Wizardry

I have to apologize, but I've dealt with these all out of the order in which they were posted.

Well, in quite a few of the scenarios that have been presented thus far, these light-sensitive molecules are developed in the systems that control movement, and thus automatically give the organism the ability to respond to light. In fact, this is the most probable scenario for the data involved; phototaxis(the ability to respond to light) shares a common mechanism with chemotaxis(the ability to respond to chemicals, at least in eukayrotes and some archaebacteria. This article identifies a common mechanism in chemo and phototaxis, histadine kinases:

Along the same lines, I found the following abstract in Nature:

Note the reference to a "common mechanism" for both chemotaxis and phototaxis. In an evolutionary perspective this suggests one of the following two possible scenarios (1)chemotaxis developed before phototaxis, and phototaxis is a modification of the receptor or (2)chemical and light receptors developed before taxis and when the mechanism for taxis emerged, it made use of both the chemical and light receptors.

Now, my money's on (1), and moreover, I'd say that phototaxis probably originally appeared in a photosynthetic bacteria because of the rather obvious advantage that would provide. But you may be asking, (and I believe you already have) "What if it's scenario (2) and photoreceptive molecule evolved before an organism used it to influence its movement? What possible good is a photoreceptor, such as rhodopsin or something very much like it, if it doesn't help an organism respond to light?"

I'm glad you asked. Let me introduce you to (dum dum dum!) bacteriorhodopsin. Same 7-helical transmembrane structure, same retinal co-factor, same transformation upon incidence with a photon, but a whole different purpose. It's main use is a light-driven proton pump. It absorbs a photon, which causes a rapid change in its electronic structure, which allows it to pump protons across the cell membrane. What good is that? That proton gradient can be used to drive a second membrane protein, ATP synthase, which as any biologist will tell you, is extremely useful.

I'm going to try to head off your next question here, assuming your next question is "But how did bacteriorhodopsin wind up in a common process with ATP synthase? How did that whole system develop?" ATP synthase is a very common transmembrane protein that turns a proton gradient into usable energy; it exists in a number of systems, notably the mitochondria. It probably predates bacteriorhodopsin by quite some time. Once bacteriorhodopsin appeared, its function as a protein pump combined with the abundance of light made it an effective energy generator. There's no complicated mechanism here. Bacteriorhodopsin creates gradient. ATP synthase uses ambient gradient to create energy. It's very simple, really.

That's not true at all. Phototaxis, even in its most primitive form, is widespread in the biosphere. It's especially important for photosynthetic organisms, but nearly all organisms function better with a certain amount of light, among other conditions.

Here is an alternate explanation for phototaxis in amoeba:
Note that phototaxis in this case does not involve a photoreceptive molecule and yet occurs anyway (this particular species of amoeba is also interesting for its partial multicellularity). Now imagine if, instead of using cyclic AMP for its phototaxis, it were able to use a molecule that sensed light directly, say by mutation of one of the proteins used for chemotaxis. Then light intensity or charcoal would not influence phototaxis, which could be quite useful in environments where that prevented proper phototaxis using this mechanism. The advantage in such a circumstance would be substantial.

Let's see if I can find 5% of an eye for you. Here's Euglena, a protist(single celled eukaryote) that manages to get by with nothing more than a little red eyespot on its anterior. The eyespot can sense the direction and intensity of light, which allows a Euglena to orient itself toward light and at an acceptable intensity. That's about five percent of an eye, no? And quite useful, at least for our photosynthetic friend here.

Evolution doesn't require that this happen, but it does sometimes anyway. Genetic drift all by itself will do it. (By the way, genetic drift is the random change in allele frequencies due to a finite population. This talk.orgins article explains it.) Here's a Java applet that pretty much answers your question. Set p to 0.1, generations for 250, play around with N and see what happens. In small populations especially, genetic drift alone, with absolutely no selective pressures leads to total domination of the population by the gene about once every eight times.

The founder and bottleneck effects, in which a larger population is reduced to only a few members, whose genomes may be unrepresenative of the original population, which accelerates genetic drift, is also in play quite frequently in evolutionary timeframes.

Also consider that a gene that confers absolutely no advantage may increase in frequency if it occurs in an individual that does has another gene that provides significant survival advantage. Genes are not independent of each other, they occur together, although sexual reproduction and viral recombination does alleviate this effect.

But in any event, there are a number of ways that a gene that doesn't confer any advantage can come to dominate a population.

That's not really relevant though, since in most cases we are talking about genes that confer a reproductive advantage, even if it is very slight. Try this applet, giving as slight an advantage as you can to a gene with a very low frequency. It still comes to dominate, eventually.

