I See Red (not quite protein-protein binding)

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There is a wonderful article in todays issue of Nature on bioluminescent organisms in the deep seas. We like to think of the deep seas as dark, since virtually no light filters into the abyssal depths from above. However, the deep sea abounds with bioluminescence, bacteria and sea life of all sorts glow gently in the depths, enough to seriously hamper the Antares deep sea neutrino telescope that is searching for the flashes of light the represent the rare interactions of neutrinos with other matter (subscription required).

As fascinating as bioluminescence is in its own right, the article links to an amazing paper. One that puts yet another dent (if that is possible) in Dr. Behe’s key thesis; that multi-amino acid binding sites are difficult to evolve. But how does the ability of a fish to see red refute a central argument of Dr. Behe’s “Edge of Evolution”

In the abyssal depths, most fish (and other organisms) are sensitive to blue light, as red light is heavily absorbed by the depth of water overhead. In fact, most are blind to red light, a fact that marine biologists use to observe deep sea denizens unobtrusively, by illuminating the study area in red light. However, some organisms have evolved to take advantage of this red blindness. Some species of befanged dragon fish have developed red bioluminescence, which allows them to see, but remain unseen, in the dark depths.

One of these dragonfish species is even more remarkable, in that it has no red sensing pigment itself, but uses bacteriochlorophyll to harvest the red light. Chlorophyll is the pigment plants and many bacteria use to capture light for photosynthesis. How dragonfish acquire this chlorophyll is not clear at the moment.

Right now you are scratching your heads and saying, “Alright, that’s pretty amazing, but how does dragonfish seeing with chlorophyll have any bearing on Behe’s claim that protein-protein binding sites are hard to evolve?”

Proteins bind to each other by matching up knobs and depressions on the proteins surfaces, in much the same way that a key fits into a lock. It is a bit more complicated to be sure, as well as matching shapes, the amino acids that makeup the proteins surface cam be neutral, charged or oily, and these properties have to match as well. Also, both the lock and the key are “floppy” as proteins are flexible and can (and do) move and flex so that what you think are not complementary shapes can flex into shapes that bind. Nonetheless, the lock and key analogy is helpful to visualize proteins binding to each other.

lock&key.gifLock and Key binding using the small molecule adrenaline as an example

Now, where does chlorophyll fit in? The above lock and key model is also valid for binding of small molecules. Everything I said about protein-protein binding applies exactly to protein-small molecule binding. Small molecules have to fit the shape, charge and “oilyness” of the protein “lock” too,

Dr. Behe claims that at least 3 or more amino acids must be mutated simultaneously before a partner protein can bind to another protein with high affinity (and a selectable activity). The same should hold for small molecules as well, if Dr. Behe’s assumptions are true, as most bind to proteins in special pockets to three or more specific amino acids. So, if Dr. Behe’s claims are true, then we would expect it vanishingly unlikely for any random small molecule to bind with reasonable affinity to a protein and result in a selectable activity. This is where chlorophyll comes in.

bacteriochlorophyll.jpgheme.pngChlorophyll (top) and Heme (bottom)

Chlorophyll is a copper magnesium containing molecule[1] that is similar to the iron containing heme molecule; the oxygen-binding component of haemoglobin. When red cells break down, there release their heme. Free heme is mildy toxic, and the body has fairly efficient ways of getting rid of it. You can also imagine that there is selection against heme binding for those proteins that don’t actually use it (such as haemoglobin and other enzymes that use iron as a catalyst), clamping a mildly toxic compound to the outside of a protein is not a good survival plan. So one would expect that the surfaces of non-heme proteins would be under selection pressure to avoid binding heme like molecules like chlorophyll. Wouldn’t you?

To determine how chlorophyll works as a visual pigment, researchers injected mice with a water soluble metabolite of chlorophyll (see the free online paper ). Remember, chlorophyll is a plant pigment that is alien to the tissues of vertebrates. This molecule was not only selectively taken up by the eye, but was concentrated almost exclusively in the retina, in the pigment layer.

And that’s not all; the injected mice were now able to respond to red light! The chlorophyll metabolite was acting as a visual pigment, harvesting light and passing the energy on to the visual pigments of native mouse photoreceptor cells.

Chlor_Rhod_comp.jpgComparison of the structure of the bacterial chlorophyll binding protein and Rhodopsin, the mammalian visual pigment

In order to transfer energy to the visual pigment protein, the chlorophyll must bind to it. Now, the diagram above shows the bacterial protein that normally binds chlorophyll, and the visual pigment protein. You can see immediately that they are very different proteins (one is like a clamshell, the other a tube, and the visual pigment, rhodopsin, is not a heme binding protein). The coordinating amino acids that bind chlorophyll in the bacterial protein (or the plant protein for that matter) are absent in the visual pigment protein, so it’s not a case of chlorophyll binding to a similar molecule and doing what it did before.

