Intelligent Design

Microbe evolution virtually finished 2.5by ago

Spread the love

With all the major evolution done so early, microbe evolution has been retired for a very long time. No wonder we can’t evolve new pathways in the lab!

From ScienceDaily

New research shows that for microbes, large-scale evolution was completed 2.5 billion years ago.

“For microbes, it appears that almost all of their major evolution took place before we have any record of them, way back in the dark mists of prehistory,” said Roger Buick, a University of Washington paleontologist and astrobiologist.

All living organisms need nitrogen, a basic component of amino acids and proteins. But for atmospheric nitrogen to be usable, it must be “fixed,” or converted to a biologically useful form. Some microbes turn atmospheric nitrogen into ammonia, a form in which the nitrogen can be easily absorbed by other organisms.

About 2.5 billion years ago some microbes evolved that could add oxygen to ammonia to produce nitrate. These microbes are on the last, or terminal, branches of the bacteria and archaea domains of the so-called tree of life, and they are the only microbes capable of carrying out the step of adding oxygen to ammonia. This indicates that large-scale evolution of bacteria and archaea was complete about 2.5 billion years ago, Buick said. “Countless bacteria and archaea species have evolved since then, but the major branches have held,”

“All microbes are amazing chemists compared to us.” Buick said.

97 Replies to “Microbe evolution virtually finished 2.5by ago

  1. 1
    tribune7 says:

    For microbes, it appears that almost all of their major evolution took place before we have any record of them, way back in the dark mists of prehistory, . . . SO WE CAN BE CERTAIN IT HAPPENED!!!!!
    Some call that science. I think it more resembles a Greek mythological creation story.

  2. 2
    critiacrof says:

    The only thing that can rescue evolution is believing that evolution is like a ninja cat that only moves when you’re not looking. http://www.youtube.com/watch?v=79dt9HRif8g

  3. 3
    Domoman says:

    Tribune7,

    Exactly what I was thinking. Well, I didn’t think of the Greek mythology part, but, you know, that works too. lol

    Funny how evolutionists will claim IDists and those of religious believes are supporting, at best, pseudo-science, but they admit to things they haven’t witnessed, and cannot witness, themselves.

  4. 4
    uoflcard says:

    I am no longer surprised by accidental admissions of blind faith by neoD’s. It is inevitable. There is no logical reason to believe matter and energy is all there is and all there ever was. Eventually all beliefs lead back to some type of faith. Only naturalists/atheists/neoD’s are the ones claiming their worldview requires no faith at all.

  5. 5
    steveO says:

    In Biblical terms, convincing arguments for evo-materialism would now require the wisdom of a Solomon.

    But going by the tone of some of their leading spokespersons, all they have is the Life of Brian.

  6. 6
    bFast says:

    I find this whole thing to be kinda bewildering. From 3.75 to 2.5 billion years ago the microbial world evolved.

    Around 0.5 billion years ago the multi-cellular organisms suddenly started to evolve.

    What do they call the period of time between 2.5 bya and 0.5 bya, the evolutionary dark ages? And more importantly, if evolution rested for 2 billion years, how did it suddenly get going 0.5 billion years ago? Oh yea, I forgot, the algae created oxygen which infused a bunch of information — how dumb of me.

  7. 7
    russ says:

    These microbes are on the last, or terminal, branches of the bacteria and archaea domains of the so-called tree of life,…

    I took from a recent blog entry here that we no longer have a “tree of life”. Is that why it’s prefaced with “so-called”?

  8. 8
    Collin says:

    The emperor is nekked.

    By the way, how long does wordpress keep the rest of you logged on? It seems like I have to re-sign in all the time.

  9. 9
    Collin says:

    “All microbes are amazing chemists compared to us.” Buick said

    This is like that one guy who told us that Darwinism is true by using the analogy of the evolution of automobiles. Incredible!

  10. 10
    magnan says:

    “What do they call the period of time between 2.5 bya and 0.5 bya, the evolutionary dark ages?”

    They call it the period during which Eucaryotic single-celled organisms evolved, containing a nucleus and organelles like mitochondria. Including single celled animals like protists, and single celled fungi like yeast. These had to come about in order to build multicellular animals and plants.

    It seems to me it is unclear how the long-ago end to major evolution of bacteria relates to ID. It could be argued that the structural and biochemical potentials of the bacterial form had been exhausted. I.E. maybe the next step available to the basic system was to jump to a much larger single cell with organelles. That did happen. The issue is how did it happen.

  11. 11
    Collin says:

    magnan,

    I don’t see how to reconcile your comments about Eucaryotic single celled organisms evolving and Buicks claim that the evolution of single cell organisms was essentially completed 2.5 million years ago. What am I missing here?

  12. 12
    Jason Rennie says:

    ““For microbes, it appears that almost all of their major evolution took place before we have any record of them, way back in the dark mists of prehistory,””

    Well that sure is convenient. If we have no record of the major evolution of bacteria then how can people be so sure they did evolve ? Am I missing something here ?

    Do I just lack the appropriate Magica… I mean … “scientific” perspective ?

  13. 13
    pharmgirl says:

    Collin-
    I believe the article is only referring to archaea and bacteria, which are prokaryotes. (I could be wrong though.)
    However, his point is moot if eukaryotes really evolved first as suggested by the article Joseph linked us to in “Questioning the Role of Gene Duplication-based Evolution in Monarch Migration”.
    http://www.msnbc.msn.com/id/12853798/
    “Can evolution make things less complicated?
    Instead, the data suggest that eukaryote cells with all their bells and whistles are probably as ancient as bacteria and archaea, and may have even appeared first, with bacteria and archaea appearing later as stripped-down versions of eukaryotes, according to David Penny, a molecular biologist at Massey University in New Zealand.
    Penny, who worked on the research with Chuck Kurland of Sweden’s Lund University and Massey University’s L.J. Collins, acknowledged that the results might come as a surprise.
    “We do think there is a tendency to look at evolution as progressive,” he said. “We prefer to think of evolution as backwards, sideways, and occasionally forward.””

  14. 14
    R. Martinez says:

    Collin (#8): “The emperor is nekked.”

    If so, why do you accept microevolution or even common ancestry? Is the Emperor, in fact, partially clothed?

    Michael Behe doesn’t accept a naked Emperor.

    Ray

  15. 15
    bFast says:

    magnan: “They call it the period during which Eucaryotic single-celled organisms evolved…”

    What, single-celled eucaryotes are not microbes? I thought all single-celled organisms were microbes.

  16. 16
    Platonist says:

    The Darwinian tree of life is bogus. There have been many posts on the site about that.

    Lets be optimistic. Universal common ancestry, macroevolution is toast.

    All the best everyone. I got a date tonight.

  17. 17

    Neither Penny’s hypothesis about the origin of eukaryotes nor the evidence upon which it is based (which is very thin and ambiguous) are widely accepted by most evolutionary biologists. On the contrary, most of the evidence (especially at the genomic level) points to the conclusion that prokaryotes (i.e. bacteria and archaea) preceded the appearance of eukaryotes by at least two billion years.

    By the way, the name for the period of time between the origin of nitrogen metabolism in bacteria and the origin of eukaryotic cells is the Proterozoic Eon. And one answer to the question “why did eukaryotes ‘wait’ until the end of the Proterozoic?” is that there is very good evidence that the entire Earth was covered with glacial ice for about 215 million years.

    This happened during the Cryogenian Period, which lasted from 850 to 635 million years ago. The Cryogenian Period was the second geologic period of the Neoproterozoic Era, and there is mounting evidence that the “defrosting” of the “snowball Earth” (combined with the increase in atmospheric oxygen and the concomitant increase in oceanic calcium carbonate) during the Archaean and Proterozoic Eons set the stage for the origin of the eukaryotes, and especially the metazoa.

  18. 18

    Like the term “germ”, the term “microbe” has no technical definition. It means (roughly) “something so small you need a microscope to see it”. So yes, both bacteria and some unicellular eukaryotes qualify as “microbes”.

    There are no bacterial cells (indeed, no prokaryotes) large enough to be seen as single cells without a microscope. Yes, colonies of bacteria can be seen with the unaided eye, but such colonies contain millions or even billions of individual cells.

    By contrast, there are many eukaryotic cells that can be seen without a microscope. Currently, the largest eukaryotic cell is an unfertilized ostrich’s egg (some dinosaur eggs were bigger). However, most of the unicellular Protista can be seen without a microscope, and of course almost all of the multicellular eukaryotes are visible with the naked eye.

  19. 19

    As to the question of why bacteria have not evolved much in the past two billion years, the question reveals a basic misunderstanding of cellular evolution. Yes, no new major metabolic pathways have evolved since the nitrogen-fixing and nitrifying bacteria evolved about two billion years ago. However, that’s because there is no new element (that is necessary for life) that has a reservoir in the Earth’s atmosphere.

    All four of the major elements necessary for life – hydrogen, oxygen, nitrogen, and carbon – participate in biogeochemical cycles that have a major reservoir in the atmosphere (and, in some cases, the ocean). Once bacteria had evolved the two major nitrogen metabolic pathways, there were no new major metabolic niches to exploit.*

    In other words, once the four major (HONC) biogeochemical cycles had evolved, the only “new” ecological niches available were for new types of cells (and, eventually, multicellular organisms), not new metabolic pathways. These new cell types (and multicellular organisms) had to wait until the “snowball Earth” melted enough to allow sunlight to penetrate to sufficient depths in the epicontinental oceans to allow for macrophytic photosynthesis, which set the stage for macrophagy and the evolution of the metazoa.

    *However, science fiction author Hal Clement (Harry Clement Stubbs) published a novel in 1980 in which he proposed that a widely distributed oceanic bacterium evolved the ability to combine the nitrogen and oxygen in the atmosphere, thereby depleting virtually all free atmospheric oxygen (O2) and leaving mostly nitrogen (N2), with traces of water, nitrogen oxides and carbon dioxide in the atmosphere. This would leave the ocean as a dilute solution of nitric acid, and would, of course, kill almost all forms of life on the planet.

    This has happened once before, when non-cyclic photosynthesis evolved among the cyanobacteria, releasing a corrosive, explosively reactive, toxic gas into the atmosphere…

    …oxygen (O2).

  20. 20

    And yes, there is no single-rooted “tree of life”. It’s a mangrove, with its roots in the muddy water of the Archaeon Eon.

  21. 21
    Domoman says:

    I wonder: why there is light, and life can just so happen to see? I do not mean, that life could not have evolved eyes (although, I honestly do not believe it could by chance), but rather, why is it such that properties exist within the universe that specifically allow life to have eyes? For that matter, why can life hear? And why can it eat substances to maintain its existence? Why can it recycle the substances it eats? I’m not looking at evolution as a possible answer. This is already assuming that evolution could create life as it is (even though I highly doubt unguided evolution). This is asking why life can specifically be the way it is, period.

    Is it not strange that light, sounds waves, availability of substances to eat, to recycle substances, and to touch (to give a few examples) can even exist?

    Would it not, given a chance creation of a universe, be more likely to have light but not the ability of life to see (that is, it may be, for instance, physically impossible to see)? Or sound waves without ears? Or mouths without edible substances? Or, even differently, why do we not have ears and yet only have light and a complete lack of sound waves? Or vise versa-eyes but only sound waves?

    Seems to me that chance isn’t even a reasonable answer. This is a bit of philosophical approach to the reason why existence is exactly what it is, rather than scientific, but I’ve been thinking about it lately.

    Seems to put evolutionary just-so stories in perspective…

    BTW: Platonist, enjoy your date!

  22. 22
    Domoman says:

    And another BTW:

    My comment above would have to do with an atheistic world view. If you’re a believer of a creator of the universe, and even believe in evolution, the questions don’t so much apply. Nor am I suggestion that evolutionists claim that evolution has anything to do with the universe (although Richard Dawkins has actually suggested there is some sort of Darwinian mechanism for the reason the universe is the way it is.) In fact, Richard Dawkins would do good to honestly evaluate my above questions…

  23. 23
    pharmgirl says:

    Collin #8
    I seem to have stayed logged in all day…I don’t think I’ve logged in for days actually.

  24. 24
    mad doc says:

    Re:Allen McNeill

    “These new cell types (and multicellular organisms) had to wait until the “snowball Earth” melted enough to allow sunlight to penetrate to sufficient depths in the epicontinental oceans to allow for macrophytic photosynthesis, which set the stage for macrophagy and the evolution of the metazoa.”

    Which storybook did you find this in?

    Oh! This one:

    “*However, science fiction author Hal Clement (Harry Clement Stubbs) published a novel in 1980…….”