As I think I have shown in this post, light sensitivity, and even proto-eyes precede the development of multicellularity, much less the development of a nervous system. Take a look at this page(for kids!, but nevertheless). Sensory specialization occured sometime around the medusa, with many different forms of sensory data developing simultaneously(spacial orientation, light, chemicals, tactical pressure), well after the development of phototaxis. So the issue of when the eye got hooked up with the nervous system is really a question about the development of the nervous system, or at the very least cell specialization, making the following exchange:

... a bit puzzling, unless the fact that photoreceptors originated long before it made sense to talk about a nervous system has relieved this particular objection.

I think I'm about done for now.

MrDarwin

Not sure if this is relevant here, but the nervous system is remarkably flexible. For example, in some cases of polydactyly the extra finger (or toe) is fully-formed and functional. So even though the brain and nervous system are not "programmed" to be wired to a sixth digit, on those rare cases when it happens it works. This doesn't even require any evolution; a whole extra organ is added and the nervous system is able to integrate it immediately! So I really don't see, on a cellular level, why a mutation affecting a particular molecule to produce a new molecule the cell has never "seen" before could not likewise be integrated into that cell's responses, especially if the molecule is only slightly different from its predecessor.

Peez

??? I was not aware that there were several "views" presented, and I am not certain of what you mean by "incrementalism," but the process of evolution generally occurs by small increments, the fact of evolution generally involves small increments, and the theory of evolution generally deals with small increments.There is no evidence that mutations are "guided" in the sense of showing any tendency to produce "beneficial" traits, and certainly the theory of evolution does not require "guided" mutations.It is not particularly important that the mutations be "incremental" (if you mean that they produce only small differences). The point is that larger differences are probably less likely to be beneficial, so it is usually the small changes that are favoured by natural selection.This is a straw man: natural selection only occurs when a trait confers an advantage in terms of average reproductive rate, as I have explained a number of times.If I understand you, you are saying that you can accept the fact of evolution, but not the theory. That is, you can accept that living things have evolved, but you do not believe that the theory of evolution is a sufficient mechanism to explain such evolution. Is that accurate?I cannot speak for others here, but it is unlikely that "the masters of the field would find the notion nauseating." Note that I have a Ph.D. in evolutionary biology, so I guess that I am a "master" in the field.Of course I am physically capable of doing that, but my sense of intellectual honesty would not permit me.I mean that I do not know enough to make any kind of useful judgement on the issue.I have personally seen the process of evolution, and it is trivially simple to demonstrate. All the process of evolution is, is a heritable change in characteristics of individuals in a population from one generation to the next.Fair enough, this will help to focus the discussion.I believe that position is sometimes called "theistic evolution," though there are a number of different ways to use that term.I don't know where you got the idea that anyone believed that evolution by natural selection could proceed at all when the genes in question "don't confer any advantage." This is perhaps the most fundamental concept in the theory of evolution, so it is important that you learn it if you wish to understand even the most basic and general concepts involved. If a gene confers no advantage to the organism, then it is not favoured by natural selection and it is very unlikely to spread in the population. The reason that adaptations evolve is that the genes that produce these adaptations (by definition) confer some advantage and are therefore favoured by natural selection.

The basis of your argument seems to be that the intermediate states between some modern trait (such as our eye) and the earlier trait (say a heat-sensitive cell) confer no advantage at all. If they did not, I would agree that it is virtually impossible that the eye would evolve. As far as I know nobody would disagree here, nobody is claiming that "genes that don't confer any advantage come to dominate a poplulation [sic]." The disagreement seems to be concerning whether or not the small changes would each confer an advantage. Am I correct?Let's be clear, are you now saying that "if we were merely talking about (relatively simple) morphological structures (bones, limbs, etc.) evolution would be much more believable to me."? If so, then is there some problem with the model of the evolution of the eye from a simple light-sensitive cell?Sorry, I did not mean to imply that one or more deities had to be involved to use a "god-of-the-gaps" argument (I certainly understand that it was natural for you to interpret it as you did). The point I was trying to make is that you are objecting to the theory of evolution based on the fact that biologists don't know everything, rather than based on some weakness in the theory.Actually you are wrong from square one, since survival is not the point, reproduction is. Also, you are barking up the wrong tree: "survival of the fittest" is not how biologists define natural selection. Finally, if I may be frank, this is a silly objection. Any definition of any word may be challenged with the same argument. I will open my dictionary haphazardly, point at a page without looking, and I find:So, all it is saying is that something that is humid is humid. Of course! The fact is that fitness, as used by biologists, is well-defined and can be (and often is) quantified and measured.I had, but perhaps in a way that was not clear to you. I will try again.