So, in the absence of any mutations, a small molecule that needs to bind to multiple amino acids of a protein in a distinct orientation to work, can bind to a completely different protein, unrelated to its normal binding partner in a species that never normally sees this small molecule in its tissues and provide a selectable function, right off the bat.

That is astounding. According to Dr. Behe’s arguments (which apply equally well to small molecule-protein interactions as to protein-protein interactions), this sort of interaction is vanishingly unlikely. Yet we see it. This shows once again that Dr. Behe’s arguments about binding and selectability are fatally flawed.

It’s enough to make an ID supporter see red.

[1] Yeah, major dimness attack, I could even see the magnesium ion in my own diagram!

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Dear Gentle Readers: At the bottom of this essay, I’m collecting links to reviews of Behe’s book The Edge of Evolution, replies to reviews and so forth. Well, now the burden is off me, and I can devote my book-reviewing time to good books,... Read More

40 Comments

Great post, Ian!

Irreducibly complex pigments have made Behe Blush Before (in principle, anyway).

Cheers & salutations, Dave

trivial-error nazi mode again:

Chlorophyll does not contain copper, as you state; it contains Magnesium (as shown in your illustration).

Otherwise, a fascinating post. Light-trapping pigment from a completely different branch of the tree, preferentially sequestered in the retina! Whood’a thunk it?

Ian, the binding doesn’t seem all that unlikely, since rhodopsin contains the cofactor retinal, which has a similar hydrophobicity to the long hydrocarbon tail of chlorophyll. What is astounding is that the absorption of light by chlorophyll can bring about the same conformational change in rhodopsin as does retinal when it isomerises in response to light absorption. This conformational change then triggers the signalling cascade that initiates a nerve impulse.

In a similar vein, proteins can form quite specific interactions with other proteins that do not encounter each other in their normal environments. A good example of this is when a (recombinant) mammalian protein is expressed in bacteria. Occasionally, a host cell protein will co-purify with the recombinant protein. Sometimes, the interaction between the bacterial protein and the mammalian one is so strong that it becomes a significant challenge to purify the recombinant protein without the bacterial protein associated with it.

In these cases, although I am not sure how much work has been done to look into these interactions (we do not have a very good library where I work), the interaction is so persistent that it almost has to be specific binding. Thus, this is a case of two random proteins forming a specific interaction with one another due simply to their individual surface chemistries, without the requirement for any mutations at all.

So, while you make the point that proteins need to adapt to avoid binding small molecules that would confer a disadvantage to the function of the protein, there are also examples of proteins that need to be adapted to avoid binding to other proteins where the interaction would be disadvantageous. Which makes Behe’s incredulity of specific protein-protein interactions all the more ludicrous.

Hmmm, reading that back I’m not sure I’ve been very clear, but I hope the core point gets across.

Quite true Nigel. One interesting aspect of protein evolution that is, of course, always overlooked by the ID/Creationist crowd is that in terms of binding, and even enzymatic reactions, proteins pretty much always carry out spurious side reactions/bindings to greater or lesser extents depending on concentrations of protein/binding partners/substrates, etc. One thing that we are quite certain has happened in many cases is where we can look at a protein family that has evolved through gene duplication and divergence. The common ancestor was more flexible and loose, carrying out many reactions with some specificity. As duplicates accumulate then individual duplicates, through mutation and selection, are refined for individual reactions, binding conformations, etc.

Of course this is coupled with other methods of duplication and divergence schemes were new functions are evolved in their entirity. Evolution isn’t always about gaining enw complexity but in many cases about reducing interactions and reactions and refining one of many strategies.

That’s really astonishing- I would never have expected immediate function like that.

Cue creationist claims of front-loading in 3…2.…1.…

Absolutely amazing. This makes me wonder about life on other worlds, perhaps on some of the gas giant moons or Mars. If life on this planet is driven to explore such extremes, then surely evolution must be no less relentless elsewhere in the universe.

So if we find life beyond Earth, we should expect it to display a similar (allowing for differences in its home environment) depth and breadth of diversity, function and adaptation.

One of our local creationist gadflies is always yammering, along the lines of finding “John Loves Mary” written in the sand, that

Information in genetic code cannot be explained from naturalistic factors. … Complex specified information (CSI) is, without exception, always observed to be generated by intelligent agents.

Ian has provided a striking counter-example. I discuss what this kind of flexibility would look like in English here.

Cheers, Dave

How come we don’t all have chlorophyll in our visual systems already? It seems that it would have been useful during the cretaceous, when mammals were sneaking around in the dark to avoid the dinosaurs.

