Evolution of complexity/information

I guess its' not so much 'abhour' as feel unconfortable when people use 'complexity' as an argument for ID. Confidently describing what complexity is, and then failing to actually link it back to biology.For example, could you describe an example of : that has been used by ID theorists, that is not just 'too complex to understand."?

I don't think any biologist would deny that your average E. coli was less complex than a human being. There are more cells, more organisation involved, and a far larger genome (encoding far more proteins).Equally, I don't think any biologist would see that increase in complexity as a problem, as it is all a matter of a series of steps. Its' not simply a matter of bacteria to man (as you seem to want to imply), its' a matter of bacteria-eukaryote-multicellular-complex multicellular-vertebrate-tetrapod.......all the way to human. So where's the uphill task with complexity? Which step is the problem? And here's the big stumbling block. How do you measure complexity objectively? If you tried to measure it by genome size for example we'd be about as complex as a banana. Brain size/weight ratio would probably see us neck and neck with a dolphin (at best). Its' not that simple. The best thing I can think of is to look at duplications in gene families, which tend to increase in number as you go 'up' your percieved complexity gradient. I doubt this is what you're looking for though, as this supports the step-by-step hypothesis of evolution: a protein which has one function in one organism duplicates and diversifies to provide more information and more complex function.So, what scientific way could you devise to measure complexity that does not just boil down to "look bacteria...human...WAAY more complex, right?" This is exactly what is being done at the moment. Certain steps are recognised as being important by looking at the fossil record and molecular evidence. Work is then done to determine what could have caused such events. A number of things (like origin of eukaryotic organelles as symbiotic bacteria) are relatively well established. Others (like the origin of cartilage and bone) are still fairly vague but that's no reason to start inserting the deity of your choice in all of the gaps in our knowledge - nothing suggests that there was a huge leap in complexity that could not be explained by good old fashioned descent with modification.

How about webbed feet?It's a small step I know, but as I said before - its' all a matter of small steps (by the way, which small step from bacteria to man did you have a problem with?).Here's how it goes:What's the main difference between a duck's foot and a chicken's foot? That's right, the webbing! At a certain stage in embryo development, both the chick and the duck have webbed feet but the expression of a protein called BMP in the chick instructs the cells in between the digits to die - so when it hatches there is no webbing.Ducks produce the same BMP, in the same place but retain the webbing because the cells in between the digits gain the ability to express another protein called Gremlin, which inhibits BMP function. To me this is a gain of information (the cells have been told "don't die"), and the duck sure as hell hasn't lost any ability, so where's the problem?Similar examples of cells gaining the ability to express proteins have also gone a long way to explaining the formation of the forebrain, the evolution of tetrapod digits, and the polarity of limbs.

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"Anything that is true of E. coli must be true of elephants, except more so." -Jacques Monod

I could see your heart wasn't in it though Besides, as crashfrog pointed out there hasn't been any loss of ability: the cells still have their cell death machinary fully intact, they've just gained the ability to ignore the death signal. This is true but only if chickens evolved from an aquatic bird, which I don't think is the case.

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"Anything that is true of E. coli must be true of elephants, except more so." -Jacques Monod

Thanks for the reply, Ah! The old ‘macro-evolution is not the same as micro-evolution’ chestnut again. I thought that might be the response {sigh}. But at least we can now agree to put the myth that 'a gain in ability means a loss of another function' well and truly to bed I’ll try and show you that the same kind of mechanisms are in effect, whatever scale you look at. Let’s look at another one of the examples I gave you — the evolution of the tetrapod limb from the fish fin — I’d have thought that that’s at the macro end of things, wouldn’t you?Again, its’ another case (like the duck foot) of proteins being produced where they were not produced before. I’ll try and explain :The fish fin and the tetrapod limb develop fairly identically to begin with. The first parts of the limbs share homologous structures, which are controlled by the same pair of control genes (known as HoxD11 and HoxD13). The part where the two types of limbs differ is at the tip of the limb: the tetrapod limb has an extra structure which has the digits radiating from it. This new feature (and the digits) seems to be have formed by a duplication of the bones that make up the rest of the limb. How does this duplication occur? A new set of cells in the limb have gained the ability to produce the HoxD11 and HoxD13 master switch proteins.Hope this is clear — feel free to ask questions if it isn’t, or if you want more details. I tried to find a picture on the ‘net but didn’t get any joy.So, what we have again is an increase in information, and an increase in complexity — both gained by a simple, non-deleterious mutation. Can you think of a ‘complexity step’ on the path from bacteria to man that could not involve this kind of simple change?