    TEE HEE

  25. 25
    Winston Macchi says:

    It seems to that that many of the traits we are most knowledgeable about when it comes to microbes are genes/proteins related to pathogenicity. Clearly, if evolved, they would not have evolved until a host was present (a Type Three Secretion System is of little use unless there is a host to secrete you virulence factors into). So my question is, given the extreme complexity of many of these virulence systems, along with things like quorum sensing which allows bacteria to talk to each other when they are in large groups (like infecting the gut), what is the basis for a ‘large-scale’ evolutionary change talked about? Must it only be metabolic?

  26. 26

    In #24 maddoc asked:

    “Which storybook did you find this in?”

    Peterson, K., McPeek, M., and Evans, D. (2005) “Tempo and mode of early animal evolution: Inferences from rocks, Hox, and molecular clocks.” In Vrba, E. & Eldredge, N. (2005) Macroevolution: Diversity, Disparity, Contingency; Essays in Honor of Stephen Jay Gould, The Paleontological Society, vol. 31, no. 2, ISBN #1891276492, pp. 36-55

  27. 27
    jerry says:

    Allen,

    You and the other evolutionary biologists may be backing yourself into an undesirable corner. The claim since Darwin has been we need time, deep time for evolution to work. Lord Kelvin squashed Darwin with his calculations that the earth might be at best 300 million years old but then the discovery of radio activity showed that the earth was billions of years old. And all was well in the Darwin camp.

    Now the earth for evolution is shortened again and is there enough time for all this miraculous change to take place. After all even the punctuated equilibrium people say it takes tens of millions of years for one protein to form through mutations.

    The whole argument will be won on the likelihood of novel proteins forming in a specified time. Are all those hox and other regulatory genes capable of forming by chance in so short a time. I don’t think so.

  28. 28

    The question of why we have the senses that we do is a very interesting one. As just one example, consider the sense of sight. As a type G-0 yellow-white dwarf star, the sun gives off a relatively narrow range of electromagnetic radiation, including (from longest wavelength to shortest) radio waves, infrared radiation, “visible (red, orange, yellow, green, blue, and purple) light”, and ultraviolet light. Almost all of these wavelengths of electromagnetic radiation can penetrate the Earth’s atmosphere (although the shorter wavelengths of ultraviolet light are somewhat attenuated by absorption by ozone/O3 in the upper atmosphere).

    So, which wavelengths of electromagnetic radiation can we perceive? The answer depends on who you define as “we”. Vertebrates have visual pigments in the cone cells of the retina that can absorb only three of these wavelengths: red (absorbed by the rhodopsin protein erythrolabe, which absorbs sunlight in the range of 564–580 nanometers), green (absorbed by the rhodopsin protein chlorolabe, which absorbs sunlight in the range of 534–545 nanometers), and blue (absorbed by the rhodopsin protein cyanolabe, which absorbs sunlight in the range of 420–440 nanometers). So, we vertebrates can only directly perceive red, green, and blue light (that’s why color computer monitors generate only red, green, and blue pixels).

    However, most insects (including honey bees) have different visual pigments, and so see very different colors than we do. They do not have a visual pigment that corresponds to vertebrate erythrolabe, and so cannot perceive the color we call “red”. However, they have a visual pigment vertebrates do not have, which can absorb light in the near ultraviolet range. Hence, insects can see colors (including ultraviolet) that we cannot see, and so the world appears very different to them.

    So far, no organism on Earth has been discovered that can perceive the radio waves given off by the sun. This is probably because to do so would require absorptive structures several meters in length (the wavelength of most radio waves).

    So, one answer to Domoman’s question is that, taken as a whole, living organisms can perceive (or at least absorb) a range of light from the far infrared to the near ultraviolet, but lack receptors for most of the electromagnetic spectrum (such as radio waves, gamma radiation, etc). In other words, the range of electromagnetic radiation that can be perceived by living organisms matches quite closely the range of electromagnetic radiation given off by the sun and transmitted through the Earth’s atmosphere (with the exception of radio waves, which are too long to by absorbed by any known biological molecule).

    That this is the case is exactly what one would expect to have evolved by natural selection, which can only work with what is available. Furthermore, it illustrates one of the basic ideas of evolutionary descent with modification: that the solutions to evolutionary problems vary from group to group as the result of historical contingency. Vertebrates see red, green, and blue, while insects see green, blue, and ultraviolet because two of our visual pigments (chlorolabe and cyanolabe) evolved before the divergence of insects and vertebrates from our common ancestor, while the third visual pigment evolved independently in the two groups, resulting in two different sets of perceived colors.

    Compare this to the answer that ID provides: vision is the way it is because that’s how the “intelligent designer” intended it to be. Which of these answers to Domoman’s query involves detailed empirical scientific investigation, and which simply relies on unsupported assertions?

  29. 29

    In #27 jerry wrote:

    “Now the earth for evolution is shortened again and is there enough time for all this miraculous change to take place.” [sic]

    Sorry, this phrase doesn’t make sense. What did you mean to write?

  30. 30
    jerry says:

    Allen,

    Apparently, you have no imagination. It must be selection. Yes it would be easier to see what I meant if instead of “earth” the word “time” or “period for the development of life on earth” was substituted but I took a literary license and used the concept of the earth being shortened again after it was lengthened to 300 million years from 6,000 years and then to 4.5 billion years and now it is back to 600+ million years under your ice scenario.

    Is that difficult to understand?

  31. 31
    jerry says:

    Allen,

    Before you make a big deal of it. I know Lord Kelvin published a range and I used 300 million to be on the generous end of the range for evolution. It is meaningless now since he was wrong.

  32. 32
    SeekAndFind says:

    I believe I know what the Darwinian response would be to this…

    The Evolutionist’s (non-ID supporter) working principle is — Once you find something that works really well you stick with it.

    So their reasoning would be — We can tell that bacteria have evolved by evidence of common descent. And we can tell that bacteria DO evolve by studying them in the lab.

    Just presenting this to everyone for their consideration. Responses welcome.

  33. 33
    bFast says:

    Jerry:

    to 300 million years from 6,000 years and then to 4.5 billion years and now it is back to 600+ million years under your ice scenario.

    Is that difficult to understand?

    Jerry, please don’t make us IDers look too illinformed. Allen_MacNeill has presented no new timescale. If you read the discussion on this board for the last few years you will see that the cambrian explosion, where multicellular life blossomed into all of its glory has always been about 600 million years ago (actually more like 550, but that’s hair splitting.)

    Again, the timeline has not changed for many years.

    First life — about 3.5 billion years ago. Multicellular life (there is some question of when the first multicellular came into being) about 600 million years ago. Allen_MacNeill’s level of twiddling with the timescale — zero.

  34. 34
    jerry says:

    Allen,

    You must be aware that it was those pesky little worms that only left trace fossils that may have ended the ice planet. One scenario is that they produced methane which is a greenhouse gas and this caused the exponential rise in global warming we see in the various markers for temperature. Similar to what we see with our fondness for Big Macs may be costing us by the increase in cow methane in the atmosphere.

    And I guess as James Burke used to say there was a trigger effect or connections. These make nice stories and in all these stories there is some truth. But as I said the war will be won on information generation and not climatic changes.

    Did you also know that the earth was probably situated in the galactic arm at the time of the Cambrian. I am surprised this is not brought forward as an opportunity for massive mutation rates from our neighbors.

    We are here to help but it is information that is the key.

  35. 35
    Michael Tuite says:

    Hello Allen,
    WIth respect to your note about micorbes: Thiomargarita namibiensis is a giant at nearly 1 mm and quite visible to the human eye. Most of its volume, however, is in the form of stored nitrate, not living tissue. Still, a genuine macrobe.

    Michael

  36. 36
    jerry says:

    bfast,

    I never said anything about a timeline changing. Actually I am making us more informed than Allen. The 600 million + is for multi-cellular life. That is where the action is and what Darwin was concerned about.

    At 600 million years ago the best there might have been is a few worms crawling around leaving trace fossils and then presto a relatively short time later there was the Cambrian Explosion and before that all those irreducibly complex systems had to arise to give rise to eyes, nervous systems, digestive systems, immunity systems etc. Hox genes, pax genes, sox genes, __x genes, etc. (These people must have read Dr. Seuss’s Fox in Sox.)

    What the Darwinist fall back on is all the changes in the environment driving the endless variety of novelties but they still have to deal with the information requirements that had to arise out of nowhere. How did they just poof into existence.

  37. 37
    Joseph says:

    Neither Penny’s hypothesis about the origin of eukaryotes nor the evidence upon which it is based (which is very thin and ambiguous) are widely accepted by most evolutionary biologists.

    That is because it poses too many problems for them. Mainly that eukaryotes contain too much complex specified information to have arisen first from non-living matter.

    Also the paper is just a couple of years old. In comparison the SET has been around more than 10x as long.

    Yet it too is built on evidence that is very thin and ambiguous.

    Compare this to the answer that ID provides: vision is the way it is because that’s how the “intelligent designer” intended it to be.

    Please provide the reference or admit you are just erecting another strawman.

  38. 38
    Joseph says:

    That this is the case is exactly what one would expect to have evolved by natural selection, which can only work with what is available.

    But the original population(s) of single-celled organisms didn’t have eyes/ vision systems.

    Come to think of it they didn’t have bones either.

    So the question is how did we get eyes/ vision systems and bones from the sightless and bone-less?

    And another question is if we do not know what genetic sequence(s) are responsible for the development of the human vision system*, how can we test the premise that it evolved via an accumulation of variants, ie modifications?

    *Andrea Bottaro said the following over at the panda’s thumb:

    Eyes are formed via long and complex developmental genetic networks/cascades, which we are only beginning to understand, and of which Pax6/eyeless (the gene in question, in mammals and Drosophila, respectively) merely constitutes one of the initial elements.

  39. 39
    magnan says:

    I think it is futile to dispute the main (rather vague) outlines of the actual history of prokaryotes and eukaryotes as summarized by Allen MacNeill, based on the actual fossil record and reasonable biochemical speculations.

    I think Allen came up with an adequate explanation for the original topic’s question: why major microbial evolution was over 2.7bya. No more available biochemical energetic pathways. In other words, the basic structure’s potentials were exhausted. Not an issue for ID.

    The first reliably established eukaryotic fossils are apparently algal mats, which are speculated to be already fully functioning, complex, eukaryotic algae. The “best guess” currently is the very first arose somewhere between slightly less than 2bya and 2.7bya. How did the this vast amount of new biological information specifying eukaryotic nuclei, plastids in algal cells, mitochondria, etc. etc. come about from stochastic fluctuations plus selection? No problem for Darwinists, for whom this is a dogmatic assumption.

  40. 40
    jjcassidy says:

    Allen, how is the idea that things work with the stuff that they have around to work with is inconsistent with any school of thought?

    That we needed to have a presence of a nourishing substance before being nourished is consistent with the idea of God making manna in the desert and Jesus making a feast out of a few loaves and fishes.

    Now, this is not to support miracles, but to show how universal some idea of this conception is. Along those lines, I’ve never heard ID proponents suggest that a cell needs something that is not present to function and thus proves design. So, on the speculative level of Domoman’s doubts, that organisms work with what they can be proven to have dependence on says nothing about ID–there is no counter case, to be shown in the light of the pragmatic “it works with what it has available”.

    One can be a complete phenomenologist and believe that the perception of what something is depends on the matrix that we perceive it to depend upon as a continued phenomena. There is really no extra “scientific” force behind the principle.

  41. 41
    jerry says:

    For modern microbe evolution done in the laboratory see the following article where they eventually hope to replace all the genes in a bacteria with completely new DNA.

    http://www.foresight.org/nanodot/?p=2977

    Be patient with the link. It took a few minutes for it to load. The interview is with a venture capitalist named Steve Jurvetson who graduated in 2 1/2 year first in his class at Stanford in EE and then got a masters in EE and MBA from Stanford. So he is a wunderkind.

    I do not know if any of their stuff is published since they are a private concern.

  42. 42
    Oramus says:

    Allen McNeil: “Vertebrates see red, green, and blue, while insects see green, blue, and ultraviolet because two of our visual pigments (chlorolabe and cyanolabe) evolved before the divergence of insects and vertebrates from our common ancestor, while the third visual pigment evolved independently in the two groups, resulting in two different sets of perceived colors.”

    That’s a nice story and ‘could’ be true. Plausible enough but so is this:

    1) All of life’s information was already present at the beginning stages of life.
    2) Each life form broke off from the mother (common parts) and took with it what was needed to fulfill its niche needs.
    3)So insects because they required the green, blue, AND ultra-violet vision had those modules put in their bag and said their farewells to the mother.
    4)Vertabrates, not needing ultra-violet vision didn’t get that module but instead got the red pigment module, more suitable for their niches.

