Potential falsifications of the theory of evolution

Are we talking about functions or mutations? You need to pick one and stick with it. I will fully agree that functions are not random. It is mutations that are random with respect to fitness.Where in the paper does it conclude that mutations are non-random with respect to fitness?Edited by Taq, : No reason given.

They certainly shouldn't be read by someone who doesn't understand what the paper is saying prior to publishing.

Shadow and Bolderdash,Perhaps this would be easier if we actually look at an experiment and the results of that experiment.Here is the initial observation.Bacteriophage are viruses that kill bacteria. They actually lyse the bacteria after they start replicating inside of the host. For this experiment we take a population of E. coli that was raised from a single bacterium and add some bacteriophage (phage from here out). We observe that the liquid culture goes from opaque to translucent indicative of phage replicating and lysing the bacteria. However, we come back a few hours later and see that the culture is opaque once again. The bacteria have grown back. Not only that, but further experiments show that the phage particles aren't even able to bind to the bacteria. The bacteria that grew back are phage resistant.What happened? How did these bacteria become resistant to phage? For expedience, assume that phage resistance is caused by a mutation. When do you think this mutation occurred according to your hypothesis of non-random, deterministic mutations and genetic engineering systems?

Take a look at the paper, Taq.
It's an opinion piece. (Note to shadow: that means no peer review!)
The underlying references are hilarious.Not only do we have one that claims DNA is self aware, there's another that claims to analyze the genome using Chomsky. The language of genes, D. Searls, Nature 420, 211-217 (14 November 2002).And the epilogue is priceless. Where's barbara when you need her?
This is right up her alley.

Journals can and do publish off the wall stuff like this. Scientists enjoy provocative papers like these, even if they ignore them in the long run. What I find more interesting is the academic affiliation. Here we have physicists and astronomers telling microbiologists what is what.My coworkers and I will catch some of these off the wall papers and enjoy going through them as a group. I remember one paper that ran experiments showing that bacteria actually make sound. That is pretty funny. A more down to Earth epilogue would have related bacterial communication with cell-to-cell communication seen in metazoan tissue differentiation. A very interesting bacteria to study in this area is myxococcus. They actually produce organized multicellular structures in response to environmental stimuli. Pretty cool bugs.

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Pattern formation: fruiting body morphogenesis in Myxococcus xanthus

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Lars Jelsbak and Lotte Sgaard-Andersen

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Department of Biochemistry and Molecular Biology, University of Southern Denmark, Campusvej 55, 5230 Odense M, Denmark

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Available online 29 November 2000.

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Abstract
When Myxococcus xanthus cells are exposed to starvation, they respond with dramatic behavioral changes. The expansive swarming behavior stops and the cells begin to aggregate into multicellular fruiting bodies. The cell-surface-associated C-signal has been identified as the signal that induces aggregation. Recently, several of the components in the C-signal transduction pathway have been identified and behavioral analyses are beginning to reveal how the C-signal modulates cell behavior. Together, these findings provide a framework for understanding how a cell-surface-associated morphogen induces pattern formation.

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molbiogirl writes; I assume you are referring to Barbara McClintock, who for 20 years would not publish because of the abuse and ridicule she endured by the world's "greatest scientists" for her discovery of Tanspositon.Molbiogirl writes; I thought that was the theory of Darwinian evolution. That all that is comes from descent and distribution in a random way from the origin of life that we don't know anything about.Molbiogirl do you ever read Dan Dennett the hero of Dawkins and secular materialism?If you beleive this complexity seen in the lowest bacteria is a result of some natural phenomena, then I have a bridge I would like to sell you.

Well, since we really know very little about the inner workings of a cell, it is impossible to say for sure what is going on to cause these rapid adaptations.But if we really want to consider if mutations are having a completely random effect on the fitness of the organism, the easiest way to consider that might be to see what percentage of the mutations that the generations of organisms are experiencing are beneficial. In a truly random assortment of anythings possible mutations, you would expect there to be an overwhelming number of deleterious mutations compared to beneficial ones. For example, if your computer is broken, and you decided to fix it by just random hitting on the circuit boards with a hammer, you are much more likely to damage it worse, then you are to luckily hit it in exactly the right spot to fix a broken connection, or wipe out a harmful resistor but restore usability. This is how randomness would work.If however a higher percentage of mutations turn out to be useful, we are clearly seeing something other than randomness at work.I believe the evidence is not showing many many smashed circuit boards, and broken CPUs compared to solutions.