Genetic material in cells is DNA. The sequence in DNA determines the sequence in the proteins that carry out various functions in a cell (and, in multicellular organisms, elsewhere in the organism). Typically, a particular protein is coded for only once in the DNA, and many copies of the protein are produced based on that code (so they are all identical). For example, you only need one bit of DNA code for beta-globin (part of haemoglobin), but a cell can make many millions of molecules of that protein using that bit of DNA.

All the cells in your body descend from a single cell (the fertilized egg, called the zygote). Thus, except for errors made in DNA copying and various other mutations that occur, each cell in your body inherits exactly the same DNA. As a result, all the cells in your bones that are producing haemoglobin normally produce exactly the same haemoglobin (there are exceptions to this, but they need not concern us here).

Now, a single point mutation in the DNA may change the code for the beta-globin. If the zygote has this mutation, then every cell in the body will almost certainly inherit it. Of course, most do not use this particular bit of DNA, but certain cells in the bones do. Since they are all pretty much genetically identical, they will all produce the same haemoglobin. The point here is that a mutation is a change in a DNA molecule, but the result is a change in all proteins produced from that molecule.

Now, let us return to the hydroid example. Before the mutation, we have an organism with a simple nerve net (it can hardly even be called a nervous system): sensory nerves (those that respond to the environment) connect directly to muscles. Thus, stimulating a particular sensory nerve cell will result in a signal being carried directly to a muscle which will then contract, and the organism therefore responds to the stimulus which excited the nerve cell. In this model, the hydroid has, among other things, sensory nerves which are excited by chemical X. This means that the DNA of this hydroid includes the code for a protein molecule that folds into a channel with a non-polar region, and opens when chemical X comes in contact, and then allows certain ions to pass through which initiate a nerve impulse. All the cells in the hydroid have this DNA, but only certain sensory nerves translate the DNA code into these proteins, and so only those cells will respond to chemical X. When they do, the impulse generated is carried by the nerve to a muscle which contracts and in so doing shrinks the hydroid.

Now, this hydroid grew from a single cell, a zygote. One hydroid zygote has a mutation in the DNA that codes for the specified protein. This small change in the sequence on the DNA translates into a small change in the sequence that makes up the protein, and when this slightly different protein folds up and embeds in the plasma membrane of the nerve cell (it is still produced only in the sensory cells mentioned), it will still open in response to chemical X. However, now it will also open in response to light. When light falls on this molecule of protein, it will open up, ions will pass through the membrane, and a nerve impulse is carried to muscles which contract and the hydroid shrinks. Note that we are not talking about one individual molecule here, we are talking about every molecule produced based on that bit of DNA. In other words, if the hydroid had 10,000 identical molecules which allowed it to respond to heat, the mutant hydroid would have 10,000 identical molecules which respond to heat or light.Since my example with the hydroid described a change in the nervous system, the light-sensitivity was already integrated into the nervous system when it appeared. In my earlier example, the light-sensitivity evolved before there was even a nervous system and so it was not necessary for it to be integrated.This is not what I have been doing. For the record, the first mention of the eye by you was:It seems pretty clear that the objection voiced here is that there is "no way, in principle, that an eye can be formed in incremental steps," no mention of the nervous system. That being said, since I have explained how it could evolve in the nervous system, it evolves already integrated.Ouch! ;( I would not agree that it is "morphologically perfect," but assuming that it is no longer connected to the optic nerve then I will not see out of it.No argument there.Please go back and reread the explanations. There are two obvious ways for light-sensitivity to evolve: before there is a nervous system (no need to be integrated), and through a change to the nervous system (already integrated).Please explain the relevance. In my example of a hydroid, it has evolved the ability to respond to light. Why should I worry about what "5%" of this sensitivity even means?If I understand you, the suggestion is that if you make the change small enough, then no benefit would exist. I suppose that this is correct, but in any event it is irrelevant. Nobody is suggesting that evolution proceeds through infinitely small changes, or even through changes that are so small that they offer no advantage. As I have explained using the hydroid example, a simple change from a single point mutation can confer sufficient light-sensitivity to be beneficial.Dawkins and his "camp" (that being the scientific community) are referring to 5% of a complex eye like that of a human (one can hardly call a light-sensitive cell an "eye"). So, when they talk about "5% of an eye" they are talking about a primitive structure that responds to light but is much less complex than the human eye.LOL!!Explained above.You are incorrect.If you wish, though it is utterly irrelevant to the model presented. Without going into a long exercise in mathematics, the proportion of individuals with light-sensitive molecules starts at 50%, but generation after generation might go up a little or down a little, at random (since neither has any advantage). This is a kind of random walk, and if you wait long enough the proportion of individuals with light-sensitive cells will eventually increase to 100% or decrease to 0%, just by random chance. There is a 50% chance that it will increase to 100%, and a 50% chance that it will decrease to 0%. Once again, this is irrelevant because in the model presented the organism did have the ability to respond to light, and the hydroid example above shows how this could happen.The same logic applies, except that now there is a 1% chance that the light-sensitive gene will eventually take over, and a 99% chance that it will disappear. Thus, if the mutation occurs 100 times we would expect it to take over. Again, this is irrelevant.Answered earlier, and above in more detail.Your example "proves" no relevant point.I have been, have you been reading mine?Note that I never stated that the protein reacted "specifically" to sugar before the mutation, nor that it reacted "specifically" to light afterwards.Note that I never stated that a change in colour would translate into it opening in response to light, I was simply explaining how a simple change could easily result in a change in colour, so that you might see that a simple change could result in a protein going from being colourless (absorbing no energy from light) to being coloured (absorbing light energy).I never mentioned any cell wall, and I did not say anything about letting sugar through, and I did not say that what was being let through was changing at all, let alone to "anything."I have no idea what a "bi-polar" molecule is.See above.