Of course, if evolution has to proceed by individual, viable steps, it makes sense that a chemical that’s never been found in the vertebrate line would not suddenly appear. But if evolution is under the control of an Intelligent Designer, why wouldn’t he have done something useful, like give us night vision, instead of harrassing us with chloroquinine-resistant malaria?

Not entirely on topic, but a couple of interesting upcoming papers concerning proteins and evolution:

http://www.biomedcentral.com/conten[…]509-1-49.pdf

http://www.biomedcentral.com/conten[…]807-7-79.pdf

The hoary puccoon questions: “But if evolution is under the control of an Intelligent Designer, why wouldn’t he have done something useful, like give us night vision, instead of harrassing us with chloroquinine-resistant malaria?”

If the Designer is Popeye then you have your answer. Eating your spinach would provide large quantities of chlorophyll. The problem arises in chlorophyll metabolism. The types and quantities of chlorophyll metabolites available for uptake by the human retina would take some further research.

Delta Pi Gamma (Scientia et Fermentum)

hoary puccoon said: “How come we don’t all have chlorophyll in our visual systems already?”

IANAB, and my question is, where do the deep-sea fish encounter chlorophyll? (Probably differently from rabbits, who, as everyone knows, don’t wear glasses because they eat all the carrots on their plates.) Before you can bind to something, you have to obtain it in a form that you can use.

Even though binding may be easy, the alarm bells go off when Ian says: “Remember, chlorophyll is a plant pigment that is alien to the tissues of vertebrates. This molecule was not only selectively taken up by the eye, but was concentrated almost exclusively in the retina, in the pigment layer.” I can visualize an IDer crowing: “Look! A perfect example of a design event! Gthe designerod put the chrolophyll in the fish for the express purpose of giving them night-vision goggles. QED.”

Olorin Wrote:

IANAB, and my question is, where do the deep-sea fish encounter chlorophyll? (Probably differently from rabbits, who, as everyone knows, don’t wear glasses because they eat all the carrots on their plates.) Before you can bind to something, you have to obtain it in a form that you can use.

IIUC, chlorophyll in the deep sea is available from both dead phytoplankton and bacteria (bacteria also make chlorophyll).

From Ian’s post:

Ian Musgrave Wrote:

[the dragonfish] uses bacteriochlorophyll to harvest the red light. Chlorophyll is the pigment plants and many bacteria use to capture light for photosynthesis. How dragonfish acquire this chlorophyll is not clear at the moment.

So it seems that the dragonfish have no mechanism whereby they can synthesise the bacteriochlorophyll, so they must acquire it from their environment. But how they do so is a mystery. Isn’t science wonderful?

“If the Designer is Popeye …”

I yam what I yam, and that’s all that I yam. ; }

Jeh offers a Designer quote: “I yam what I yam, and that’s all that I yam. ; }”

That could be construed as a take off on scripture. Remember Intelligent Design is not about religion, it is about cartoons. By proposing Popeye as the Designer I am merely suggesting a possibility. Its testability lies in developing a series of hypotheses about the nature of the Designer and then testing these against known information about Popeye, in other words watching cartoons. For example, the problem of “who designed the designer” is easily addressed in Popeye cartoons.

Delta Pi Gamma (Scientia et Fermentum)

I don’t know about the Popeye hypothesis, Bruce. While the absence of canned spinach during the cretaceous era is a plausible explanation for why we don’t have chlorophyll in our eyeballs, your whole approach seems MUCH too rational for Intelligent Design.

Nigel D wrote:

Ian, the binding doesn’t seem all that unlikely, since rhodopsin contains the cofactor retinal, which has a similar hydrophobicity to the long hydrocarbon tail of chlorophyll.

Except in the experiments, it was a chlorophyll metabolite, chlorin, which was used. Chlorin lacks the long hydrophobic tail, yet can still bind and transfer energy to the visual pigment, so it can’t just be mimicking retinol. I’m still amazed by this.

Your other points are well taken Nigel, but these are the sorts of interactions Behe specifically excludes (I know it’s silly, but see EoE chapter 8 and the Open Letter thread , esp Open letter 6).

hoary puccoon wrote:

How come we don’t all have chlorophyll in our visual systems already? It seems that it would have been useful during the cretaceous, when mammals were sneaking around in the dark to avoid the dinosaurs.

Mammals developed high sensitivity black and white vision instead. The whole preferable extinction of red light is only relevant in water. At night in terrestrial environments all wavelengths are reduced. Also, reptiles aren’t red blind (not that they can see red as the colour red, just that red photons will stimulate their visual systems), so developing red searchlights with red sensitive vision to go with it isn’t as useful in a terrestrial night environment as it is in the deep sea. Some vertebrates have developed infrared sensitivity though and use that for hunting (pit vipers etc.)

The hoary puccoon said: I don’t know about the Popeye hypothesis, Bruce.