There's much we don't know about intracellular processes, but I wouldn't call what we do know very little, and regarding adaptation through random mutation and selection we know a great deal.In Taq's example bacteria experiment there are billions of bacteria that reproduce (divide into two, also known as fission) every 15 or 20 minutes. Each division results in some number of mutations, let's say 10. And let's say there are a billion bacteria. That means the population as a whole experiences 10 billion mutations every 15 or 20 minutes. That's 10 billion trial-and-error experiments. If the bacterial genome has a million nucleotides then it is very, very likely that every nucleotide is affected by a mutation in every generation. Most mutations are neutral or deleterious, but some are beneficial with regard to tolerating the phages, and the bacteria with those mutations will be the ones that populate succeeding generations because they will out-reproduce bacteria which do not have those mutations.A bacteria which divides every 15 or 20 minutes can grow from a population of 1 to a population of billions in less than a half day.Just to reiterate one point let me respond to this: It is already well established that deleterious and neutral mutations far outnumber beneficial mutations. There's no debate about this. Deleterious mutations are what natural selection filters out. Neutral mutations are responsible for genetic drift. Beneficial mutations pass through the filter of natural selection much more successfully, and it is this success that is the measure of fitness.But it is very important to understand that a mutation's effect on fitness can only be known *after* the mutation occurs, not before. Fitness is judged by the success of an organism's descendants, and no amount of cellular machinery can know that in advance.--PercyEdited by Percy, : Grammar.

Do you understand what kind of mutations we're talking about? We're talking about the only mutations that could mean anything in evolution. It's apparent that you are talking about a different kind of mutation, ones that are meaningless to evolution.The only meaningful mutations are those that can be inherited by offspring. Those mutations are purely genetic and not physical; ie, they only constitute changes in the DNA. And they are only in the germ cells, not in the body cells.Changes in the body during embryonic development that are caused by factors other than the inherited DNA (eg, by alcohol, drugs, chemicals, diet) are meaningless, evolutionarily speaking, since they will not be inherited by the next generation. Mutations in body cells resulting from exposure to chemicals or to radiation (eg, skin lesions caused by years of exposure to sunlight) are also meaningless, evolutionarily speaking. Clearly, only mutations in the DNA that will be passed on to the next generation could possibly have any evolutionary meaning. You seem to be fixated, like many creationists, on the wrong kinds of mutations.Of the meaningful kinds of mutations, there are only a few. Ernst Mayr John Maynard Smith named only four, which I will have to list later, since my book is at home.One such mutation is base substitution, in which a base (A G T or C) is replaced by a different base. If it's part of the gene for creating a protein, then three bases together form a codon which specifies an amino acid in the protein. Some amino acids are specified by more than one codon, so a base substitution could result in no change in the protein. In addition, many amino acids in a given protein are not specified, such that any amino acid could fit there, or only for certain types of amino acids, such that more than one amino acid could be substituted and not change the protein. Only a small number of sites on the protein need to be specific amino acids. For examples of the great diversity of amino acid sequences that a given protein could have, just compare its amino acid sequences across many different species. So with base substitutions, there's a very good chance that most mutations would have little or no effect and a small number would be deleterious.Before you dream up analogies for something, you really should try to learn something about it first.PS
The book is Evolutionary Genetics by John Maynard Smith (Oxford University Press, 1989). On pages 53-54:

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Mutation
The Nature of mutation
A mutation can be defined as any change in the base sequence of the DNA in the genome. Mutations may involve:
1. Base substitution: the replacement of one base by another.
2. The insertion or deletion of single bases. Such mutations involve a 'frame shift' in the process of translation.
3. Inversion of a section of DNA. ... this results in the insertion into the transcribed strand of an inverted portion of the complementary strand, and is therefore likely to be lethal if it occurs in an essential region of the DNA. Viable insertions presumably involve breaks in non-essential regions, and are such that the instructions concerning which strand is to be transcribed are preserved.
4. Duplication or deletion of a section of the DNA.

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These kinds of mutations occur at different rates, and are differently affected by mutagenic agents, but there's no reason to think that there is any constraint at the level of the DNA on what mutations can occur. Some kinds (for example, type 2) are almost certain to be lethal if they occur in an essential region of the DNA. But this is a constraint on what mutants will survive, and not on what will occur in the first place. In any particular species there will be severe limitations on the kinds of adult mutant phenotypes one observes: one will not find adult insects, or vertebrates, with an occluded gut. But these constraints arise from physiology and development, and not from the mutational process itself: so far as we know, there is no class of DNA sequence that cannot arise by mutation.