    Just as plausible a scenario. Commom parts breaking off the mother and recombining in a seamingly endless array of life forms created what we have today.

    And how was the mother made? Dividing and condensing light.

  43. 43
    AussieID says:

    Allen, Allen , Allen …

    I really enjoyed your writing on wavelenghts that are accessible to our planet’s fauna. But you made a complete hash of your piece when trying to explain it: “That this is the case is exactly what one would expect to have evolved by natural selection …”

    Living things would have to have acquired, beginning with just the raw chemistry, all the myriad of complex systems we observe today. But for the acquisition of every new system an increase of information is obviously required. Biological systems derive from information. For every postulated evolutionary advance that you write you name it as ‘natural selection’.

    Natural selection, though, adds no information. It only EVER reduces it. If you are trying to invoke mutations, then all known ones are (again) a loss of information. If you contend that reducing the information in populations is evolution-in-action, then you are misguided.

    If you really believe that the ‘downhill’ process of natural selection can take you further ‘uphill’, then what you believe mutations can achieve that ‘lose’ information is like the merchant who lost a little money on every sale but who thought he could make it up on volume.

  44. 44
    mullerpr says:

    Hallo Jerry,

    Your reference to Steve Jurvetson’s interview was very insightful. I would like to comment about the dangerous and illegitimate claim that “beneficial change” i.e. adaptation is a natural phenomenon (I concur that information in nature’s hand can only degrade, based on all observations). Adaptation is something that can only be attributed to intelligence, there is no evidence to the contrary, and “Microbe evolution virtually finished 2.5by ago” supports a design hypothesis. Just referring to the Cambrian explosion undermines the notion of naturalistic adaptation. What I suggest is that a clever guy like Steve should use analogies of intelligence and design in human behavior if he wants to extract new ideas. Evolution is such a lame and human degrading metaphor!

    I have to conclude with a defense of my position by making reference to various pathogens that apparently “adapt” to survive. The “pour things” are actually just DYING IN STAGES because we (intelligent humans) are attacking just a small selection of a vastly complex set of pre-existing gene code. True adaptation would create, for the pathogens and all microbes, more novel features not less. This insight will help scientists to be prepared for the consequences of their fight against pathogens, i.e. prevent them from turning “good microbes” into pathogens. They will also try to focus on deciphering the knowledge contained in more “aboriginal microbes” to come to knowledge of the current pathogens next “dying kick”.

  45. 45
    uoflcard says:

    Allen, a few thoughts on your post about wavelengths.

    First, it was very interesting. Thank you for posting.

    Second, you missed the point of Domoman’s questions. He was asking a purely philosophical question (Why is there light? Why does it have properties that allow us to sense it? etc.). He specifically said:

    I’m not looking at evolution as a possible answer. This is already assuming that evolution could create life as it is.

    Also, I have a problem with your final paragraph:

    Compare this to the answer that ID provides: vision is the way it is because that’s how the “intelligent designer” intended it to be. Which of these answers to Domoman’s query involves detailed empirical scientific investigation, and which simply relies on unsupported assertions?

    First of all, most of your post is about common descent, which ID by itself does not challenge. In fact, most that are regulars here at UD accept common descent just as neoD’s. All of the actual science you mentioned is applicable to ID just as neoD. I do not see the logic in your final assertion that ID’s reliance on/acceptance of purposeful design excludes it from the science you mentioned before.

    Finally, the only thing that separates your view from ours IS an “unsupported assertion”, which is that natural selection and mutation did everything without any guidance or pre-programming. It is a common assumption for neoD’s to assume that just because something is/was beneficial, it means a random genetic mutation “discovered” and exploited the benefits. See Richard Dawkin’s youtube videos for the evolution of the eye. If I recall correctly, he said eyesight began as just a flat, photosensitive patch/cell, and as mutations and variation made the patch more concave, the perceieved direction of the light become more focused. It is a fascinating theory (some of which I have a hard time believing, but that is another story). But what is passed off as nothing for neoD is the origin of the photosynsetic patch, in the first place! Even the most primative eye sight is a very complex system. But of course, it happened on its own, “because it was beneficial”.

  46. 46
    bFast says:

    uoflcard:

    But what is passed off as nothing for neoD is the origin of the photosynsetic patch, in the first place!

    Sometimes IDers clamp onto challenges that realy aren’t that challenging. Consider, for instance your “photosynsetic patch”. Put on a really good blindfold, one that lets in no light. Now stand in the sun. Can you tell which direction the sun is coming from. Yes, one part of your body will be warmer than the others. You will find it quite easy to turn your face towards the sun.

    Conclusion, any heat-sensitive nerve is a natural precursor to your “photosynsetic patch”. To add to that, we have a natural phenomenon that makes a heat-sensitive nerve particularly easy to develop by accident. That is that most chemical reaction happen faster in the presence of heat than otherwise. The challenge is not to come up with the “photosynsetic patch”.

  47. 47

    In #43 AussieID wrote:

    “Natural selection, though, adds no information. It only EVER reduces it. If you are trying to invoke mutations, then all known ones are (again) a loss of information.”

    This quote demonstrates a basic misunderstanding of the process of natural selection. According to Darwin (and virtually all evolutionary biologists), natural selection has three prerequisites:

    1) Variety (generated by the “engines of variation”

    2) Heredity (mediated by the transfer of genetic material, either vertically – from parents to offspring – or horizontally – via viral transduction, retrotranscription, etc.)

    3) Fecundity (reproduction, usually at a rate that exceeds replacement).

    Given these three prerequisites, the following outcome obtains:

    4) Demography: some individuals survive and reproduce more often than others. Ergo, the heritable variations of such individuals become more common over time in populations of those organisms.

    Natural selection is synonymous with #4; it is an outcome of the three processes listed first, not a “mechanism” in and of itself.

    Ergo, the real dispute here is not over natural selection per se, but rather the properties and capabilities of the “engines of variation”. I have written extensively about these here:

    http://evolutionlist.blogspot......ution.html

    and here:

    http://evolutionlist.blogspot......awman.html

    Yes, natural selection (i.e. #4, above) is conservative not creative. It produces no new genetic nor phenotypic information, which is why Darwin eventually came to prefer the term “natural preservation” rather than “natural selection”.

    However, it is also abundantly clear that the “engines of variation” – that is, the processes the produce phenotypic variation among the members of populations of living organisms – are both extraordinarily creative and extraordinarily fecund. The real problem in biology is not producing new variation, but rather limiting the production of new variation to the point that the “engines of variation” do not cause the rapid disintegration of living systems.

    As just one example of this problem, the genetic elements known as transposons generate a huge amount of new genetic variation, much of which is either phenotypically neutral or deleterious to the organism. There are biochemical mechanisms by which cells can monitor the incidence of transposition in themselves, and limit its consequences (up to and including the active self-destruction of the cell via apoptosis).

    At the same time, there is very good evidence in the genomes of many organisms that retrotransposition events mediated by transposons have produced genetic changes that have resulted in increased survival and reproduction of the organisms in which such events have taken place. There is a large and growing literature on this phenomenon, all of which points to the inference that retrotransposition via transposons both creates new genetic and phenotypic variation, and that in some cases such variation can provide the raw material for evolutionary adaptations, which are preserved via natural selection.

    So, if you really want to find out where the “intelligent designer” might create new variations, you should follow the lead of Darwin’s good friend, Asa Gray, and look for the telltale evidence for such intervention in the “engines of variation”. Of course, you will have to show pretty conclusively, using empirical investigations and statistical analysis, that such “creation events” are not the result of purely natural, unguided processes. If you can do this, you will undoubtedly win a Nobel Prize and a Crafoord Prize (plus a MacArthur or two).

    Notice that this will involve looking carefully into the mechanisms by which new variations are produced, rather than pointing to the outcomes of such processes (i.e. natural selection) and simply asserting that “you can’t get here from there”. Simply asserting (without empirical evidence) that something can’t happen isn’t “doing science” at all. In fact, it’s doing just the opposite…

  48. 48

    In #45 uoflcard wrote:

    “…the origin of the photosynsetic patch…happened on its own, “because it was beneficial”.”[emphasis added]

    Nope; according to evolutionary biologists, the origin of the photosynthetic patch was literally an accident. That is, it was produced by the “engines of variation” which I have cited in comment #47. There is absolutely no hint that the mechanisms listed in those links produce variations because they are beneficial. Indeed, most of the variations they produce are either selectively neutral or deleterious. Only occasionally do such accidental “creations” have the effect of increasing the survival and reproduction of the individuals within whom they have occurred. It is only under such conditions they can become the raw material for evolutionary adaptations.

    The idea that new variations are “created” because they are “beneficial” was originally proposed by Darwin’s close friend, Asa Gray, in 1860, who also proposed that this was how the Judeo-Christian-Muslim-Mormon deity shaped the process of descent with modification in order to produce life as we observe it today, and especially the production of humans via a guided process of evolution via natural selection.

    Ergo, William Paley (an English philosopher and theologian) and Asa Gray (an American botanist and evolutionary biologist), along with Darwin’s “partner”, Alfred Russell Wallace, should be recognized as the founders of the modern “intelligent design” movement, not Michael Behe or William Dembski (and certainly not Phillip Johnson, whose only contribution to the movement has been in the form of propaganda, not science). Behe and Dembski have only supplied a gloss on Paley, Gray, and Wallace, who were the real originators of the “guided evolutionary hypothesis”.

  49. 49
    uoflcard says:

    bfast

    Sometimes IDers clamp onto challenges that realy aren’t that challenging. Consider, for instance your “photosynsetic patch”. Put on a really good blindfold, one that lets in no light. Now stand in the sun. Can you tell which direction the sun is coming from. Yes, one part of your body will be warmer than the others. You will find it quite easy to turn your face towards the sun.

    Conclusion, any heat-sensitive nerve is a natural precursor to your “photosynsetic patch”. To add to that, we have a natural phenomenon that makes a heat-sensitive nerve particularly easy to develop by accident. That is that most chemical reaction happen faster in the presence of heat than otherwise. The challenge is not to come up with the “photosynsetic patch”.

    First of all, I made a typo. I meant to say “photosensitive”. I doubt “photosynsetic” is even a word, although it does sound official.

    To my knowledge, eyes have evolved independently many times, some of which were deep in the ocean, where the sun’s radiation is much less significant. But that is beside the point(s). The evolutionary benefit Dawkins spoke of was not detection of the direction of the sun’s light, but the direction of the light reflected off of predators. And the radiation coming from a predator is MUCH less significant, and is also independent of light reflection (if we stood in a dark room, you could theoretically feel the radiation from my body, although most of the heat you would feel from me would probably be convective). Also, your “easy” evolutionary pathway (which I disagree with, anyway) still ignores my original thought, which is that you skip over the most challenging part, developing the complex system to detect light. Our eyes are not heat-sensing devices. We cannot see heat (although we can see evidence of it, such as flames, red hot coils, etc.), and conversely we cannot “feel” light. A blind person can tell when they’re standing in the sun, but they can’t tell when I’m shining a flashlight at them (unless it is REALLY powerful or very, very close to their skin, so they can feel the radiation and/or convection).

    Also, your final statement that the heat would speed up the process is arbitrary regarding this argument, for several reasons. Some eyes evolved deep underwater, w/o the extra heat. Also, most neo-Darwinian critics do not posit that there was slightly too little time for these complex structures to develop, but that it would require many orders of magnitude more time in order to make their random appearance probabilistically believable (or a series of slight incremental, beneficial mutations…I’m not talking about the evolution of the eye like Dawkins explained, but the actual structures that sense light). Therefore, even if the extra heat were to double or triple the supposed rate of development, it wouldn’t affect our argument. Also, we’re not talking about a chemical reaction, we’re talking about gene variation/mutation between generations. Does heat have some effect on this process? If so I’d be interested to learn about it (not sarcastic). Finally, this does not apply to any complex biological system that evolved in a cold environment or away from the sun’s radiation, so I don’t see its use here. If it is necessary/beneficial in this instance, there are countless other systems that had to have developed without the benefit.

  50. 50
    uoflcard says:

    #48 – Allen

    Nope; according to evolutionary biologists, the origin of the photosynthetic patch was literally an accident.