I was just trying to generate a reason for watching old Popeye cartoons. Framing my excuse as a testable ID hypothesis seemed the simplest way to approach the problem. If a useful paradigm could be developed along the way that illustrates the inadequacies of ID so much the better. It is a trivial matter to generate a hypothesis but a vast majority of hypotheses are easily tested and discarded. ID is short on hypotheses which should not be a problem for a new active area of research. A well constructed and testable hypothesis take work, something ID seems short on.

Delta Pi Gamma (Scientia et Fermentum)

You don’t need specific binding to rhodopsin. This is probably excitonic energy transfer; it happens over quite a long distance; as long as the chlorins partition into the rod cell membrane, which is plausible, they probably can do the transfer.

It’s an interesting paper, but it doesn’t prove what you want it to prove: i.e. specific chlorin-rhodopsin interaction.

Ian Musgrave Wrote:

Except in the experiments, it was a chlorophyll metabolite, chlorin, which was used. Chlorin lacks the long hydrophobic tail, yet can still bind and transfer energy to the visual pigment, so it can’t just be mimicking retinol.

Ian, thanks. I seem to be learning more with every comment here.

Gerard Harbison Wrote:

You don’t need specific binding to rhodopsin. This is probably excitonic energy transfer; it happens over quite a long distance; as long as the chlorins partition into the rod cell membrane, which is plausible, they probably can do the transfer.

And more learning still. Thanks to you too, Gerard.

Except about Popeye - he is merely a tool of the true designer, Olive Oyl. Hence the lack of canned spinach in the Cretaceous (and I think you’ll find a lack of canned spinach throughout the Permian, Triassic and Jurassic, too). :)

Nigel D concludes: Hence the lack of canned spinach in the Cretaceous (and I think you’ll find a lack of canned spinach throughout the Permian, Triassic and Jurassic, too). :)

I think with some careful thought you will realize that the cations required for proper functioning have to come from somewhere. Well they leach out of the can of course (pirouette, sidestep, ignore physiology). My testable hypothesis is that paleo spinach cans will be found in the fossil record. In some obscure shale layer little fossil imprints of spinach can labels lie waiting to be uncovered confirming Popeye as the Designer. It’s not too late to pay homage and watch Popeye cartoons, it is certainly more enjoable than watching Dembski narrated cartoons.

Delta Pi Gamma (Scientia et Fermentum)

Gerald Harbison wrote:

You don’t need specific binding to rhodopsin. This is probably excitonic energy transfer; it happens over quite a long distance; as long as the chlorins partition into the rod cell membrane, which is plausible, they probably can do the transfer.

Firstly, chlorin is water, not lipid soluble, so you will not get significant lipid partitioning (yes, I checked the Rf values). Secondly, even if it was substantially lipid soluble, without specific binding to the photoreceptor pigment, chlorin would be present equally in all cell membranes throughout the body, not specifically bound to the photoreceptor layer (it is very dramatic in the microscope images). As well, in photosynthetic systems, the excitonic transfer is from chlorophyll directly to a protein that is binding the chlorophyll closely, no lipids involved.

So the evidence is that it is binding to the rhodopsin.

Curses, I misread a part of Gerard’s comment. I was taking it as specific binding to the protein (but not necessarily in the same pocket as retinal), not as partitioning into the membrane. Of course, Ian is correct in his responses there.

If the chlorin binds to the protein in any kind of specific or preferential way (and thus becomes concentrated within the same regions of the body and of the cells in those tissues) then nonspecific electron transfer may indeed play a role. Otherwise, it could not initiate the visual transduction cascade.

Thus, either the chlorin is binding specifically to the protein but is effecting nonspecific electron transfer to bring about the conformational change in the protein, or the chlorin is genuinely mimicking the role of retinal, and is bringing about a specific conformational change in the proetin in response to absorption of a photon of red light. Cool!

Ian Musgrave Wrote:

Firstly, chlorin is water, not lipid soluble, so you will not get significant lipid partitioning (yes, I checked the Rf values).

Rf? The chromatographic mobilities? What solvent, who stationary phase? Do you mean the octanol water partition coefficients? Funny you didn’t cite the work.

In the paper you cite, the chlorin was extracted 3:1 chloroform-methanol, a very common solvent cocktail used for lipids, and immisicble with water. Chlorin-e6 has a hydrophilic edge and a hydrophobic edge, and therefore likely sits in the membrane with the carboxyls interacting with the headgroups and the ring system and hydrophobic sidechains buried.

