wrong. You assume modern systems evolving independently. You are misusing probability calculations, which means your maths are both wrong and incomplete.

 

 

In the original thread, the narrow issue under discussion was whether it was possible or reasonable for a new enzyme system to arise by "natural" phenomenon in the 250 million years between the preCambrian period and the Cambrian explosion. We made the (reasonable) assumption that we would have had to see the expression of at least one new enzyme system in the 250 million year period. This has nothing to do with abiogenesis.

 

I have not had a chance to read your references in the post yet, but I would be highly surprised if anyone has demonstrated anything related to this since I last researched this in detail a year or two ago.

 

Wow, where have I read this one before? Oh yeah, on Panda's Thumb, where biologists debunk creationists on a regular basis:

The Panda's Thumb: Meyer's Hopeless Monster

Meyer’s paper, therefore, is almost entirely based on negative argument. He focuses upon the Cambrian explosion as an event he thinks that evolutionary biology is unable to account for. Meyer asserts that the Cambrian explosion represented an actual sudden origin of higher taxa; that these taxa (such as phyla) are “real” and not an artifact of human retrospective classification; and that morphological disparity coincides with phyletic categories. Meyer then argues that the origin of these phyla would require dramatic increases in biological “information,” namely new proteins and new genes (and some vaguer forms of “information” at higher levels of biological organization). He argues that genes/proteins are highly “complex” and “specified,” and that therefore the evolutionary origin of new genes is so improbable as to be effectively impossible. Meyer briefly considers and rejects several theories proposed within evolutionary biology that deal with macroevolutionary phenomena. Having rejected these, Meyer argues that ID is a better alternative explanation for the emergence of new taxa in the Cambrian explosion, based solely upon an analogy between “designs” in biology and the designs of human designers observed in everyday experience.

 

The mistakes and omissions in Meyer’s work are many and varied, and often layered on top of each other. Not every aspect of Meyer’s work can be addressed in this initial review, so we have chosen several of Meyer’s major claims to assess. Among these, we will take up the Cambrian explosion and its relation to paleontology and systematics. We will examine Meyer’s negative arguments concerning evolutionary theories and the origin of biological “information” in the form of genes.

How is your argument different from the failed creationist argument above?

 

There are not "plenty" of examples. There are a number of instances where biochemical machinery (or substrates) are reused for starkly different purposes. This is indeed interesting, but does not avoid the problem of the remarkable efficiency of lysosomes (in all eukaryotes) degrading foreign or abberant proteins. There are almost NO extra proteins floating around in cells. We have found and named most of them. Intracellular trash is FAR less than 1% of intracellular protein volume. This means there are VERY few chances for multiple, functional enzymes to be formed, survive and associate. If a new enzyme system (of at least 6 enzymes) were to be expressed through a set of random natural events (e.g., UV damage to DNA), each of the 6 functional enzymes would have to survive in some sort of presursor form, survive degradation by lysosomes, and end up being physically associated with each other at a particular intracellular locus.

 

Then, the feedback mechanism to maintain the quantity of the enzyme (based, presumably, on metabolic requirements) by the DNA feedback loop described above would have to be live as well to maintain the new enzyme system.

 

Associating this problem with "creationists" is a false argument.

Associating your arguments with creationists is precisely what will be done when you post creationist arguments.

You are suggesting that enzyme systems are "irreducibly complex", which is a common ID/creationist argument.

also:

http://letmegooglethatforyou.com/?q=evolution+metabolic+path

 

I'm going to ask you again: is there any published, peer reviewed work by evolutionary biologists supporting your contention? What you are making is an extraordinary claim, and will require at the very least a normal standard of scientific evidence.

[Galapagos]

I read through your examples, and they seem to be irrelevant, although the E Coli instance is the most interesting.