    I admit my mistake. But my fundamental argument still stands, that this accidental occurence is no problem for neo-Darwinian theory, like someone born with 6 toes instead of 5. It just happens, eventually. The period of time and number of mutating organisms is enough to make the appearance of these proteins and systems likely. This is the point of contention.

    btw, about a blind person/animal not being able to sense light, apparently there are such proteins as cryptochromes, which react to light. Plants have them to know when to unfurl their leaves, etc. But they are still complex systems and components

  51. 51
    PaV says:

    Allen:

    Your argument that bacterial evolution was halted 2.5 bya because of a lack of new biochemical pathways may have some merit. But I don’t see how explaining that for 215 years—out of a 2 billion year period—ice covered the earth help explains why ‘evolution’ was halted. What about the other, roughly 1.8 billion years? Why didn’t anything happen then?

  52. 52
    jerry says:

    Allen,

    You come here in bursts, maybe between classes or after the children are asleep, and expound. A lot of it is good but you fail to read most of what is posted here. You are starting to preach to the choir. Yes, Allen, we are your choir but you do not know it. You have never said anything that is in conflict with ID.

    We have long said the debate in evolution is about the source of variation and that is the Achilles heel of the evolutionary synthesis. Your 47+ engines of variation are interesting but the real issue is whether they ever produced any novel functional complex capabilities. That is the issue. I have just read Jurgen Brosius’s discussion of genetic change and do not see in it any definitive support for anything dramatic. He asserts the changes come from what he describes but the actual changes laid out and delineated are missing in action.

    So please do not get so patronizing when it us who have told you about the real issues in evolutionary biology for nearly two years. You are starting to learn more about evolutionary biology from us. Now before you get yourself in a huff and a puff as you normally do, this is said tongue in cheek.

    And reflect that there is little if anything that you say that is in conflict with ID. If you think that is not accurate, then start listing the issues and we can discuss them. But please, keep the rhetoric down.

  53. 53
    Joseph says:

    Allen,

    The book “Not By Chance” does exactly what you suggest.

    Dr Spetner came to the inference that most mutations are not random, rather they are directed.

    To confirm that however, we need to be able to look at the programming of the organisms.

    For example in C++ there are statements that you cannot see by looking at the outcome- ie the running program.

    Therefor to figure out the program one needs to be able to download it and read it.

    Therein lies the problem- we cannot (yet) download nor read biological programs.

    And that is where the origin of life comes in:

    If living organisms did not arise from non-living matter via unguided processes, ie an accumulation of accidents, then there would be no reason to infer the subsequent evolution to be driven solely by those types of processes.

  54. 54
    Joseph says:

    Nope; according to evolutionary biologists, the origin of the photosynthetic patch was literally an accident.

    Do those evolutionary biologists have a way to test that premise?

    Or is this just more “science by decree”?

  55. 55
    Joseph says:

    And thank you Allen.

    That is thank you for understanding that intelligent design is not a spin-off of Creation because of some court-case in the 1980s.

    Ergo, William Paley (an English philosopher and theologian) and Asa Gray (an American botanist and evolutionary biologist), along with Darwin’s “partner”, Alfred Russell Wallace, should be recognized as the founders of the modern “intelligent design” movement, not Michael Behe or William Dembski (and certainly not Phillip Johnson, whose only contribution to the movement has been in the form of propaganda, not science). Behe and Dembski have only supplied a gloss on Paley, Gray, and Wallace, who were the real originators of the “guided evolutionary hypothesis”.-Allen MacNeill

    Phil Johnson admits to his role and I have never heard Behe nor Dembski, nor Johnson for that matter, say anything about being a founder of ID.

    And what, pray tell, do evolutionary biologists do if not put that gloss on Darwin?

    Even though they know more than Darwin because the technology has advanced, they have not come any closer to answering the questions.

  56. 56
    uoflcard says:

    Joseph (53) –

    Dr Spetner came to the inference that most mutations are not random, rather they are directed.

    To confirm that however, we need to be able to look at the programming of the organisms.

    For example in C++ there are statements that you cannot see by looking at the outcome- ie the running program.

    Therefor to figure out the program one needs to be able to download it and read it.

    This reminds me of an article I ran across last year, about results from the massive study of the human genome (discovering that junk DNA is not as useless as so many assumed) (emphasis added):

    ‘Junk DNA’ not so useless after all

    …the ENCODE consortium were surprised to find that the genome appears to be stuffed with functional elements that offer no identifiable benefits in terms of survival or reproduction.

    The researchers speculate that there is a point behind this survival of the evolutionary cull. Humans could share with other animals a large pool of functional elements – a “warehouse” stuffed with a variety of tools on which each species can draw, enabling it to adapt according to its environmental niche.

  57. 57
    Domoman says:

    Allen @ #28,

    You did a very good job at explaining, in detail, how living organisms can see, and I commend you for that. Unfortunately you completely missed my point. My question wasn’t, “How does life see?”, but rather, “Why does life see at all?”

    Why is it that the these very specific proteins can allow life to see at all? Why should they exist, as opposed to not exist? And why, even if they could exist, should they have the specific properties to allow organisms to use them for sight? Why should the universe have varying wavelengths and yet not allow for organisms to see? Why not sound waves, but no ears? Why not mouths but no substances fit to be eaten? And going even further, granting that substances exist that are edible, why should life be able to digest them, as opposed to not being able to digest them? These questions are very similar to the question of, “Why does anything exist as opposed to nothing?”

    It’s far more likely, that if we grant the universe as a freak accident, that life should very much not be what it is. It would be more likely that the universe have sound waves, but the inability to have ears; or light waves but the inability to have eyes; or sensory organs but substances that totally escape the ability to feel; or mouths but the inability to digest; or mouths but the lack of edible substances.

    But then, we realize that sound waves exist, light waves exist, edible substances exist, objects can be felt, and then life just so happens (out of all other objects within the universe) to be able to respond to all these. The universe just so happens to exist so that we can hear, and see, and eat, and feel. Is not this strange, given an accidental, unintended cause of the universe? Perhaps you do not see this as a strange, but if you don’t, I think you may seriously underestimate the miracle that is life.

  58. 58
    Domoman says:

    Joseph @ 54,

    *quoted user*Nope; according to evolutionary biologists, the origin of the photosynthetic patch was literally an accident.*quoted user*

    Do those evolutionary biologists have a way to test that premise?

    Or is this just more “science by decree”?

    It’s science by decree I’m pretty sure. Considering that “science” must be completely materialistic, of course it follows that it was an accident. Of course this would be impossible to prove, but you know, it must be true. xD

  59. 59
    uoflcard says:

    Joseph (53) –

    And that is where the origin of life comes in:

    If living organisms did not arise from non-living matter via unguided processes, ie an accumulation of accidents, then there would be no reason to infer the subsequent evolution to be driven solely by those types of processes.

    Flipping the question around, if it does turn out that evolution is guided, perhaps by “junk” DNA, it seems to me that this entire debate will hinge on whether the system arose naturally. While an incredible system of meta-inforation (information about information) seems obviously designed, so do some very complex biological structures, yet the thought of them possibly being designed is laughed at by a dogmatic many.

    Let’s assume for a moment that it does turn out that “junk” DNA is actually a “warehouse” of information allowing a species to respond to changes in its environment, etc. What could falsify any naturalistic theory of origin would be if information in that warehouse existed before it was needed. Studying this would require a thorough understanding of the functions of “junk” DNA, as well as developing an encyclopedia of the entire genomes of as many species as possible. We’ve only got a few so far, to my knowledge, but as technology exponentially develops, it will probably get easier and easier to do this.

    A completely hypothetical example with no thorough knowledge of how “junk” DNA theoretically works: We discover a segment of “junk” DNA in a certain land animal that allowed it to respond to something only a land animal would encounter (air-borne particles, or something). If a species that lives on the floor of the ocean, whose ancestors have never been above water, shares the same DNA sequence, and that sequence has no other known uses, it would be fair to propose that the sequence was PRE-programmed, only explainable by one of three possibilities:

    – Intelligent origin of life

    – Absurdly lucky generation/selection of the sequence much earlier in evolutionary history

    – The sequence has some other unknown use, which must have been useful much earlier in evolutionary history

  60. 60
    Joseph says:

    uoflcard,

    IMHO ID will be “proven” once it is demonstrated that genetic information is NOT reducible to the sequence, just like a computer’s information is not reducible to the medium on which it resides.

    For example scientists have synthesized a ribosome but it does not function. Had it been reducible to its chemical make-up it should function.

    IMO synthesized ribosomes will not function until we learn how to program them.

  61. 61
    R. Martinez says:

    Allen_MacNeill (#48): “The idea that new variations are ‘created’ because they are ‘beneficial’ was originally proposed by Darwin’s close friend, Asa Gray, in 1860, who also proposed that this was how the Judeo-Christian-Muslim-Mormon deity shaped the process of descent with modification in order to produce life as we observe it today, and especially the production of humans via a guided process of evolution via natural selection.”

    And Charles Darwin published a stern rebuke of Asa Gray’s proposal (Darwin, “The variation of animals and plants under domestication” 1868:432, Vol.2). Charles Darwin is, of course, the founder of the evolutionary theory that was accepted; therefore his subjective opinions are the objective claims of the theory.

    For Allen to suggest that evolutionary theory allows the dead-on-arrival proposal of Gray is an attempt to deceive undecided Christian readers into accepting the same biological production theory that all Atheists accept.

    Allen_MacNeill: “William Paley (an English philosopher and theologian) and Asa Gray (an American botanist and evolutionary biologist), along with Darwin’s ‘partner’, Alfred Russell [sic] Wallace, should be recognized as the founders of the modern ‘intelligent design’ movement, not Michael Behe or William Dembski (and certainly not Phillip Johnson, whose only contribution to the movement has been in the form of propaganda, not science). Behe and Dembski have only supplied a gloss on Paley, Gray, and Wallace, who were the real originators of the ‘guided evolutionary hypothesis’.”

    Egregious ignorance or misrepresentation.

    William Paley in no way shape or form ever advocated evolution. He was the arch-enemy of evolution and Atheism. He was, of course, a Creationist and ordained Minister. These are basic undisputed historical “round earth” facts. Paley produced the very famous Watchmaker thesis (1802) which both Darwin (1859) and Dawkins (1986) were a reply. For Allen to say Paley advocated anything evolution is a premeditated lie. Again, this is why over half of all adults in the U.S. are anti-evolutionists, Creationists and/or IDists: evolutionists are recognized to be brazen liars.

    Allen can assert Asa Gray to be the founder of guided evolution.

    A.R. Wallace did NOT advocate guided evolution except for the production of the human brain. Wallace’s views had no correspondence whatsoever to Paley ID or Dembski and Behe ID since he rejected the existence of the Biblical Theos (= Atheism). Again, for Allen to leave out these all important facts is inexcusable.

    Again, Allen is engaged in equivocation because he is attempting to whitewash the pro-Atheism claims of Darwinism. All Atheists would not be evolutionists if Darwinism supported God or the Bible in any way.

    William Paley is the undisputed sole founder of Intelligent Design.

    Phillip Johnson, William Dembski and Michael Behe are the founders of DI IDism. DI IDism and Paley IDism are fundamentally different. The latter plainly admits the obvious: ID = God; while the former, for the advancement of a misguided political and legal agenda, denies. The denial is subjective.

    And Christian scholar Phillip Johnson, contrary to the predictable opinion of Atheist-evolutionist Allen Mac Neill, has contributed greatly to science. He has published many books showing the falsity of Darwinism.

    Ray

  62. 62
    Domoman says:

    Joseph,

    IMHO ID will be “proven” once it is demonstrated that genetic information is NOT reducible to the sequence, just like a computer’s information is not reducible to the medium on which it resides.

    For example scientists have synthesized a ribosome but it does not function. Had it been reducible to its chemical make-up it should function.

    IMO synthesized ribosomes will not function until we learn how to program them.

    Dude, if we find out that ribosomes were programmed, I might actually cry. That is with joy of course. ^_^

  63. 63
    AussieID says:

    Allen,

    I will play along with your terminology that ‘natural selection’ is now merely the outcome and not the mechanism (please edit changes in textbooks): Variety, Heredity, Fecundity and tied up with Demography (something we use to know by shorthand as ‘natural selection’) still reduces and specialises information and DOESN’T produce new information.

    Natural selection (through the processes of V,H,F & D!) is a conservative process that usually eliminates variables. It is ‘predominantly’ conservative and NOT a creative force. Mutations that have been observed generally degrade the genetic information, even when so-called ‘beneficial’ to the organism’s survival. Losing wings off a beetle’s back (through mutation) so it doesn’t get blown off the island ISN’T adding new information!

    So, back to your original point: “That this is the case is exactly what one would expect to have evolved by natural selection …” (So, just to be clear, are you talking about the outcome or the mechanism!!!!)