Note that I previously offered an apology for any part I had in raising hackles unnecessarily, are you up to it yourself?

Peez

Doubting Didymus

Ahh, brilliant! A thousand thanks to MrDarwin for digging this gem up:

Evolution of the archaeal rhodopsins: evolution rate changes by gene duplication and functional differentiation.

This seems to directly adress some of luvluvs primary objections.

For example, that the nervous system needed to be involved:

The precursors to our opsins are present in single-celled archea, which naturally have no need for a nervous system. In unicellular world, if you have any working protein in your cell membrane, it's as fully connected to you as it ever needs to be.

Here, we see the functions of the opsins in the archea:
Looks like the hypotheticals that myself and others were proposing were right on the money: a gene enconding for a protein that already does somehting in the cell was duplicated, and the copies progressed in different directions like so:

Most importantly:

We get our modern rhodopsins from phoborhodopsin, which is already a photoreceptor for directing movement away from blue-green light. In other words, these little buggers go way back. No doubt phoborhodopsin itself has still more ancient predeccessors. If you remember, I hypothesised earlier that a molecule that causes a phobic reaction to heat could become sensitive to the heat generated by a certain wavelength of light. This would result in the organism being phobic to BOTH heat and light. Going by this article, the wavelength was blue-green light. That molecule is still in existance in our ancestors, and a duplicateof it went on to become sensitive to more and different wavelengths of light. The changes we're thinking of are basic, tiny point mutations. The benifit comes from being suddenly able to hide in shady places.

The point is, these things are being built up on things that are already existing, and they in turn were built on something preexisting, going right back to the first replicator. Duplications provide more and more raw material for this to happen, so that nothing ever has to come into being ex-nihilo.

MrDarwin

Glad to be of help, DD. I've emailed you a prediction of sorts, based on this latest bit of data. Let's see how long it takes to be fulfilled.

luvluv

I'm still here, guys.

I'm reading through these links and I'm gonna respond sometime today.

Just moving this back onto the front page...

Edited to add....

Umm, D.D. or MrDarwin...

Anybody care to translate that last link into something resembling english?

MrDarwin

(1) Rhodopsins are not unique; they can be classified into four groups that serve a variety of functions at the cellular level.

(2) Some of these rhodopsin-like molecules are used for non-sensory functions.

(3) Some of these rhodopsin-like molecules are used for sensory functions other than detecting light.

(4) These rhodopsin-like molecules and the genes coding for them them are similar enough to each other that they almost certainly arose by gene duplication, with subsequent mutation taking the duplicates in different directions.

Fair summary, DD?

Doubting Didymus

I would only add that the organism we're talking about here are archea. Little buggers, single cells, NOT technically even eukaryotes, and yet they're using these opsin proteins that are similar to the ones we still use today. The main point here, (well, the main point relevant to luvluvs objections), is that the light sensitive molecules we've so far traced the problem of 'how cometh the eyeball', have been in existence before anything had anything even remotely like an eye. It never has to be "hooked into" the nervous system, because it was already around well and truly before nervous systems ever existed. It was never a problem battling with the probability of the protein just happening to occur in a photocell, because they've been waiting in the wings for a billion years beforehand.

Once you go so far back as to be explaining how a protein that was busily doing one thing became also active when struck by light, you've gone waaay past explaining the evolution of the eye.

Non-praying Mantis

Are you still there luvluv?

(bump)

NPM

Principia

Come on, NPM, it's been only a week or two. Give luvluv a chance to revisit PJ's Darwin on Trial for the appropriate rhet... um, scientific response.