Evolution of the Eye

There was a study once that I saw where they set up a GA to evolve an eye; they programmed in the ability to create a few types of components - transparent layers, light sensitive cells, etc. It started out with an eyespot, then developed a thin layer of transparent material, then the eyespot started to curve inward, then the thin layer began to form a lens... (etc). Each increment just happened to be positively correlated with better eyesight.I can probably track down the article if you'd like.------------------
"Illuminant light,
illuminate me."

Again, you need to be more specific. What interaction between rods and cones are you talking about? Are you talking about how a rod or a cone could evolve? Or how one type of cone could differentiate from another? Or the concept of rods, cones, and other parts of the eye evolving in tandem?We need specifics to be able to get you what you're looking for. ------------------
"Illuminant light,
illuminate me."

In short, he doesn't know what he's talking about, and decided to name some random parts of the eye and random chemicals to prove his point?Let's take a look at this. Vitamin A aldehyde acts as a light absorbing pigment. Of course, vitamin A is used all over the body, in - in the skin around bodily openings, for example. I'd be surprised if it took more than a few BP mutation to attach an aldehyde to a gene duplicate. I'm not sure what they're talking about concerning alcohol - are they talking about the effect of drinking on vision? If so, that's a neural issue. Which proteins is the person concerned about? Ospins, perhaps? Any protein that initially interacted with vitamin A in any manner could easily become an ospin - it just needs a new piece of functionality tagged on which causes it to trigger a response. Ospins from over 30 different species, from flies to humans have been examined. Guess what? The similarity between different ospins (as always) matched the evolutionary tree. There are analogues to the common segments between different ospins in bacteria which are unrelated to light detection - small mutations in these proteins made them trigger a response when the variant of vitamin A is triggered. The rod ospin has changed very little between species, while the cone ospins all seem to be variants of the rod ospin and of each other. Of course, *these too* follow the evolutionary tree. Cones are overall a clear progression from rods, and have since evolved from each other. The code sequence for red and green cones is almost identical. In some rare cases, women have been found with a fourth type of cone, between red and green - again, another duplicate-then-change genetic artifact. Some animals have many more; birds and turtles usually have 4 or 5. The mantis shrimp has an astounding 16 types rods/cones, invaluable in its bright coral reef habitat (they also can see polarized light, and can see well into the UV spectrum; their total count of distinguisable colors is believed to be about 10 times ours, and they can garner additional information from light via the polarization detection than we can).On the other hand, there is plenty of evidence that the design of the eye was not created. The rods and cones are aimed *backwards* (unlike the eyes of some invertebrates), making them less able to absorb light. This also means that the nerve fibers have to pass in front of the cells, blocking out more visual ability. The human eye only has one focal point, unlike many birds. Additionally, no eye has evolved to contain multiple lenses in front of each other, acting to enable zoom vision. If humans were to ever design sentient "robot beings", they almost certainly would have this simple and very useful add-on. However, there is no simple linear path to successive lenses in a row. I could go into all sorts of problems with the design of the eye, from the "blind spot" to the loose attachment of the sclera to the "upside down" orientation of vision. Mollusks, who took a different visual evolutionary path, do not have these problems. We've sort of dead-ended ourselves, unfortunately.It looks even worse when you look at other animals. Take the mole rat, for example. It has eye sockets, and optic nerves, which have been since rerouted for other tasks. There is a complete structure designed to hold an eye, which now contains a defunct glob of eye cells with skin grown over and into it. Why on earth would a designer do this?------------------
"Illuminant light,
illuminate me."[This message has been edited by Rei, 09-24-2003]

Hey, Fred! Have you ever actually read the paper by Dan Nilsson and Susanne Pelger ("A pessimistic estimate of the time required for an eye to evolve"), or are you just spouting out about an inaccurate summary you read? They didn't even spell Pelger's name right!In the paper, they outright admit that they are not attempting to simulate the inner workings of the cells. They provide the different types of tissues as a "given" - light receptive layers, transparent layers, etc. If this article's complaint is that they didn't go into how the cells work, the author is an idiot, because that was accepted as a given at the beginning of the paper.They *did* do their calculations on a computer. It wasn't a GA, but the caluclations were done by computer.The change from eye spot to fish eye took 1829 generations using 1% bends in components of the eyes, and never going to a more poorly adapted version. Do you think that 1% improvements is unreasonable?There final number (364,000) generations is assuming a very poor rate of a successful mutation sticking (1 in 200 chance).Despite the suggestion that Berlinski tries to put across, Nilsson and Pelger do *not* attempt to explain how the nervous system that interprets it, nor the individual tissues, develop (and function). They *do* show that there is a completely linear progression in eye shape from an eyespot to an eye. If you disagree, explain why. No hand waving.If you agree, we can move on to things that their paper did *not* go into, such as the wiring of the brain or the functioning of different tissues.------------------
"Illuminant light,
illuminate me."

Convergence is more of a problem for creation. If two organisms were "designed" for the exact same niche, how come they approach it in radically different ways, with traits that match up with a steady progression of animals from outside that niche in progressively different niches?The very fact that traits are retained along lines even as two species try to fill the same niche is a strong piece of evidence *supporting* evolution.------------------
"Illuminant light,
illuminate me."

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Wow, a beneficial mutation rate of 100%, and a deleterious rate of 0%. Very impressive!