Of course, there is also copious experimental data for partitioning into lipid membranes. I don’t have access to more than most of the abstracts until Tuesday (I’m away from my department), but I can get PNAS.

http://www.pnas.org/cgi/reprint/88/[…]0.pdf?ck=nck

This paper shows unconjugated chlorin-e6 localized in the nuclear membrane, the cell membrane, and the mitochondria. And I quote:

Fluorescence of unconjugated Ce6 is present diffusely in most cellular membranes in a pattern similar to that of porphyrins (38); the localization of unconjugated Ce6 within membranes is consistent with its reported lipophilicity (37).

In the paper you cite, they showed localization in the outer and inner segment layers, but that’s likely because photoreceptor outer segments are just chock full of lipid membranes.

http://en.wikipedia.org/wiki/Photoreceptor_cell

The partitioning of chlorin-e6 into membranes has been well-known for 20 years.

Nigel D:

Curses, I misread a part of Gerard’s comment. I was taking it as specific binding to the protein (but not necessarily in the same pocket as retinal), not as partitioning into the membrane. Of course, Ian is correct in his responses there.

If the chlorin binds to the protein in any kind of specific or preferential way (and thus becomes concentrated within the same regions of the body and of the cells in those tissues) then nonspecific electron transfer may indeed play a role. Otherwise, it could not initiate the visual transduction cascade.

Thus, either the chlorin is binding specifically to the protein but is effecting nonspecific electron transfer to bring about the conformational change in the protein, or the chlorin is genuinely mimicking the role of retinal, and is bringing about a specific conformational change in the proetin in response to absorption of a photon of red light. Cool!

Nigel

Visual transduction has nothing to do with electron transfer. 11-cis retinal is covalently bound to apo-rhodopsin; there are no aldehyde groups on chlorin-e6 to allow similar covalent binding, and its shape is utterly different, so it’s highly implausible that it could bind to the same site. There is no evidence - nada - in the paper for specific binding of chlorin-e6 to rhodopsin. The paper shows is that within the retina it localizes in a tissue layer that has stacked sheets of lipid membranes; and it’s already known to bind to lipid membranes (see citation in my previous comment).

re: copper

perhaps you were thinking of vegetables cooked in copper kettles, where the magnesium atom is replaced by copper and the green color is more resistant to fading in low ph

The link provided to the paper is dead (at least to me). Can someone post the citation in conventional format? thanks,

You guys are taking Behe’s words out of context. He excluded external proteins in his argument. They fall under a different category from the edge of evolution. For Darwinism to be true any advancement would have to take place without the help of other organisms. Symbiotic relationships always help the argument for design. Your illustrations aren’t 3D therefore only hint at the complexity of shape space, and in matching up proteins for binding. When two organisms come together for a purpose then it’s design. Some of you guys are just discussing minutiae, and not contributing to the larger discussion.

For Darwinism to be true any advancement would have to take place without the help of other organisms

Why would common descent depend on organisms never getting help from each other?

Why would accumulation of beneficial mutations depend on the organisms never getting help from other species?

Why would genetic drift depend on species never getting help from other species?

Since the answer to all those is “it doesn’t”, what aspect of current evolutionary theory implies that species never help each other? (Hint: it doesn’t.)

Henry

What aspect of evolutionary theory implies that species never help each other? Creatures helping each other is not an example of evolution. Evolution is creatures changing into something else thru random genetic mutations. Natural selection is more closely related to living things helping each other to survive. A bird finding a bee nest, and screams so that the badger can find the nest to eat its honey. Animals helping man to plow his fields, track his prey, or guard his camp etc. These examples may help the creature to survive, but are independent of evolution. Natural selection could play a role in evolution if there were really some major changes occurring in the cells, but there isn’t. That is one of the points that Behe’s book makes. Observing Malaria, HIV, and E. Coli for almost 50 years, shows that even though they have had numerous genetic mutations, none of mutations have changed them. Accurate predictions can be made about evolution, and whether it has had any effect at all on life, because of the massive populations of the three organisms, and their mutation rates. Time therefore is irrelevant. The HIV virus genetic thumbprint is so small, that any mutations to that, would have a more significant impact on it evolving into something else, then some creature with millions, or billions of genes.

Creatures helping each other is not an example of evolution.

While not evolution per se, cooperation is one factor that affects what traits work better than other traits. Ergo, cooperation affects the results of evolution.

Evolution is creatures changing into something else thru random genetic mutations.

Incorrect. Or at least incomplete. Mutations by themselves merely increase variety present in the population.

A bird finding a bee nest, and screams so that the badger can find the nest to eat its honey.

Exactly! (Assuming that the bird gets something out of it, too - does it eat some of the bees? Or some of the honey?) Anyway, if that behavior benefits the bird, genotypes that have more of that behavior than their relatives would tend to spread.

Natural selection could play a role in evolution if there were really some major changes occurring in the cells, but there isn’t.