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He then goes on to cover "The balance between mutation and selection" and "Deleterious mutations in natural populations".
Hint: it's a textbook that delves into the mathematics of population genetics.Edited by dwise1, : Hadn't cleaned up completelyEdited by dwise1, : author name correction and PS

Yes, except that we are no longer talking about single point mutations, but as Shapiro is suggesting a whole network of mutational events in orchestration.And, also as you stated, we don't know the effects until after the mutations have occurred, so there is an equal inability to identify any mutational effects as random as un-random. if we can't know all the mutations that have occurred until after we see the effect on the fitness of the organism, what standard are we using to call them random?Also, do we see large drop-off in population numbers when rapid mutations are increased? That is what we should expect initially, until the right solution is found (if it is ever found), with the population quickly diminishing due to the great increase in deleterious mutations.

First, Taq's example experiment wasn't about Shapiro. It was intended as an illustration of how random mutations with regard to fitness combined with selection result in improved adaptation.Second, Shapiro is not proposing "a whole network of mutational events in orchestration." I'm not sure that an increase in the mutation rate is part of Taq's example, but you are correct that high mutation rates can overwhelm natural selection.--PercyEdited by Percy, : Improve clarity.

As with most of your assumptions, you are completely wrong. He is referring to the poster "barbara" on this forum, and not the Barbara whose work on transposition was published in the Proceedings of the National Academy of Sciences, whose work on maize was supported by the National Science Foundation and the Rockerfeller Foundation, and who was awarded the National Medal of Science, the Albert Lasker Award for Basic Medical Research, the Wolf Prize in Medicine, the Thomas Hunt Morgan Medal, the Louisa Gross Horwitz Prize and the Nobel Prize for Physiology or Medicine by her grateful and admiring peers.

Sorry for the second reply, I originally intended to respond to this, let me do so now: But we *can* see all the mutations that have occurred. How do you think we know that the bacterial mutation rate is approximately 10^-8 per base pair per generation, and that the human mutation rate is around 2.4 x 10^-8 per base pair per generation?To determine which mutation or mutations were responsible for phage resistance in Taq's bacterial experiment example, experimenters would have sampled the bacteria periodically during the experiment and sequenced their genomes. Which mutations were responsible for the resistance would then be readily identified.It is through the same type of sequencing that we know that mutations occur randomly throughout the genome. We also know that bacterial populations under stress experience higher mutation rates, but where they occur is still random.The goal of science is to figure out how things actually work in reality. To do this scientists devise experiments, sometimes very complex and difficult to replicate experiments, but their attitude is never that there are things "we can't know," which is how you characterized our chances of figuring out which mutations occurred.To tie this back in to Shapiro, he emphasizes mutation-causing processes within the cell (as opposed to random chemical accidents) and calls them non-random, but the mutation's effect on fitness is still random.It should be pointed out that humans can cause mutations, too. It is now common for human experimenters to insert specific foreign genes into their experimental subjects. To the organisms receiving the new gene it is, of course, a mutation. One type of gene commonly inserted is for fluorescence, helpful to experimenters because it makes organisms that inherit the gene easy to identify. This could be considered an example of intelligent directed evolution, because having observed the fluorescence gene in other organisms we know precisely what it will do, as opposed to intracellular processes which haven't got a clue as to the effect of any mutation.--Percy

Nope. Another member of this board who has some rather special ideas about bacteria. I think you might want to let Shapiro know about that bridge.

We know a lot more about the inner workings of the cell than you think. One minute you are lambasting us for ignoring the supposedly obvious evidence that mutations are non-random and deterministic, and the very next minute the cell is impossible to understand and a complete mystery. Which is it? None of this relates to the mutation in the experiment. What do you think is happening with respect to the mutation conferring phage resistance in this experiment? When should this mutation appear according to the hypothesis of non-random, deterministic mutations? Should it appear once the bacteria sense the presence of the phage? Will 1 in every 100 bacteria produce this mutation in response to the presence of phage? What percentage does the hypothesis of non-random, deterministic mutations predict?Edited by Taq, : No reason given.Edited by Taq, : No reason given.