 

That lizards (for example) can rapidly change morphology argues strongly AGAINST a genetic alteration driven by selection. Rather, it argues that the species has a precoded adaptive mechanism (e.g., mammals grow more hair in cold climates, and less in warm climates). These examples are typically reversible when the environment reverts (as with Darwin's famous finch examples). Ergo, they are extremely unlikely to be driven by genomic change. Rather, there are pre-existing adaptive mechanisms (i.e., both morphologies exist in the genome) and the preferential expression is expressed when keyed by an environmental challenge.

 

This bolsters my case, not yours. These are examples of adaptation that is very probably NOT due to genomic change.

 

There is no way you had enough time to read through those papers.

 

You also seemed to miss the part about genetic analysis in the paper about the lizard population:

Genetic mitochondrial DNA analyses indicate that the lizards currently on Pod Mrčaru are indeed P. sicula and are genetically indistinguishable from lizards from the source population

Samples and Phylogenetic Analysis.

Islands were visited in spring and summer of 2004, 2005, and 2006. Lizards were caught by noose and transported to the field laboratory or measured in situ. Small tail clips (±4 mm) were taken from all individuals and stored in 100% ethanol for genetic analysis. To corroborate morphological identifications, a subset of specimens from both islands (Pod Kopište, n = 8; Pod Mrčaru, n = 7) and a set of reference specimens of P. melisellensis from Lastovo Island (n = 7) were subjected to DNA sequence analysis. Total genomic DNA was extracted by using the QIAamp DNA Mini Kit (Qiagen). Two mitochondrial DNA fragments (12S rDNA and 16S rDNA) were amplified by PCR by using the primer pairs 12SaL (5′-AAACTGGGATTAGATACCCCACTAT-3′)[...]

 

Also, see figure 5 for phylogeny:

http://www.pnas.org/content/suppl/2008/03/14/0711998105.DC1/11998Fig1.jpg

 

 

edit--IF what is being asked for is observed production of novel genes, I would refer the back to this massive list of articles showing just that:

Related Articles for PubMed (Select 11682312) - PubMed Results

 

From the first result in the above list:

Evolution of novel genes. [Curr Opin Genet Dev. 2001] - PubMed Result

Much progress in understanding the evolution of new genes has been accomplished in the past few years. Molecular mechanisms such as illegitimate recombination and LINE element mediated 3' transduction underlying exon shuffling, a major process for generating new genes, are better understood. The identification of young genes in invertebrates and vertebrates has revealed a significant role of adaptive evolution acting on initially rudimentary gene structures created as if by evolutionary tinkers. New genes in humans and our primate relatives add a new component to the understanding of genetic divergence between humans and non-humans.

[Biochemist]

I am curious, why is this a problem? Or is it a problem? If indeed recycling the old enzymes works and is easier than making totally new ones why would you expect to see new ones evolve in the past 250,000,000 years? I don't see why this is a reasonable assumption.

Thanks for the question MM. You are indeed describing the reigning hypothesis, but the support is weak. I may have done a poor job of explaining the problem.

 

A great many of the statistical problems in lower life forms (bacteria, insects) are often swept under the rug because these life forms have so many progeny per generation (thousands to millions), and/or they have such rapid generations (multiple per year).

 

Things get much more problematic once we get to the "sudden" advance of speciation during the Cambrian explosion (-540 million BC and following) after the phyla get more sophisticated. There are about 250 million to 300 milllion years between the first multicellular life form, and the first mammal. The first mammals show up about 200 million year ago.

 

The statistical problem is that once the generations are a) annual, and :) small in number, there are VERY few opportunites for adaptations to 1) be generated by genomic alteration, 2) survive lysosomal degradation, and 3) assemble into complex structures.

 

Ergo, in the example above, I was trying to discuss the probabilistic issue of getting a single six-sequence enzyme system through this process in 250 million years. There are probably a dozen enzyme systems that showed up in this window in higher mammals (bone metabolism, muscle creation and metabolism, autocoids and hormones, etc) that were not present previously. Again, we are not discussing whether the enzyme systems showed up (they certainly did). We are discussing how.