    No it’s not. Mutations and natural selection do not account for the information created in the genome.
    NS, through the process of through the processes of V,H,F & D, removes variety.

    Allen, repeat after me: no random process can be expected to create information placing well-designed structures in the right place at the right time.

  64. 64
    jerry says:

    “repeat after me: no random process can be expected to create information placing well-designed structures in the right place at the right time.”

    This is not what they say. There is no right place and right time. They say random processes are busily creating changes to genomic parts that are not functional, maybe thousands of places in any one organism and this multiplied by the number of organisms represents a very large number of places where changes are being made. If just one of these places somehow turns into something that causes a morphological difference then it may now be added to the gene pool.

    And if this morphological change affects reproduction then it may be selected for or not depending upon the environment. And presto we have a new protein or some other form of control in the genome. There is no right time, right place or right combination. But eventually there will be a change that will affect the organisms, maybe in small ways or maybe in a much bigger way as a result of these random processes.

    This is the theory. Whether it ever happened or not is the question. Of course it probably happened a few times but how many and were they big enough changes to cause the formation of new complex capabilities. I doubt it because it would leave a forensic trail in the genome to look for but we do not see the examples. But this is the theory.

  65. 65
    pharmgirl says:

    It seems that the more we learn the less likely this idea of nearly neutral mutations in nonfunctional areas of the genome becomes. Here’s a link I gave in another post I made earlier. It’s a very interesting article about the human genome from Dr. MacNeill’s blog.
    http://evolutionlist.blogspot......-gene.html

  66. 66
    AussieID says:

    G’day Jerry,

    “This is not what they say.”

    Mmmm. But that’s what they SHOULD say.

  67. 67

    aussieID:

    You include the “V” in your list of the processes that “can’t” produce new information, but you completely miss the point that “V” stands for variety, which is produced by 50+ genetic, epigenetic, developmental, and ecological processes, all of which produce genuinely new information.

    In #64 jerry actually has a very concise and pretty accurate summary of the position held by most evolutionary biologists. It is clear that jerry has done some homework and understands at least the basics of what could be called “varianomics”. However, jerry ends with this:

    “I doubt it because it would leave a forensic trail in the genome to look for but we do not see the examples.”

    In fact, there is considerable evidence for precisely the kind of “forensic” evidence that jerry suggests we should look for. Scientists in the fields of genomics and proteomics are finding such evidence every day, and virtually all of it supports the hypothesis that the new variations generated by the 50+ mechanisms are virtually all “unguided”, in the sense that the majority of them appear to have come about “by accident” (as shown by the fact that they have no detectable effect on phenotypes and rapidly degenerate into non-functional “nonsense” information).

    As J.B.S. Haldane showed almost a century ago, however, it doesn’t take much of a beneficial effect to cause huge changes in allele frequencies in a surprisingly short time (geologically speaking). There is reliable “forensic” evidence that such “accidental” events as retrotranspositions can produce phenotypic changes that result in increased survival and reproduction of the individuals within which such changes have occurred.

    So, jerry, you are correct when you assert that “this is the theory”, but you need to do some more homework, because the evidence you say we should be looking for has already been accumulating for almost two decades.

  68. 68
    jerry says:

    “So, jerry, you are correct when you assert that “this is the theory”, but you need to do some more homework, because the evidence you say we should be looking for has already been accumulating for almost two decades.”

    Well, then someone present it. I did not see it in Brosius’s article. Only assertions. After all this time, we come down to finally summing up the theory, now is the time for the evolutionary synthesis people to walk the walk.

    The ID position is that the attainment of more than a few functional proteins is beyond the scope of the process described.

  69. 69
    AussieID says:

    Allen,

    You are missing not only the big picture, but the very brushstrokes that cause it. (More on this later)

    ‘Variety’ – the end product of your machines of variation – involves no addition of complex new genetic information. Most of the variation in populations arises from reshuffling of previously existing genes and from mutations.

    Variety, Allen, does not provide new genetic information. For example, what has occured in bacteria, in many cases, is that bacteria already had the genes for resistance to the antibiotics. Some bacteria, retrieved by thawing sources which had been frozen before antibiotics were developed, has shown to be antibiotic-resistant. Now apply antibiotics to a population of bacteria: those that are lacking resistance are killed off. Any genetic information they carry is destoyed. The survivors are carrying less information but they are all still resistant.

    We find that the same principle can apply to insects supposedly ‘evolving’ resistance to pesticides. The resistance was already there. Animals without this resistance are eliminated. This also applies to rat colonies.

    On the other hand, some antibiotic resistance is the result of a mutation. There is not a known case otherwise where a mutation does not destroy information or render it neutral. Resistance to the antibiotic penicillin is a case in point.

    The appearance of a new trait doesn’t have to add new information via the DNA coding. It is so unlikely that it could ever be the basis for the increased information needed for evolution as you tout it.

    Information content is measured by the specified complexity of a base sequence or the protein amino acid sequence. A mutation could never do anything but scramble the information, thus reducing the information.

    Of the many studies of antibiotic, insecticide herbicide and resistance mechanisms studied at the biochemical level, none have added specified complexity in the DNA. New traits, due to mutations, that have arisen all involve LOSS of information.

    Variety is everywhere. But not because of the build up of new information but the imparting and reshuffling of existing information. I’ll try an analogy: consider the colour wheel. We’ll go for the red/blue/yellow primaries. By examining the inter-relationships between the colours the variety of colours that can be created from these three is immense. With shades and tints of black and white the colours able to be produced is, almost, immeasurably extended. Now, with all these abilities to combine tertiary, secondary, intermediate, ect. with black and white, then the variety that can be witnessed is massive.

    Now make the colour silver.

    Or bronze.

    What about copper?

    You may say they are variations of grey, brown or yellow. Correct, but there is new information required that isn’t present in the original to create these metallic shades. I know that the colour wheel can not show all colours, but this is not my premise. You need new information to create new colours. Variety can be immense, but not a useful tool in this case.

    You write, that variety “produce(s) genuinely new information.”

    Nope. You are wrong.

  70. 70

    In #69 aussieD wrote:

    “There is not a known case otherwise where a mutation does not destroy information or render it neutral.”

    Here’s just one example (out of thousands):

    In 1975 a team of Japanese scientists discovered a strain of Flavobacterium living in ponds containing waste water from a factory producing nylon that was capable of digesting certain byproducts of nylon 6 manufacture, such as the linear dimer of 6-aminohexanoate, even though those substances are not known to have existed before the invention of nylon in 1935. Further study revealed that the three enzymes the bacteria were using to digest the byproducts were significantly different from any other enzymes produced by other Flavobacterium strains (or any other bacteria for that matter), and not effective on any material other than the manmade nylon byproducts.

    This discovery led geneticist Susumu Ohno to propose that the gene for one of the enzymes, 6-aminohexanoic acid hydrolase, had come about from the combination of a gene duplication event with a frame shift mutation. A series of recent studies by a team led by Seiji Negoro of the University of Hyogo, Japan, suggest that a different mutation was involved in the evolution of the 6-aminohexanoic acid hydrolase.

    Scientists have also been able to induce another species of bacteria, Pseudomonas aeruginosa, to evolve the capability to break down the same nylon byproducts in a laboratory by forcing them to live in an environment with no other source of nutrients. The Pseudomonas aeruginosa strain did not seem to use the same enzymes that had been utilized by the original Flavobacterium strain. Other scientists were able to get the ability to generate the enzymes to transfer from the Flavobacterium strain to a strain of E. coli bacteria via a plasmid transfer.

    To sum up:

    There is a scientific consensus that the capacity to synthesize nylonase most probably developed as a single-step mutation that survived because it improved the fitness of the bacteria possessing the mutation.

    Sources:

    Kinoshita, S.; Kageyama, S., Iba, K., Yamada, Y. and Okada, H. (1975) “Utilization of a cyclic dimer and linear oligomers of e-aminocaproic acid by Achromobacter guttatus” Agricultural & Biological Chemistry 39 (6): 1219?23.

    Kinoshita S, Kageyama S, Iba K, Yamada Y, Okada H (1981) “Utilization of a cyclic dimer and linear oligomers of ?-aminocapronoic acid by Achromobacter guttatus K172″. Agric. Biol. Chem. 116: 547-551.

    Negoro S, Taniguchi T, Kanaoka M, Kimura H, Okada H (July 1983) “Plasmid-determined enzymatic degradation of nylon oligomers”. J. Bacteriol. 155 (1): 22–31.

    Ohno S. (April 1984) “Birth of a unique enzyme from an alternative reading frame of the preexisted, internally repetitious coding sequence” Proc Natl Acad Sci USA. 81 (8): 2421–5.

    Yomo T, Urabe I, Okada H (May 1992) “No stop codons in the antisense strands of the genes for nylon oligomer degradation”. Proc Natl Acad Sci USA. 89 (9): 3780–4.

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

    Okamura K, Feuk L, Marquès-Bonet T, Navarro A, Scherer SW (December 2006) “Frequent appearance of novel protein-coding sequences by frameshift translation” Genomics 88 (6): 690–7.

    Negoro S, Ohki T, Shibata N, et al (June 2007) “Nylon-oligomer degrading enzyme/substrate complex: catalytic mechanism of 6-aminohexanoate-dimer hydrolase” J. Mol. Biol. 370 (1): 142–56.

    So, your assertion that there is no known case where a mutation does not destroy information or render it neutral is completely and demonstrably false.

    You can make all the unsupported assertions you want, but doing so doesn’t make them true. Indeed, unless you present empirical evidence and cite who obtained the evidence, where and when it was published in a peer-reviewed scientific journal, and how we can all read it for ourselves, then all you have done is express your uninformed (and, in this case, mistaken) opinion.

  71. 71

    In #68 jerry wrote:

    “…now is the time for the evolutionary synthesis people to walk the walk.”

    For many documented examples of how transposons and retrotransposition have played important roles in evolution, start here:

    http://www.evol.nw.ru/labs/lab.....intro.html

    and then follow up the embedded links.

    And while you’re doing that, please post some citations to published empirical research that indicates that “attainment of more than a few functional proteins is beyond the scope of the processes described.” Thanks!

  72. 72
  73. 73
    jerry says:

    Allen,

    Do you want to hold up these references as the cutting edge of evolutionary biology change? Is this it? I fully expect you can dig for more but the nature of these examples is telling.

    Now I admit I am not a biologist so what I have to go on is what is claimed by these studies and others that you have introduced. And because I am not an expert in this, it will take me some time. Are these covered in any textbook or any review article on macro evolution. After all the references you gave me are 11-20 years old and the article by Brosius which is a review article did not list a lot of examples. I want to be able to put them in layman’s language so that I and others can judge them accordingly.

    Remember that ID does not dispute that your 50+ (to replace the 47+) engines of variation exist and can cause many changes to a genome and occasionally some are selected for. But new selected for characteristics is not necessarily something that will lead organisms on the path from microbes to man. The issue has always been the origin of complex new capabilities or the creations of systems within the organism that did not exist before as the result of changes to the genome by your engines of variation. Do you want to offer these up as examples of such? Otherwise it is just another diversion and does not reflect well on any synthesis that people adhere to in evolutionary biology if a published exposition of major changes leading to new functionality of organisms does not exist. All the microbe examples while interesting do not represent such changes.

    I am sure that new research will provide more examples and I always maintain that until there are substantial mappings of genomes and an understanding on just how all the genomic elements affect the operation of the organism and development we will still be in a guessing game. Until that time it looks like the 50+ engines as the driver of macro evolution will be just speculation. Thank you for all the stuff you provide us. We learn each time you help us.

  74. 74
    mad doc says:

    Allen #70

    “This discovery led geneticist Susumu Ohno to propose that the gene for one of the enzymes, 6-aminohexanoic acid hydrolase, had come about from the combination of a gene duplication event with a frame shift mutation”

    Gene duplication + “frame shift” = no new information.

    Back to the drawing board, Allen.

  75. 75
    AussieID says:

    Allen, firstly the “empirical” science lesson I got from a mate:

    Much research has flowed from this discovery of the two species (Flavobacterium sp. K172 and Pseudomonas sp. NK87) that degrade nylon compounds in trying to elucidate the mechanism for the apparently novel ability of these bacteria.

    There are three enzymes involved in Flavobacterium K172: F-EI, F-EII and F-EIII, and two in Pseudomonas NK87: P-EI and P-EII. None of these have been found to have any catalytic activity towards naturally occurring amide compounds, suggesting that the enzymes are completely new, not just modified existing enzymes. Indeed no homology has been found with known enzymes. The genes for these enzymes are located on plasmids: plasmid pOAD2 in Flavobacterium and on two plasmids, pNAD2 and pNAD6, in Pseudomonas.