How so? Actually, not so. All it takes for natural selection to act is for one genotype to outproduce another in the same population. All that requires is for one genotype to produce a slightly different behavior, a slightly different proportion of some body part, a slightly different protein, or some other change that gives its carrier an edge in producing more descendants. A major change might cause evolution to proceed faster, but that isn’t a requirement for evolution to occur.

Maybe one of the resident experts can go into more detail on these points. (Or correct anything I might have gotten wrong.)

Henry

You really need to read BeHe’s latest book so I don’t have to answer every question myself. Again he shows that there is no change occurring in creatures. This is the scientific evidence, from studies done with Malaria, HIV, and E.Coli. When some one speaks of evolution it entails the dogma of all life coming from a single cell organism, or from a rock, or from the vacuum of space, whatever was here before the big bag. They also believe that the Big Bang is a product of evolution. Evolution is both a political movement, and a religious movement, that’s why its adherents fight so ardently in the face of impossible odds. Something doesn’t come from nothing. Also the creation of the universe shows fine tuning, without which there would be no life on earth. Taking small incremental steps, one mutation at a time in order to evolve life is impossible. It takes a completed created cell to make another complete created cell. ATP needs to be contributed to the ATP creating process, in order to make more ATP. Where did the first ATPs come from before the cell made ATP? Where did the info in DNA come from? etc.

Something doesn’t come from nothing.

OK, then where did all this life come from, if not “from nothing”? What’s your theory?

Alveno, you should find out what the theory of evolution is before spouting off about it. It has nothing to do with the Big Bang theory. It says nothing about the origins of life, about which there are indeed many questions.

Evolution is both a political movement, and a religious movement

There are conservatives, liberals, socialists, communists, libertarians and no doubt fascists who accept the theory of evolution. There are Christians, Moslems, Jews, atheists, agnostics, Shintoists, Buddhists and others who accept the theory of evolution. It is complete and utter twaddle to suggest it is a political and religious movement.

Have you read any of the reviews of Behe’s book by scientists? Read and think about them, and you will discover that Behe is wrong about many things. For example, he says that intraflagellar transport is required to make cilia, not realizing that his prime example, Plasmodium, does without. Remember, his book is a popular work, not a scientific publication and is not subject to the same level of quality control. He has never published this work in the scientific arena because he knows it will not withstand scrutiny by people are capable of assessing it.

You really need to read BeHe’s latest book so I don’t have to answer every question myself.

You should read textbooks to offset the effect of the propaganda you’ve been reading.

The problem is that your “answers” have already been refuted.

Most of them are probably addressed here: http://www.talkorigins.org/indexcc/index.html

If any of your claims aren’t addressed there, ask here and maybe somebody will answer it.

Henry

Oh boy, a whole new pile of misunderstanding to correct (or should that be “rectify”?).

Alveno Kondyles Wrote:

“What aspect of evolutionary theory implies that species never help each other?” Creatures helping each other is not an example of evolution.

No, not “an example” of evolution, but neither required nor precluded by evolutionary theory.

The real question, since you bring this up, is: why do you consider it to be relevant?

Evolution is creatures changing into something else thru random genetic mutations.

No, it isn’t. Evolution, as defined by evolutionary biologists, is the change of gene frequencies within a population over time (my paraphrase).

Over a large amount of time (e.g. tens of millions of years), this often results in gross morphological changes, but that ain’t necessarily so. The coelocanth, for instance, has changed little over the last 100 million years.

Why is this? Because it has not been subjected to any significant selection pressure. Evolutionary change mostly happens in response to changes in the organism’s environment. If the environment does not change significantly, why would the organism?

Natural selection is more closely related to living things helping each other to survive.

Quite the opposite. Natural selection arises as a consequence of living things competing for limited resources. If two organisms both benefit from helping one another, in terms of competing with the dozens of other organisms that occupy the same habitat, then coopoerative behaviour will evolve (e.g. an anemone living on the shell of a hermit crab, which is an example of commensalism, in which both organisms benefit from the relationship).

A bird finding a bee nest, and screams so that the badger can find the nest to eat its honey.

This is only an example of natural selection if both organisms benefit and are better able to compete as a consequence.

Are you citing this as an actual or hypothetical example?

Animals helping man to plow his fields, track his prey, or guard his camp etc.

These are examples or artificial selection. Humans intervene in the natural process by, for example, limiting the choice of mates available to dogs with particular traits that are desirable to the humans.

These examples may help the creature to survive, but are independent of evolution.

Not so. Artificial selection is an evolutionary process. How else could so many different breeds of dog arise from the natural ancestor in so short a time?

Natural selection could play a role in evolution if there were really some major changes occurring in the cells, but there isn’t.

No. This is just wrong. Natural selection is a mechanism of evolution: it can act upon any situation in which a selection pressure exists. The resultant changes are most often very gradual (requiring hundreds or thousands of generations to become obvious).