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So, Fred, is their conclusion that an eye would evolve in around 1829 generations? What? It's not??? But they came to the conclusion that there were only 1829 1% modifications needed (of which some can occur in parallel). And, thanks to your wonderful ability to read context (of which I'm sure 3rd graders are envious over), you've come to the conclusion that they were using 100% beneficial mutations. So, my bright friend, how did they end up with a number of years *FAR* more than that?The answer is that they were only assuming a small rate of the genes fixing into the population, using a standard population genetics equation. Yes, they assume that in the long run, bad genes don't fix into the population as a whole. Do *you* debate this? And, when it comes to good genes, they effectively give a 1 in 200 chance.

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the 80129540 steps

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Be mature. You know better. 81029540 is a quantification of the extent of changes; 1829 is the number of steps.

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So, it doesnt matter which step occurs, by golly it has a selective advantage!

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Hey, Fred! If you were working on the design for an airplane and had an entire design team to work on the problems that you're encountering, and you had two choices: A) Have everyone work independently on the same part that is failing - and then as soon as someone comes up with their independent solution, move everyone along to the next failure (again, everyone on the same failure); or B) Have everyone work on different failures. (B) is clearly advantageous. There's absolutely no reason that different organisms can't quite effectively evolve different components at the same time, as long as there is A) sexual reproduction, and B) natural selection.I know you hate to admit it, but they showed they showed that there *is* a continuous path between an eyespot and a fully functional eye, assuming that the types of tissues used in eyes exist. There's not even the slightest question about that - there *IS* a linear path.

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To look at it another way, they are claiming that the required mutations are fixating at an average of 220 every generation!

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Wow, there's your wonderful context reading again! Now you're impressing the 1st graders. *You Read The Number Inverted*. It's one beneficial adaptation fixating out of every 200, not 200 beneficial adaptations in every generation. This is the overall effect of the standard population genetics formula, R=h^sup 2^i*V*m. How can you read something like this *backwards*?Perhaps you should go embarass yourself elsewhere.For those of you just joining us, here are the assumptions underlying Nilsson and Pelger's paper:1) The individual tissues involved can have evolved on their own, as can the nerves; this is only a study of eye morphometry.
2) The initial eye is a small bundle of photoreceptors, surrounded by a small layer of dark pigment, and covered in a thin protective layer.
3) Bad mutations don't fixate into the populations. One in every 200 beneficial mutations fixates.
4) Changes are in 1% steps, linearly.
5) Changes can be stretching, dimpling, growing, shrinking, thickening, thinning, etc.There are legitimate criticisms of the paper out there. They don't weigh in the cost to improvements of the eye (everything in nature bears a cost). They don't list enough of their calculations (although they're fairly simple). They don't pursue alternative routes that could occur at the same time. Etc.The things you brought up, however, did not address any relevant points. You did little more than slander their paper with utmost inaccuracy.------------------
"Illuminant light,
illuminate me."

Fred, Fred, Fred. Notice how you didn't respond to my tearing apart of your post. I can understand why, though, since all you can manage is argument from personal increduility. And, if you had read it, you'd realize how silly you look when you claim that their model is not accounting for genetic deaths - that's included in the population genetics equation that leads to about one in 200 successful mutations fixating in the popuation. If they weren't taking into account genetic deaths, it would only take 1829 generations.Enough slander, address the issue!

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each step is represented by less than 1 substitution

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What? You're saying that the change of an entire allele would need to cause more than a 1% change, or that things would need to happen in parallel? No, you've got to be kidding! That could never happen! Are you aware that a 2 BP mutation in the human on the SRY gene has led to an XY person being completely female? We're not talking about 2 alleles - we're talking *2 BP*. Of course, that was just an occurance which led to the deactivation of the gene, not the creation of a new one, but the point is clear - an allele can make a *huge* difference.You are correct, however, that the steps do not have to be in order. Of course, that helps Nilsson and Pelger's case, instead of hurting it. Congratulations!------------------
"Illuminant light,
illuminate me."

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That is exactly what convergence does, and is a major stumbling block to phylogeny construction. Do you at least agree with the last sentence, that convergence offers a major stumbling block to phylogeny construction?

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If Loudmouth knows anything about the subject, they won't. The difficulty in constructing phylogenies in modern times exists almost completely at the genus and species level. Thanks to evolution, creatures that converge keep obvious traces that they are unrelated; in modern times, genetics have confirmed this. For example, the tazmanian wolf and the dingo have converged on the same niche. Because of this, they look more similar in appearence than, say, a wolf looks to a hyena (and they're in the same genus). However, evolution predicts that, since the divergence of placentals from marsupials occurred long ago, they'll have quite different genetics despite the mostly similar appearence. Genetics confirms this, of course.In modern times, the difficulty at the species level is largely due to interbreeding, and the genus and occasionally family levels have the difficulty of defining what makes a distinct enough trait to warrant being a separate species (or genus). In very fews cases is there actually any question about how closely related they are.BTW, now that your slander about the Nilsson/Pelger paper has been shot down, are you prepared to offer more to the discussion of the paper than personal incredulity? Such as a rebuttal to your false statements about the paper? If not, we might as well just close the thread.------------------
"Illuminant light,
illuminate me."

Fred, when are you going to give up on the out of context quotes? How many times do I need to waste my time digging up the source material to shoot you down on this one? This time, you're going Gish on me, using several at once so that I don't have time to handle them all.Pick one so that I can put you back in your place by adding the context to it.------------------
"Illuminant light,
illuminate me."

And the thing is, the paper doesn't say that, it says quite the opposite. This has been pointed out to Fred several times (in fact, every claim he made against the paper has been torn apart), and he has yet to respond.------------------
"Illuminant light,
illuminate me."