    So, is this evidence consistent with random mutation generating the new genes? Thwaites [Thwaites, W.M., New proteins without God’s help, Creation/Evolution 5(2):1–3 (issue XVI), 1985.] claimed that the new enzyme arose through a frame shift mutation. If this were the case, the production of an enzyme would indeed be a fortuitous result, attributable to ‘pure chance’. However, there are exceptionally good reasons to doubt the claim that this is an example of random mutations and natural selection generating new enzymes, quite aside from the extreme improbability of such coming about by chance.

    Evidence against the evolutionary explanation includes:

    1. There are five transposable elements on the pOAD2 plasmid. When activated, transposase enzymes coded therein cause genetic recombination. Externally imposed stress such as high temperature, exposure to a poison, or starvation can activate transposases. The presence of the transposases in such numbers on the plasmid suggests that the plasmid is designed to adapt when the bacterium is under stress.

    2. All five transposable elements are identical, with 764 base pairs (bp) each. This comprises over eight percent of the plasmid. How could random mutations produce three new catalytic/degradative genes (coding for EI, EII and EIII) without at least some changes being made to the transposable elements? Negoro speculated that the transposable elements must have been a ‘late addition’ to the plasmids to not have changed. But there is no evidence for this, other than the circular reasoning that supposedly random mutations generated the three enzymes and so they would have changed the transposase genes if they had been in the plasmid all along. Furthermore, the adaptation to nylon digestion does not take very long (see point 5 below), so the addition of the transposable elements afterwards cannot be seriously entertained.

    3. All three types of nylon degrading genes appear on plasmids and only on plasmids. None appear on the main bacterial chromosomes of either Flavobacterium or Pseudomonas. This does not look like some random origin of these genes—the chance of this happening is exceptionally low. If the genome of Flavobacterium is about two million bp, and the pOAD2 plasmid comprises 45,519 bp, and if there were say 5 pOAD2 plasmids per cell (~10% of the total chromosomal DNA), then the chance of getting all three of the genes on the pOAD2 plasmid would be about 0.0015. If we add the probability of the nylon degrading genes of Pseudomonas also only being on plasmids, the probability falls to 2.3 x 10-6. If the enzymes developed in the independent laboratory-controlled adaptation experiments (see point 5, below) also resulted in enzyme activity on plasmids (almost certainly, but not yet determined), then attributing the development of the adaptive enzymes purely to chance mutations becomes even more implausible.

    4. The antisense DNA strand of the four nylon genes investigated in Flavobacterium and Pseudomonas lacks any stop codons. This is most remarkable in a total of 1,535 bases. The probability of this happening by chance in all four antisense sequences is about 1 in 1012. Furthermore, the EIII gene in Pseudomonas is clearly not phylogenetically related to the EII genes of Flavobacterium, so the lack of stop codons in the antisense strands of all genes cannot be due to any commonality in the genes themselves (or in their ancestry). Also, the wild-type pOAD2 plasmid is not necessary for the normal growth of Flavobacterium, so functionality in the wild-type parent DNA sequences would appear not to be a factor in keeping the reading frames open in the genes themselves, let alone the antisense strands.
    Some statements by Yomo et al., [Yomo T, Urabe I, Okada H (May 1992) “No stop codons in the antisense strands of the genes for nylon oligomer degradation”. Proc Natl Acad Sci USA. 89 (9): 3780–4.] express their utter consternation at the findings:

    “These results imply that there may be some unknown mechanism behind the evolution of these genes for nylon oligomer-degrading enzymes.

    “The presence of a long NSF (non-stop frame) in the antisense strand seems to be a rare case, but it may be due to the unusual characteristics of the genes or plasmids for nylon oligomer degradation.

    “Accordingly, the actual existence of these NSFs leads us to speculate that some special mechanism exists in the regions of these genes.”
    It looks like recombination of codons (base pair triplets), not single base pairs, has occurred between the start and stop codons for each sequence. This would be about the simplest way that the antisense strand could be protected from stop codon generation. The mechanism for such a recombination is unknown, but it is highly likely that the transposase genes are involved.

    Interestingly, Yomo et al. also show that it is highly unlikely that any of these genes arose through a frame shift mutation, because such mutations (forward or reverse) would have generated lots of stop codons. This nullifies the claim of Thwaites that a functional gene arose from a purely random process (an accident).

    5. The Japanese researchers demonstrated that nylon degrading ability can be obtained de novo in laboratory cultures of Pseudomonas aeruginosa [strain] POA, which initially had no enzymes capable of degrading nylon oligomers. This was achieved in a mere nine days! The rapidity of this adaptation suggests a special mechanism for such adaptation, not something as haphazard as random mutations and selection.

    6. The researchers have not been able to ascertain any putative ancestral gene to the nylon-degrading genes. They represent a new gene family. This seems to rule out gene duplications as a source of the raw material for the new genes.

    P. aeruginosa is renowned for its ability to adapt to unusual food sources—such as toluene, naphthalene, camphor, salicylates and alkanes. These abilities reside on plasmids known as TOL, NAH, CAM, SAL and OCT respectively. Significantly, they do not reside on the chromosome (many examples of antibiotic resistance also reside on plasmids).

    The chromosome of P. aeruginosa has 6.3 million base pairs, which makes it one of the largest bacterial genomes sequenced. Being a large genome means that only a relatively low mutation rate can be tolerated within the actual chromosome, otherwise error catastrophe would result. There is no way that normal mutations in the chromosome could generate a new enzyme in nine days and hypermutation of the chromosome itself would result in non-viable bacteria. Plasmids seem to be adaptive elements designed to make bacteria capable of adaptation to new situations while maintaining the integrity of the main chromosome.

    Now, to look at stasis in bacteria: P. aeruginosa was first named by Schroeter in 1872. It still has the same features that identify it as such. So, in spite of being so ubiquitous, so prolific and so rapidly adaptable, this bacterium has not evolved into a different type of bacterium. Note that the number of bacterial generations possible in over 130 years is huge—equivalent to tens of millions of years of human generations, encompassing the origin of the putative common ancestor of ape and man, according to the evolutionary story, indeed perhaps even all primates. And yet the bacterium shows no evidence of directional change—stasis rules, not progressive evolution. This alone should cast doubt on the evolutionary paradigm.

    Flavobacterium was first named in 1889 and it likewise still has the same characteristics as originally described.

    It seems clear that plasmids are designed features of bacteria that enable adaptation to new food sources or the degradation of toxins. The details of just how they do this remains to be elucidated. The results so far clearly suggest that these adaptations did not come about by chance mutations, but by some designed mechanism. This mechanism might be analogous to the way that vertebrates rapidly generate novel effective antibodies with hypermutation in B-cell maturation, which does not lend credibility to the grand scheme of neo-Darwinian evolution. Further research will show that there is a sophisticated, irreducibly complex, molecular system involved in plasmid-based adaptation—the evidence strongly suggests that such a system exists. This system will once again, as the black box becomes illuminated, speak of intelligent design, not chance.

    I LOVE empirical evidence! But when scientists try to use empirical evidence to show the short-comings of Neo-Darwinian methods they aren’t published in a “peer-reviewed scientific journal”. You should have rewritten it as “Darwinian-orthodoxy-reviewed journal”. That is more appropriate, but that wouldn’t be such a good line now, would it!.

    Apologists for materialism, such as you, latched onto these findings as an example of evolution of new information by random mutations and natural selection. You obviously don’t critically evaluate anything you read as your ongoing mantra shows. To rework your own words, “… then all you have done is express your uncritical (and, in this case, mistaken) opinion.”

    Your example is irrelevant to goo-to-you evolution.

    If this is your best work, and I never know anyone to provide their B and C games to convince someone of a point, then I can confidently go back to my original point:

    “Natural selection, though, adds no information.”

    Bring on your ‘A’ game, Allen, your ‘A’ game.

  76. 76
    Joseph says:

    Carbon- nylon-6 contains carbon, which has been around for quite some time.

    And it is that carbon which the bacteria requires.

    IOW bacteria may not have known “nylon” but bacteria definitely knew carbon.

    Then all that was necessary was for the bacteria to solve the problem- how to get the carbon out of the nylon-6.

    And it looks like a solution was found.

    Why isn’t that an example of a “built-in response to environmental cues” as Dr Spetner describes in his book “Not By Chance”?

  77. 77
    Joseph says:

    Dr. Spetner discussing transposons:

    The motion of these genetic elements to produce the above mutations has been found to a complex process and we probably haven’t yet discovered all the complexity. But because no one knows why they occur, many geneticists have assumed they occur only by chance. I find it hard to believe that a process as precise and well controlled as the transposition of genetic elements happens only by chance. Some scientists tend to call a mechanism random before we learn what it really does. If the source of the variation for evolution were point mutations, we could say the variation is random. But if the source of the variation is the complex process of transposition, then there is no justification for saying that evolution is based on random events.

  78. 78
    Joseph says:

    What do the Creationists say about nylon eating bacteria?:

    Batten, D. 2003. The adaptation of bacteria to feeding on nylon waste. Journal of Creation 17(3):3–5.

    It concludes with:

    It seems clear that plasmids are designed features of bacteria that enable adaptation to new food sources or the degradation of toxins. The details of just how they do this remains to be elucidated. The results so far clearly suggest that these adaptations did not come about by chance mutations, but by some designed mechanism. This mechanism might be analogous to the way that vertebrates rapidly generate novel effective antibodies with hypermutation in B-cell maturation, which does not lend credibility to the grand scheme of neo-Darwinian evolution.11 Further research will, I expect, show that there is a sophisticated, irreducibly complex, molecular system involved in plasmid-based adaptation—the evidence strongly suggests that such a system exists. This system will once again, as the black box becomes illuminated, speak of intelligent creation, not chance. Understanding this adaptation system could well lead to a breakthrough in disease control, because specific inhibitors of the adaptation machinery could protect antibiotics from the development of plasmid-based resistance in the target pathogenic microbes.

  79. 79
    George L Farquhar says:

    Joseph,
    As that was published in 2003 are you aware of any follow ups in regard to

    Further research will, I expect, show that there is a sophisticated, irreducibly complex, molecular system involved in plasmid-based adaptation

    Has there been further research then? Has it shown that these systems are IC?

    This system will once again, as the black box becomes illuminated, speak of intelligent creation, not chance.

    Is 6 years not enougth time to illuminate this?

    Understanding this adaptation system could well lead to a breakthrough in disease control

    Has such an understanding been reached? Is anybody that you are aware of working on reaching such an understanding from a design perspertive?

    Seems alot could have been done to advance your cause in the years since that was published.

    Has it?

  80. 80
    Joseph says:

    George,

    If you write to Answers in Genesis– be nice and cordial- most likely they will answer you.

    However they may say just what the heck has this feature arising by accident advanced?

    BTW my “cause” is to get to the reality behind our existence and the existence of what we observe.

  81. 81

    Here’s another one, much more recent (2004). I’m copying the entire article from an online scientific journal that is not available to people without a subscription. I can get it for free through my university library gateway.

    ARTICLE CITATION:

    Brookfield, J. F. Y. (2004) Evolutionary genetics: Mobile DNAs as sources of adaptive change? Current Biology, Volume 14, Issue 9, Pages R344 to R345. Available online 3 May 2004.

    ABSTRACT:

    Mobile DNAs are potent sources of mutation in wild populations, but seem only rarely to have been used in adaptive evolution. A new study has revealed a mobile DNA insertion in Drosophila simulans that is associated with an apparent selective sweep and an elevation in expression level of an adjacent gene which creates insecticide resistance.

    FULL TEXT:

    The neo-Darwinian paradigm of evolutionary change assumes that mutations occur independently of any natural selection that will subsequently act on them. While such independence has been challenged in some descriptions of adaptive mutation in bacteria [1], it is still generally accepted to apply in multicellular organisms. It follows that, were one to examine simultaneously the process of mutation and the process of evolution, the kinds of mutational change that one would see should not be different in kind from the sorts of changes one sees occurring over evolutionary time, unless different types of mutation had systematically different phenotypic consequences: only selection can create a systematic difference between mutational and evolutionary changes.

    A lack of agreement between mutation and evolutionary change was first noted in the context of dominance. In the 1920s, when the neo-Darwinian synthesis was being created, it was seen that mutations in Drosophila melanogaster are usually recessive to the wild-type allele. The paradox was that if genes are evolving, then the current wild-type allele would have been a mutant when it first arose, spreading to become the wild-type because of its advantageous phenotypic effect. Why should advantageous mutations generally be dominant, when their advantageousness depends on the particular environments that they will encounter?