That is one of the points that Behe’s book makes.

And Behe’s book is wrong. Have you read any of the reviews of his book that were written by actual scientists?

Observing Malaria, HIV, and E. Coli for almost 50 years, shows that even though they have had numerous genetic mutations, none of mutations have changed them.

On the contrary, these mutations are the raw material upon which NS can act.

Remember that for malaria, 50 years is only 2 generations for one of its host species. And yet, we see chloroquine resistance arising in several populations, arising through different mutations, and occurring to different extents (although, very often, when weak chloroquine resistance arises, stronger chloroquine resistance is usually not far off).

For HIV, it has been shown that new biochemical functions have arisen. The various sub-types of HIV may well be on the way to becoming new species. Then again, the definition of “species”, especially among viruses, is entirely arbitrary. At what point do we draw the line and say “these two viruses represent different species”?

E. coli is well-adapted to its environment. The typical coli experiences very little selection pressure at all. And again, 50 years is only 2 generations for its host species, so why would you expect to see significant changes?

Accurate predictions can be made about evolution, and whether it has had any effect at all on life, because of the massive populations of the three organisms, and their mutation rates.

Not so. Making accurate predictions about the evolutionary path a population will take is fraught with difficulty. One would need to know every single relevant selection pressure that exists, and one would need to know every single interaction between the organism and its environment.

Time therefore is irrelevant.

If this is so, why do you mention mutation rates?

Anyhow, time is extremely relevant. Evolution is change over time. How could time not be relevant?

The most important point for evolution, however, is the presence or absence of selection pressure. Selection pressure leads to new adaptations arising withing a population. A very strong selection pressure may cause extinction of a population. A moderate selection pressure will cause gradual change. The absence of selection pressure still allows genetic drift, which causes change but is slower than evolution in the presence of a selection pressure. Opposing selection pressures may lead to sub-optimal, compromised adaptations (which is something we find in, for example, sickle-cell anaemia).

The HIV virus genetic thumbprint is so small, that any mutations to that, would have a more significant impact on it evolving into something else, then some creature with millions, or billions of genes.

Again, you demonstrate a misunderstanding of evolution. An organism does not evolve into “something else”. It evolves into its own descendents. What’s to say that the various subtypes of HIV are not already sufficiently different from one another that we could make a case for calling them separate species (in the which case we would have witnessed a sepciation event within about 20 years)?

Alveno Kondyles Wrote:

You really need to read BeHe’s latest book so I don’t have to answer every question myself.

I prefer to avoid meaningless drivel in my spare time, thanks all the same. I have read enough reviews and critiques of his book to have a good idea of the content.

Again he shows that there is no change occurring in creatures.

He shows no such thing. He claims it, but he has been shown to be wrong.

This is the scientific evidence, from studies done with Malaria, HIV, and E.Coli.

Studies that Behe deliberately misinterprets so that the conclusion he reaches fits with his preconceptions.

When some one speaks of evolution it entails the dogma

No. Not dogma. After all, science isn’t a religion, which is where we do find dogma.

of all life coming from a single cell organism, or from a rock, or from the vacuum of space, whatever was here before the big bag.

Make up your mind. Which creationist misprepresentation of evolutionary theory do you wish to discuss here? Are you saying all life came from a single-celled common ancestor, or from a rock, or from space? Because only one of these has anything to do with MET (modern evolutionary theory) and the others are creationist strawmen.

They also believe that the Big Bang is a product of evolution.

No-one believes this. Evolution is a theory of biology (that means living things, m’kay?). The Big Bang is a theory of cosmology (that means it deals with the universe). See if you can work out what the differences are.

Evolution is both a political movement

This is a lie. MET is science, entirely based on evidence and logical inferences from the evidence. It is apolitical.

, and a religious movement,

This is another lie. Actually, I’m starting to find this particular lie rather boring. It is trivially easy to prove it wrong, yet the creationists come up with it time after time.

that’s why its adherents fight so ardently in the face of impossible odds.

No. This is utterly wrong.

Supporters of good science fight to protect MET from lying creationists because they believe in many things, among which are such things as: (1) Freedom of speech; (2) Freedom of religious expression; (3) The ability of science to arrive at a consensual truth (i.e. conclusions obtained through science are the same for everyone); (4) The rights of high-school students to be taught good science as opposed to lying creationist pseudoscience garbage.

I could go on, but I can’t be bothered.

Something doesn’t come from nothing.

Well, I’m glad you agree that special creation is wrong. Now, tell us what you do believe in.

Also the creation of the universe shows fine tuning, without which there would be no life on earth.

Gosh, you really have swallowed the party line hook, line and sinker, haven’t you? (Please forgive the mixing of metaphors). Notice that the term “fine tuning” implies the existence of some active force or entity to carry out this tuning. What if the universe is the way it is through chance? How could we distinguish that from fine-tuning?