 

At any point in time, there is a vanishingly small number of unused proteins in a cell (so few that they are essentially unfindable). For a new 6-enzyme system to arise, the first five have to survive without any use, or each one has to have a prior use which could somewhat suddenly convert to a new purpose.

 

The fact that some proteins have multiple uses does not particularly support the case that genomic changes happen randomly, and that changes are subsequently selected by the environment.

 

We do have dozens of examples of selection (as Modest offered above) where environmental changes result in selection of a normal variant. Often, these normal variants revert to the previous morphology when the environment reverses. We also have examples of "genetic drift", where a species wanders slightly over time (e.g., the Ensatina salamander) when populations are separated by some sort of physical barrier.

 

Neither of these demonstrate the sequence a) genetic damage new functional gene, c) new functional protein d) selection in ecological niche. The first demonstrates adaptation where both morphologies are expressable in the same genome. The second reflects selection of recessive alleles that already existed even if they were not previously expressed.

 

Suggesting that there "must have been" enough time, or that each new enzyme system was able to mature step-wise from prior enzymes or structures is speculation, not fact.

[REASON]

This bolsters my case, not yours.

 

What, exactly, is "your case," Bio?

 

You are continually arguing against a "natural" explanation for speciation, for instance, yet deny supporting a "supernatural" one.

 

What else is there?

 

You haven't actually offerred a more reasonable explanation for anything you've questioned relating to this topic, you appear to seek only to discredit the current scientific understanding.

 

You offer doubt, not truth, to those who will listen.

 

I submit that your goal here is not to produce a reasoned and more reliable explanation of natural occurances, but to attemp to undermine accepted science for the sake of convincing people to open up their beliefs to the ideas generated by pseudoscientific institutions like the Discovery Institute, who you think will appear more reliable if you can show that the traditional scientific method produces questionable explanations.

 

But you actually don't have a better explanation, do you?

 

If you do, let's hear it.

[Biochemist]

What, exactly, is "your case," Bio?

 

You are continually arguing against a "natural" expanation for speciation, for instance, yet deny supporting a "supernatural" one....What else is there?... you actually don't have a better expanation, do you?

I think speciation is pre-coded in the genome of the parent species. It fits the available facts better.

 

It explains the following, each of which are at odds with speciation-by-mutation:

 

1) the apparent expression of recessive alleles that were not previously expressed

2) the speed of speciation

3) the particular issue of increased speciation with sequestered populations- recessive alleles express even when there was not necessarily adequate time to create them- and LOTs of them (addresses the mechanism of the Cambrian explosion)

4) the common biochemical roots of all life forms (e.g., DNA, RNA, the same 20 amino acids- a very troublesome problem)

5) The tendency of higher forms to have more "junk" DNA than lower forms (since non-coding DNA would be required to manage evolution of DNA, and more would be required in higher forms)

6) the fact that phylogenesis seemed to have stopped a couple hundred million year ago

 

It certainly does not address the abiogenesis problem. But we had that problem anyway. We just made that problem bigger.

[Biochemist]

I think speciation is pre-coded in the genome of the parent species. It fits the available facts better.

Further, this is a testable hypothesis. As we decode an increasing number of species, this hypothesis would suggest that daughter species are not obligated to be morphologically similar to parent species. Some (many) certainly are. But I suspect some are not. I suspect we will find that some daughter species are as different form their parents as (for example) caterpillars are from butterflies. Given that we have many known example of individual species with significantly different morphologies, it it not that great a step to suggest that daughter species could be phenotypically significantly different than the parent species.

 

I suspect this is how we got new phyla.

[REASON]

I think speciation is pre-coded in the genome of the parent species. It fits the available facts better.

 

Ok. Thank you.

 

Do you have any thoughts as to how speciation might be "pre-coded" in the genome?