    R.A. Fisher [2] and [3] suggested that the solution to this conundrum was that dominance evolves – an advantageous mutation is only co-dominant when it first arises, but, as it spreads through the population as a result of selection, evolutionary changes at other, ‘modifier’ loci cause the mutation to be dominant by the time it is fixed in the population. For Sewell Wright [4] and [5], however, the explanation was that the Drosophila mutations are recessive because they inactivate genes, so that their recessivity has a physiological, rather than an evolutionary, cause. Wright’s prediction, subsequently abundantly confirmed, implies that, at the molecular level, there is no symmetry between typical major mutations studied in laboratories and the adaptive changes occurring over evolutionary time. Major mutations represent losses of gene function, a change not often used in adaptive evolution – we do not evolve by successively losing more and more of our gene functions, but rather by subtly altering the ways in which genes work.

    Similarly, what are the evolutionary consequences of mobile DNA insertions? It has been estimated that 80% of the spontaneous mutations seen in Drosophila genetics result from transposable elements [6]. Do mobile DNA insertions similarly create 80% of evolutionary changes in this species? Without question, they do not. The most revealing observation is the almost complete absence of fixed sites of mobile DNAs in D. melanogaster [7]. A mobile DNA insertion that created an advantageous phenotype would be expected to spread to fixation in the species by natural selection. This would create a site fixed for the element throughout the species. Such sites are very rare, although they have recently been detected for the S element family in heat shock protein genes [8]. Is this simply because transposable element insertions are different in kind from base substitutions, the typical outcome of the insertion of a mobile DNA into the coding sequence being a gene inactivation? Possibly, but one can easily imagine that an insertion of a mobile DNA near to a gene could leave the coding sequence intact but could create a subtle, and potentially advantageous, alteration in the gene’s expression pattern.

    A recent study by Schlenke and Begun [9] has revealed an example of an adaptive change apparently created in Drosophila simulans by the insertion of a mobile DNA. These authors have shown that, in D. simulans, a mobile DNA insertion 5? to the cytochrome P450 gene Cyp6g1 has apparently created an adaptive phenotypic change, as a result of which it has spread to high frequency in a local population. The sign of an adaptive change first noted by the authors was a region of around 100kilobases with very low heterozygosity, but only in a D. simulans population sampled from California, and not in African samples. This appeared to be the sign of a ‘selective sweep’. A selective sweep occurs when a new advantageous mutation arises and rapidly spreads through the population. Because the mutation arises initially in a single chromosome, as it spreads, this chromosome also spreads through the population, eliminating the standing crop of genetic diversity in the region. The length of the chromosome affected by such a selective sweep depends on the relative sizes of the selective coefficient favouring the new mutation and the local recombination rate per base.

    There are, of course, difficulties in identifying, in a 100kilobase region that has undergone a selective sweep, the particular mutational change in the region that has been responsible for the selection (many variants will have recently spread from low to high frequency as a result of the sweep). The identification of the cause of the sweep in D. simulans is thus based on circumstantial evidence. Schlenke and Begun [9] noted that there is an insertion of the non-long-terminal repeat (LTR) retrotransposon Doc in the 5? flanking region of Cyp6g1, around 200 base pairs upstream from the start of transcription and absent in African D. simulans lines. While this gene is not at the centre of the chromosomal region affected by the sweep, cytochrome P450 genes are known to play a role in insecticide resistance, and thus Cyp6g1 is a candidate cause of the sweep.

    One remarkable property of the Doc insertion is that an extraneous 72 base pairs of DNA at its 5? end seems to have been translocated from a 5? flanking sequence of the mitochondrial P450 gene Cyp12c1, thereby possibly introducing new controlling regions to Cyp6g1. Certainly, the Californian lines bearing the Doc insert have a higher level of Cyp6g1 expression than African lines. There is also statistically significant evidence for enhanced resistance to the insecticide DDT in the Californian lines, although the high between-line variation in resistance among lines all with the Doc insertion implies that the presence or absence of the insertion is not the sole determinant of resistance. The size of the region affected by the selective sweep allows the estimation of the strength of selection at 2% per generation favouring the new advantaged haplotype.

    Further evidence that insertion of mobile DNAs creates an advantageous insecticide resistance at this locus comes from comparison with D. melanogaster populations. Remarkably, in a similar location 5? to Cyp6g1, Californian D. melanogaster have a high frequency insertion of the gypsy-like LTR retro-transposon Accord. This insertion occurs at a much lower frequency in other populations. Again there is evidence that this insertion is associated with DDT resistance and that a selective sweep has occurred, but one that is smaller in extent than in the D. simulans case and more tightly associated with the Cyp6g1 gene.

    If these apparent selective sweeps are indeed the result of mobile DNA sequence insertions, why are insertion mutations that alter the expression patterns of adjacent genes in a selectively advantageous way not more common? Why do these so rarely seem to spread through the species as a whole? One can clearly create a model in which insertions are eventually followed by imprecise excisions, leaving behind a small fragment only of the inserted sequence, or causing the loss of all the insertion, along with some flanking host sequences. Such a change might still create the advantageous phenotype, and thus one can imagine that an advantageous insertion is replaced by its deleted derivative. A recent sweep generated by a insecticide resistance phenotype might not have had long enough for this secondary event to have occurred.

    The other, more disturbing, aspect of this study is that the species is responding to a very strong, man-made selective pressure, as is the case with many of our best examples of recent adaptive change in wild populations. Are these sudden man-made changes in environments typical of the environmental changes that wild populations encounter, and to which they respond through evolutionary change? Or do environments more usually change in such a gradual way that the adaptive response is qualitatively different at the molecular level. In other words, just as the mutations seen in laboratories are not typical of the mutational changes used in adaptive evolution, is it possible that the mutational changes used in adaptive evolution triggered by sudden mad-made environmental changes are not typical of the mutational changes used in adaptation to the more gradual environmental changes normally encountered by wild populations?

    REFERENCES:

    [1] B.G Hall, Adaptive mutagenesis: a process that generates almost exclusively beneficial mutations, Genetica 103 (2003), pp. 109–125.

    [2] R.A Fisher, The possible modification of the response of the wild-type to recurrent mutation, Am. Nat. 62 (1928), pp. 115–126.

    [3] R.A Fisher, Two further notes on the origin of dominance, Am. Nat. 62 (1928), pp. 571–574.

    [4] S Wright, Fisher’s theory of dominance, Am. Nat. 63 (1929), pp. 274–279.

    [5] S Wright, The evolution of dominance, Am. Nat. 63 (1929), pp. 556–561.

    [6] M Ashburner, Drosophila, a laboratory handbook, Cold Spring Harbor Laboratory Press, Cold Spring Harbor, New York (1992).

    [7] B Charlesworth and C.H Langley, The population genetics of Drosophila transposable elements, Annu. Rev. Genet. 23 (1989), pp. 251–287.

    [8] X Maside, C Bartolome and B Charlesworth, S-element insertions are associated with the evolution of the HSP70 genes in Drosophila melanogaster, Curr. Biol. 12 (2002), pp. 1686–1691.

    [9] T.A Schlenke and D.J Begun, Strong selective sweep associated with a transposon insertion in Drosophila simulans, Proc. Natl. Acad. Sci. USA 101 (2004), pp. 1626–1631.

    AUTHOR’S INFORMATION:

    Institute of Genetics, University of Nottingham, Queens Medical Centre, Nottingham, NG7 2UH, UK

    COMMENTARY:

    The transposon-mediated adaptive changes cited in this article are exactly the kinds of changes I cited in my earlier post (#71, above). Furthermore, the transposon-mediated changes cited here do not involve plasmids (which eukaryotes rarely if ever have). On the contrary, they involve the random insertion of transposable elements which, upon examination and correlation with frequency in different populations, have been shown to have become more common over time.

    This is the definition of adaptive evolution: an accidental genetic change (which in its original position in the genome had no detectable adaptive value) increases in frequency in a population because the individuals carrying this change survive and reproduce more often than individuals who do not carry it.

    Now, of course, someone could go on and argue that the Intelligent Designer somehow “guided” the insertion of this transposon by some entirely unspecified mechanism, but that assertion cannot be shown to be the case using any conceivable empirical method. Ergo, it’s not science and should not be included in a scientific explanation.

    I can keep this up all day, so long as I have access to Google Scholar and the Cornell University Library Gateway. However, I would also like to hear how the alternative hypothesis – that adaptive changes are produced by the intervention of an Intelligent Designer – can be tested and either verified or falsified empirically, and by what mechanism(s) the Intelligent Designer accomplishes this.

  82. 82
    George L Farquhar says:

    However, I would also like to hear how the alternative hypothesis – that adaptive changes are produced by the intervention of an Intelligent Designer – can be tested and either verified or falsified empirically, and by what mechanism(s) the Intelligent Designer accomplishes this.

    Not only that, but can
    A) The amount of FSCI
    B) The change in the amount of FSCI
    C) The final amount of FSCI
    As defined by Kariosfocus be shown for the adaptive changes detailed in Allen’s post?

    If not, what is needed in order to be able to do so? DNA sequences? What? I’d really like to know what would be needed to work it out.

    Does anybody know?

  83. 83
    jerry says:

    “by what mechanism(s) the Intelligent Designer accomplishes this.”

    Allen, there is a whole area of study called Synthetic Biology which I am sure you are aware of. Maybe it was one of the ways they are thinking of using. But I bet it was more advanced than anything they are currently using so you may have to wait awhile.

  84. 84
    uoflcard says:

    However, I would also like to hear how the alternative hypothesis – that adaptive changes are produced by the intervention of an Intelligent Designer – can be tested and either verified or falsified empirically, and by what mechanism(s) the Intelligent Designer accomplishes this.

    First of all, not all of ID theory proposes miraculous interventions whenever some major evolution needs to happen. I am becoming more and more partial to front-loaded evolution, especially with what is beginning to be discovered about genomes, and “junk” DNA. If it is proven that some of “junk” DNA is basically programming that influences evolution (instead of random mutation/variation creating all information), I think ID’s case becomes very strong. I need to learn more about the front-loaded theory, and we all need to learn more about “junk” DNA. But I have heard for years from front-loaded theorists that our genomes could be programmed for evolution. It was easily rejected by neo-Darwinists because they were thoroughly engulfed in the dogmatic acceptance of “junk” DNA being worthless evolutionary artifacts. But now it appears there is much more to the genome than what has been unquestionably accepted for decades.

    If it turns out to be true, the evolutionary “warehouse” of DNA (a.k.a. “junk”) would be a possible mechanism.

  85. 85
    jerry says:

    Allen,

    You done it again. Thank you very much. We ask for major changes and we get back simple micro evolution which ID accepts. An interesting article. I admit I do not understand all that is being said but know enough to know that this is a minor change with positive results. Is it beneficial over all for the fruit fly or just locally because of DDT. Would the change persist in other areas with no insecticides or be selected against?

    It is still a fruit fly with a slight genomic change to add the insecticide resistance and it looks like it is the result of a jumping gene or something similar. I now know what a selective sweep is and will be on the look out for it in the future.

    Jumping genes or jumping beans. It is still a long way from true macro evolution. Remember we do not deny these changes take place and sometimes have some beneficial effects.

  86. 86
    jerry says:

    uoflcard,

    I have tried to find out what the junk DNA is supposed to do. As far as I know the only thing they know is that it gets transcribed but not translated in any way. After that they are still at a lost as to why it is transcribed and what the function of the transcribed RNA has if any. If it has none, then it may be still junk and it will be a colossal waste of energy because the cell expends energy to transcribe. Most of the DNA are repetitive elements like ABABABABABAB etc.

    Does anyone have any different insight on this? A big deal was made of the ENCODE project but I have not seen any real substance out of it except the claim made by some that nearly all the genome has function.

  87. 87
    AussieID says:

    Allen,

    “I can keep this up all day …”

    … and you do: without being able to give a real response to the question of ‘new information’. Finding articles to support your ‘idea’ but that don’t support the facts isn’t what you need to show.

    Repeat to Allen ad nauseum: “Natural selection, though, adds no information.”

    Elephant hurling, Allen, only produces a lot of big excrement.

    Here is a parallel to your article:
    The rainforest fly Drosophila birchii likes living in, not surprisingly, rainforests, where the air is humid and everything is nice and moist.

    But Australia ’s pockets of tropical rainforest are becoming more fragmented by land clearing for roads, agriculture and urban development. Increasing penetration of drier air from outside alters the ‘microclimate’ inside the rainforest—particularly humidity.