Hello again HD,I would say that whether something macro- or micro-evolution depends totally on your perspective. It seems to me that you accepted the duck-webbing example because, in your mind its 'micro' - and microevolution is OK. On the other hand, you have trouble with the development of seemingly new structures because you've already pidgeonholed it as a 'macro' event. Yet the two examples are using the same mechanism to increase complexity - cells making proteins that they didn't make before. The reason this mechanism can provide such a striking example is because, as I said HoxD11 and 13 are master switch proteins. They provide patterning information, so that when they are expressed (when the protein is made), they trigger a number of different events to occur. Its' like the genes are saying:"Right, I want a bone here, and a bone here"The mutation that caused the duplication of this expression pattern effectively turned the instruction to:"Right, I want a bone here, and a bone here. And once you've done that, do the same over there"As you can imagine, pattern duplication events like this one would be quite a powerful way of producing novel structures. There are a couple of reasons for this :1) There are mutations that cause truncation of the limbs: mutations in the HoxD13 gene have severe effects on digit formation for example. But they do not result in fins because the rest of the limb has evolved to be an arm or a leg.2) It would be silly to say that you could go from fin to hand in one step. Once the initial structure duplication event happened then a number of other 'micro' events would need to occur. In other words: there are more layers of complexity. Why do I call them 'micro' events? Because the kind of mutations required would be very similar to mutations we see in humans (like changing the number of digits or their shape and size) - so they are by your definition micro-evolution.As for your request for fossils: given that fossilisation is a fairly rare occurance, it would be a bit much to ask for a fossil snap-shot of a single mutation wouldn't it? The conclusions are drawn by looking at the expression patterns of the genes in extant fish and tetrapod limbs, and comparing their DNA sequences.If you want a general idea of the structures involved, do a google on 'Devonian times' . It gives a good overview of the basics - I think (not being a fossil man myself). But as we're talking about how complexity evolved, its's the molecular data that should speak volumes - and it does.Hope this goes some way to answering your questions.Oh yes, and the information on the HoxD11 and 13 genes: The coding region of these genes contains around 330-odd codons (the proteins contain around 330 amino acids in other words). They are both very similar proteins (caused by one of those gene duplication events that the great pink hairy one is talking about), and they are a type of protein known as transcription factors. Transcription factors act by binding to the DNA and effecting the expression of other proteins.I tried to anticipate some of your up and coming questions in that last bit - hope it wasn't too garbled.TTFNEdit: Modified the number of amino acids in the genes to get a more exact figure. I didn't want to look a bit of an idiot now that Loudmouth put up the exact bp values - Ta LM This message has been edited by Ooook!, 07-15-2004 01:46 PM

Hello,Blimey! I spend a day away from my keyboard and the whole thread careers away from me - ho hum. The statement in your post I wanted to deal with was related to the mechanism of natural selection and has already been well fielded by a number of other people, so I won't labour over it again.I suppose I could summarise it though by saying:If mutations that cause this subjective increase in complexity (ie 'better' lifeforms) can occur, and a reasonable explaination for why they would be an advantage can be suggested I see no problem with the progression from bacteria to humans. One thing that I would suggest (if you weren't doing it on this thread already) is to take a look at all of the steps on the pathway and ask - "Now how would that give it an advantage?". When doing this of course you should take into consideration the likely selective pressures at the time the change took place (if bacteria nowadays for example were to turn multicellular they would have to compete with quite a few really quite well adapted organisms). One possible stumbling block for this I can see is supposedly IC systems - but that, as you point out, is another thread.As an aside: I see your talking about the transition from prokaryotes to eukaryotes with Loudmouth, and are asking whether there is any fossil evidence. As LM quite rightly points out, internal components of cells don't fossilise - but there is other evidence that the organelles (the separate compartments) of eukaryotes were once bacteria in their own right. Mitochondria and chloroplasts contain their own genome, and their own protein sythesis machinary - and their DNA sequence shows that they are related to existing bacteria. Apologies to Loudmouth if this has already been mentioned.

Hi Hangdawg, I think you should be careful not to confuse 'leaps in faith' with 'gaps in knowledge'. One of the great strengths IMO of the scientific method (and what I percieve as one of the major problems with fundamentalism), is that it ever packs up and says "right, we know everything about that now!". In other words, there will always be gaps in our knowledge, and the only thing we can say is that "judging by the evidence, this is the most likely explanation"So (he says trying to swing back on topic), what does this mean regarding the evolution of information and complexity?1)We do know that information can increase (contrary to many creationist's claims), and we have a pretty good idea of how it would do that. Pink Sasquatch has done a good job in summarising the mechanisms (duplication, rearrangement etc).2)We know that these increases in information (ie mutations) can cause the kind of changes required if evolution is to explain the origins of all of the species alive today.3)However we do not know everything! If the only thing that will convince you that evolution occurred is a DIY mutation-by-mutation guide from primordial soup to man then you will be waiting a while.I must admit that if all we had to go on was the evidence summarised above I would find it hard to accept that life just 'found a way', but it doesn't stand on its' own. As with everthing that gets discussed here, it is just part of a larger framework of facts that support evolution (which probably explains why it is so easy to drift off-topic). Therefore by taking everything together I can confidently say that the most likely explanation is that the complexity that is me is a result of mutation and natural selection. To say that evolution can't be right because it can't explain the exact evolution of the eye is to do the rest of the evidence a great disservice.I hope that was roughly on-topic and of interest As for the other things that you mentioned in your last post: Feel free to start another topic that addresses these issues - I'm sure you won't be short of people willing to discuss them. This is touching on another topic: using DNA sequences to find common ancestry. It is true that a mitochondrial eve can be traced, but unfortunately for the creationists you mentioned, it also can be traced back even further to a 'mitochondrial Ooook'. I started a thread a while ago that kind of deals with the issues you're raising, you're welcome to join me in EvC Forum: The "common creator" myth ('the "common creator" myth'.)Shamelessly trying to drum up interest for my own topic I know but the only people who have posted anything there so far are me and Nosy (in his various guises). This message has been edited by Ooook!, 07-18-2004 08:50 PMThis message has been edited by Ooook!, 07-18-2004 09:04 PM