What’s that? We can’t? Then how can any claim of fine-tuning stand up to even casual scrutiny?

Your argument is one or personal incredulity, and it is a logical fallacy.

Taking small incremental steps, one mutation at a time in order to evolve life is impossible.

Oh, boy, you are a one for the big claims, aren’t you. Are you prepared to back up this whopper with any evidence?

Anything at all?

It takes a completed created cell to make another complete created cell.

Prove it.

Bear in mind that I could provide a recipe of the components for a bacterial cell. Many of these components are able to self-assemble and are available commercially from various suppliers of life-science research tools.

ATP needs to be contributed to the ATP creating process, in order to make more ATP.

Where did you get this nonsense from?

Someone’s been feeding you a line of prime BS, here. Why did you believe it?

Do you know what ATP is and how it can be produced in the first place, at all? Because if you don’t know this, then how can you possibly claim that it requires x or y or z for its formation?

Where did the first ATPs come from before the cell made ATP?

Irrelevant. There are plenty of other reactions that cells use to transfer energy from one process to another. If you had the faintest inkling of what you were talking about you would know this, or you would at least be considering it as a possibility.

For example, are you aware of NADH and FMNH2?

Where did the info in DNA come from? etc.

The question is meaningless unless you define what you mean by “the info[rmation] in DNA”.

Also, you need to be more specific. Do you mean the first DNA? If so, the answer is “we don’t know, but inquiring minds are investigating”. However, ignorance of one aspect of abiogenesis is irrelevant to MET, since abiogenesis is a separate field of biology.

Alveno, with this comment you are parading your ignorance as if it were something of which to be proud. It isn’t. If you are genuinely interested in the answers to your questions, then go and learn some actual biology from books written by actual scientists.

If, like so many other trolls, you don’t really want to know the answers, then at least respect the fact that the experts really do know what they are talking about.

To make an analogy, if you knew nothing about motor maintenance and you took your car to a garage where someone who has been working on cars for 20 years tells you your diff shims need replacing (and in fact, if you took your car to 7 different garages, and every mechanic told you the same thing), would you argue with them? No. You would either take their word for it, or go and learn enough about cars to understand it for yourself.

If you would accord such courtesy to motor mechanics, why can you not extend it to scientists, whose expertise is arguably deeper and more hard-won than that of any motor mechanic?

Alveno, one more point:

In what way do any of your comments address Ian’s post, in which he describes a counter-example that demonstrates that what Behe claims in EoE to be impossible really does occur?

One counter-example is all that is required to refute a claim of impossibility, but there are others.

Before the beginning there was nothing. There was not even the vacuum of space, since space didn’t even exist. Then all the mass, and energy that would ever exist spontaneously came from the nothing. Billions of years went by. Then the earth took form. Initially it was inorganic. Then spontaneously organic life came out of the rocks, minerals,water etc. That happened about 4 billion years ago. Gradually one nucleotide,one amino acid, one mutation at a time, life evolved. Until all the life that you now see came to be, including humans with billions of genes, and over 80,000 distinguishable proteins. Lets go in reverse. Human from bacteria via a googol of intermediate creatures, bacteria from inorganic elements, inorganic elements from Big Bang, and Big Bang from nothing.Therefore man came from a single cell organism via inorganic via Big Bang via Nothing. Man via Nothing.

I hope that I clarified for Nigel what I meant from the statement that “man came from a rock”. Life spontaneously coming from nothing is exactly what evolutionist believe? Right? I believe that something can not come from nothing! Therefore I must believe that a causative intelligent agent created everything. It’s only logical. One other thing. If everyone that Nigel trusts to feed him accurate info is as bias as he is, then Nigel better read the books himself. I read some comments about Coyne’s review of Behe’s book. I went to The University of Chicago web site to read his review myself. I now know that some comments were accurate, and some were in error.

[edited to fix bad html IFN]

I’m not convinved that the difference between a small molecule and a big one isn’t valid. It is a lot easier to stick a small piece of paper to a refrigerator with magnet, for instance, that a large pad. Maybe the chrlorophyll molecule isn;t really bound at all, just weakly attracted. To disprove Behe, you would have to find a three amino acid binding site on a protein that developes quickly.

gadfly Wrote:

It is a lot easier to stick a small piece of paper to a refrigerator with magnet, for instance, that a large pad.

This is where common sense falls down. At the scales we are talking about, proteins in water act more like like lumps of play-dough embedded in molasses. A small molecule and a large molecule have roughly the same ability to stick together in this environment (large ones even more so).

For rapidly developing binding sites, see the “open letter” thread referenced in the post to which you are replying.

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This page contains a single entry by Ian Musgrave published on November 22, 2007 12:08 AM.

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