    So scientists decided to test Drosophila birchii in the laboratory to see how quickly this rainforest fly would be able to adapt to a drier environment.

    They exposed flies to a dessication (drying) stress until 80 to 90% had died, and then bred from the survivors. But the offspring were no better than their parents at surviving drier-than-normal conditions. With mounting surprise, the researchers repeated the process—for 30 cycles over 50 fly generations—but still no increase in dessication resistance.

    The astonished researchers thought something must have gone wrong with that particular batch of D. birchii flies. After all, when the lab tested other species of Drosophila from less humid environments—D. melanogaster, D. simulans and D. serrata—they saw a two- to five-fold increase in dessication resistance.

    Even after dry-stressing fresh batches of the flies from four separate rainforest populations, the researchers noted that ‘the most resistant population lacks the ability to evolve further resistance even after intense selection for over 30 generations’.

    As other evolutionists have commented, this was ‘a complete surprise’. For IDists, this is a classic example of the built-in limits to genetic variation.

    Evolutionary theory claims that life arose by a process which is ultimately creative, and virtually without limits.

    When researchers found that a rainforest fly was unable to adapt to drier conditions, it was ‘a complete surprise’: Natural selection eliminates genes, it does not create new information.

    This is most noticeable in extreme environments, e.g. in dry conditions, flies that lose body moisture too quickly will die out and, without offspring, their genes will be lost from that population. But in a wet rainforest environment, there’s no advantage in conserving body moisture; what’s needed is just the opposite—the ability to withstand high humidity and the rampant diseases which thrive in such conditions. Hence Drosophila birchii populations have become highly adapted to life in the rainforest, but it has come at a cost. The price paid for such specialisation is the permanent loss of genetic information useful for survival in a drier environment.

    In contrast, the Drosophila flies from intermediate (less humid) environments, D. melanogaster, D. simulans, and D. serrata, still contain sufficient genetic variation to enable the population to adapt to drier conditions.

    So, what we have here is not evolution, just natural selection. Not a creative, limitless process, but one of culling genes already in existence.

    As Jerry notes, you aren’t able to answer the question asked: microchanges that aren’t moving to macro. I am amazed that you – in a position of educating the future – is incable of registering this fact.

    Just give us one “of your thousands” that show us the pathway of macroevolution.

    I asked for your ‘A’ game. Where is it?

    Do we have to go through your “thousands” and still continue to show you that it is microevolutionary in nature; that the mechanisms of natural selection do not provide new information; and that your science is more about faith than evidence!

  88. 88
    Joseph says:

    The mechanism the designer may have used is spelled out in “Not By Chance” by Dr Lee Spetner:

    “Built-in responses to environmental cues”.

    And as I have already stated the only way to demonstrate that is by actually learning to read the genetic programs.

    However to date the only genetic program readers are the organisms we observe.

    And exactly how is saying “genetic accident” in any way scientific?

    IOW how can it be demonstrated tat every mutation is an accident? That is besides our ignorance…

  89. 89

    In #85 jerry wrote:

    “Remember we do not deny these changes take place and sometimes have some beneficial effects.”

    If “we” includes aussieD, then yes, you do. I was specifically asked to present evidence that natural selection (which, as I have pointed out, includes the various “engines of variation”) can produce new genetic information. I did so, and apparently did so conclusively, as your tactic was to change the subject to macroevolution. On that subject, let me refer you to a recent post at my blog:

    http://evolutionlist.blogspot......dence.html

    In it, I provide exactly what you are asking for: examples and mechanisms of macroevolution, as discovered and elucidated by evolutionary biologists. And yes, I use the definition of “macroevolution” used by scientists who do the research.

    So, please provide me with examples and macroevolution via “intelligent design”, and so that we can all see the differences between what scientists do and what “intelligent design theorists” do, please include the mechanisms by which the Intelligent Designer has brought about the examples that you have provided. That way we can “play by the rules of science” in which evidence for mechanisms is part of the argument, rather than arguing via unsupported assertion.

  90. 90

    In #87 aussieD wrote:

    “Evolutionary theory claims that life arose by a process which is ultimately creative, and virtually without limits.”

    The first half of this assertion is correct, but the second half is not. On the contrary, evolutionary theory is quite clear that there are multiple limits on what can be accomplished via the various mechanisms that produce phenotypic change. Indeed, this is the crux of the argument that evolution (and especially macroevolution) is an historically contingent process. There are many examples in evolutionary biology of cases in which “you can’t get there from here”. That is, the particular genetic and/or phenotypic resources of a population do not include a characteristic that would allow for the exploitation of a new adaptive zone, so that no matter how beneficial a particular change might be, it simply doesn’t happen.

    This is clearly the case with the example you cited of Drosophila birchii. Indeed, the example you chose illustrates the point I just made quite well (and undermines yours). As you pointed out,

    “…the Drosophila flies from intermediate (less humid) environments, D. melanogaster, D. simulans, and D. serrata, still contain sufficient genetic variation to enable the population to adapt to drier conditions.”

    Exactly; these three species had evolved in environments in which dessication stress was a periodic threat, and so they had either gained or retained the genetic ability to respond to it. This was not the case with Drosophila birchii, which either lost the ability to do so, or never had it to begin with (without a complete scan of its genome, it would be difficult if not impossible to say which).

    And so, faced with the validity of my example in response to your question (and recognizing that your own examples provide even more evidence for precisely the point I was making), you (like jerry) switch questions on the fly. Now the question is not “can natural selection (a microevolutionary process) produce new genetic information?” The answer, for which you have yourself provided evidence, is “yes”. So, having given up that point, you switch to a completely different question: “Okay, so microevolution can produce new genetic information (and new phenotypic adaptations to environmental stresses, as pointed out in your examples). It still can’t produce macroevolutionary changes.”

    Note that this is an assertion, not an argument. You have presented no evidence that macroevolution can’t do this, nor have you presented evidence in support of an alternative explanation for macroevolution, nor have you attempted to provide any plausible (and empirically testable) mechanism by which this can occur.

    Rather than repost the same examples and evidence over and over again, I simply refer you to the link posted in comment #89, above. And, like jerry, would you be so kind as to provide us with examples of macroevolution that are unambiguously the result of “intelligent design”? And, so that we can all see the differences between what scientists do and what “intelligent design theorists” do, would you also please include the mechanisms by which the Intelligent Designer has brought about the examples that you have provided? Thank you!

  91. 91

    In #88 Joseph asked:

    “…how can it be demonstrated that every mutation is an accident?”

    There are several ways to do this. Probably the most effective way to do so is to compare the sequence in question with other sequences from organisms in which this sequences is either not present, or present in a different form. In almost all cases, such comparisons have shown that something like the “new” sequence (i.e. the mutation) is present in other organisms, but in a different form (i.e. some of the sequences are different):

    • the mutant sequences have different bases in specific locations, which indicates that the mutation is a point mutation, such as a substitution, insertion, or deletion

    • the mutant sequences are in a different order, indicating that the sequence was inverted during replication

    • the mutant sequences include relatively long sequences that can be correlated with similar sequences located elsewhere in the genome, indicating that retrotransposition, translocation, or viral transduction has taken place.

    All of these can be verified using statistical analysis, as developed by evolutionary geneticists over the past few decades. If you are interested, I could provide some references to textbooks in which these methods are explained and their uses (including their advantages and shortcomings) are discussed.

  92. 92
    jerry says:

    “would you also please include the mechanisms by which the Intelligent Designer has brought about the examples that you have provided? Thank you!”

    Allen, I already answered this. Se #83 on synthetic biology.

    Allen, I have told you in #52, we are your choir. Nothing you present to us has ever undermined ID. And we continually thank you for your examples and references.

    The book by Vrba and Eldredge so far has supported ID even though it is on macro evolution because there is no hard evidence in it on how macro evolution took place, only speculation. The book by Jablonka and Lamb also heavily supported ID because they could not provide any information on macro evolution either. Lots of stuff on micro evolution and it was good stuff. So we thank you for all these references supporting ID.

    Every time you fail to provide empirical evidence for macro evolution (what we call macro evolution or call it mega evolution if you wish) it is support for ID.

    The logic is inescapable. Either a study supports ID, is neutral to ID, or undermines ID. So far all of your examples have been the first two and mostly the first. The one above by Brookfield supports ID.

  93. 93
    bFast says:

    Allen_MacNeill:

    In almost all cases, such comparisons have shown that something like the “new” sequence (i.e. the mutation) is present in other organisms, but in a different form (i.e. some of the sequences are different)

    Would you say that is also the same with the human HAR1F gene. It differs by a mere 18 nucleotides, but is mutated compared to the ultra-stability found in all other vertibrates. Experiments done with bacteria seem to support Behe’s suggestion that even three simultaneous mutations simply won’t happen by chance. Eighteen non-contiguous mutations is far more than chance can account for. The ultra-stability of the gene should be very strong evidence that any one point mutation will be deleterious.

  94. 94
    PaV says:

    Allen: I await your response to my post above [51].

  95. 95
    Joseph says:

    “…how can it be demonstrated that every mutation is an accident?”

    There are several ways to do this. Probably the most effective way to do so is to compare the sequence in question with other sequences from organisms in which this sequences is either not present, or present in a different form. In almost all cases, such comparisons have shown that something like the “new” sequence (i.e. the mutation) is present in other organisms, but in a different form (i.e. some of the sequences are different):

    But that doen’t mean the new sequence occurred by accident.

    • the mutant sequences have different bases in specific locations, which indicates that the mutation is a point mutation, such as a substitution, insertion, or deletion

    OK I will grant that point mutations can be attributed to a genetic accident.

    But insertions and deletions are another matter.

    • the mutant sequences are in a different order, indicating that the sequence was inverted during replication

    Still doesn’t make it an accident.

    I would expect individuals to be different because individuals are affected by different epigenetic events.

    • the mutant sequences include relatively long sequences that can be correlated with similar sequences located elsewhere in the genome, indicating that retrotransposition, translocation, or viral transduction has taken place.

    That still doesn’t make it an accident.

    Dr. Spetner discussing transposons:

    A transposon has in it sections of DNA that encode two of the enzymes it needs to carry out its job. The cell itself contributes the other necessary enzumes. The motion of these genetic elements to produce the above mutations has been found to a complex process and we probably haven’t yet discovered all the complexity. But because no one knows why they occur, many geneticists have assumed they occur only by chance. I find it hard to believe that a process as precise and well controlled as the transposition of genetic elements happens only by chance. Some scientists tend to call a mechanism random before we learn what it really does. If the source of the variation for evolution were point mutations, we could say the variation is random. But if the source of the variation is the complex process of transposition, then there is no justification for saying that evolution is based on random events.

    And BTW the way evolutionary biologists define macro-evolution not even YECs dispute it.

    Also it carries an ambiguity- that of “species”.

    1- You are using something that NO ONE disputes to try to settle a dispute.

    2- Even your use is ambiguous because “species” is ambiguous.

  96. 96
    ShawnBoy says:

    What an absolutely phenomenal post by AussieID at #75. Bravo! The Ivy League professor’s response? Pretend it never happened, copy and paste another questionable finding, and end his ranting with the child-like “I can do this all day”. You’re better than that Mr. MacNeill……I think.

    Darwinists, here’s your problem – when you twist every finding in a way in which it’s concluded to support Darwinism – even when it does not (Liars For Darwin) – it’s not hard for the highly educated I.D. supporters to take you to school over it. Post #75 for example, or the majority of posts from DaveScot, BarryArrington, kairosfocus, and many, many more regular contributors here.

    Why I’m on the subject, why is it Darwin supporters are so reluctant to publicly debate IDists? The cop-out rational explanation I’ve seen most often is that they don’t want the public to think there’s a controversy. Here’s my problem with that: according to a recent Gallup Poll, no less than 80% of the U.S. public supports I.D. (whether they know it or not) while just 14% agree with Darwinism. If you feel your argument is so strong that it’s necessary to mercilessly insult anyone who disagrees with it, as Darwinists do, then surely you have enough confidence to publicly debate it, educate the “ignorant” public, and chip away at that 80%?

    I can’t help but think there’s another reason for your reluctance to publicly debate Darwinism vs I.D., and after studying said debate for the past year or so, I’m pretty sure I know what it is (think K.F.C.).

  97. 97
    ShawnBoy says:

    A couple of comments on my last post. That should be while not why, and cop-out should have a strike through it. It showed up o.k. in the preview yet for some reason it didn’t go through with the post. Oh well, no big deal.

Leave a Reply