Examples of new information

As I read your question, you seem to be asking for the development of a new gene, but one which does not in turn require the loss of another gene.So, using a hypothetical example.A creature has Gene A, Gene B, Gene C. They each do different things. B codes for a protein which breaks down lactose, let's say.A mutation occurs which causes B to change.The creature now has Gene A, Gene D, Gene C. New Gene D codes for a protein which strengthens hair or whatever.Even though Gene D is new and novel, you would not consider it "new information" since the net result is still 3 genes.Am I close?In that case, let's look at another example:Gene A, Gene B, Gene C again.This time there is a mutation which causes gene duplication.So, the new organism has Gene A, Gene B, Gene B, Gene C.The "new" Gene B is exactly the same as the old Gene B. It's completely redundant.A couple of generations later, a 2nd mutation occurs resulting in the switch from Gene B to Gene D.So, now the organism is Gene A, Gene B, Gene D, Gene C.The new organism can still process lactose (it has gene B) but also has stronger hair (it has gene D).Would that scenario be considered "new information" since the net gain to the organism is an additional gene with a new property while not losing the existing gene with the original property.If not, why not?

What he means by gene switching is, well, gene switching. That is, he very reasonably wants assurance that the novel characteristics of the organism are not caused by the switching on and off of pre-existing genes as a pre-programmed response to a novel environment. Your example is therefore unnecessarily complicated (besides being hypothetical).

Well, then that's useless question.Just look at the genome. Is the gene there in an earlier generation? No? Okay, it's there now. Done.E. Coli/Citrate demonstrates this with multiple mutations.Go ahead and close the thread.

Well, yes, we do seem to be done apart from the bit where d4r says "thank you". Edited because d4r isn't a creationist, he's just talking like one for no apparent reason.Edited by Dr Adequate, : No reason given.

Is this helpful or confusing? Is there any information in the second image that was not in the first image? Edited by Dogmafood, : No reason given.Edited by Dogmafood, : No reason given.

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In many experiments, we can check this very easily. We can see that gene switching is not a possibility by looking at the actual DNA sequence and finding the mutation; and we can check that it is not a result of lateral gene transfer (of plasmids or anything else) by using a clonal line --- that is, you do the experiment starting with just one bacterium, yeast cell, or whatever.

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That seems reasonable, however we need to be sure that the mutation is actually in a gene that codes a protein.

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In the case of the nylon-eating bacteria which Percy mentioned, the first condition holds but not the second, since this development occurred in nature and not in the laboratory. (However, one might in lieu of it consider the fact that prior to the invention of nylon, a nylon-eating bacterium would have starved to death, so common sense suggests that the development of the gene must involve a novel mutation.)

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How do you know that the enzyme that nylon eating bacterium used to break down nylon wasn't formerly used for something else?

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However, there are plenty of experiments where both conditions apply --- we can identify the mutation, and we can be certain that the founder of the population didn't have it. One example would be Lenski's experiment, which you may have read about.

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I could not find any info on the specific mutation that allowed these bacteria to digest citrate. How do you know it was not a mutation to a gene controller?

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Afterthought added by edit: another way we can rule out gene switching is if we can watch the process of change and know that it didn't happen immediately. If it was a pre-programmed response to environmental factors, then it would take place on introduction to the organism into the new environment, whereas if the change is a result of genuine evolution this will hardly ever be the case. So it is not always necessary to look at the gene directly.

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That seems reasonable but it doesn't rule out gene switching.

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For example, when we watch the evolution of multicellularity in chlorella, not only does it not happen instantly, but we can observe several steps in the process as the first crude mutation is progressively refined to the optimal form. If this change was pre-programmed, then we'd see every organism in the experiment switch to the optimal form within the first generation, would we not? If it looks like evolution and quacks like evolution, it's probably evolution.

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You mention how a crude mutation is modified to produce multicellular. This example seems like the silver bullet I am looking for. What type of genes were these mutations happening in?I am currently exploring the evolution of decreased risk of stroke and heart disease in some people. I will try to explore your examples further but I will admit genetics is not my thing.
Apolipoprotein AI Mutations and InformationThanks for the examples!Edited by Admin, : Fix quote.

If you can find the mutation in the sequence, you'll know whether its in an Open Reading Frame or not. So we know that the mutation is in a gene that encodes a protein. Because bacteria did not intrinsically possess nylon-eating activity prior to the mutation. If they'd had the nylonase enzyme from the get-go, all related bacterial species would have immediately been able to metabolize nylon just as soon as there was some nylon to metabolize. Direct DNA sequencing. No, it does rule it out, that's the point. If it's just a matter of switching on a gene that all bacteria have, then every bacteria will switch the gene on in response to the environmental need. That's the point of having a "switch." A good example is the lac operon - bacteria can produce the enzyme beta-galactosidase they need to metabolize lactose, but they won't do it if there's no lactose, and they won't do it if there's lactose but also glucose.It's only when they're in an environment where lactose is the only sugar that they'll switch the gene for beta-galactosidase on and start to metabolize lactose. Every single bacterium with this gene switching mechanism does it in response to an environment with lactose but no glucose.On the other hand, only a small number of bacteria gained the ability to metabolize nylon in response to the presence of nylon in the environment. That's what proves that it was a new ability gained by mutation and not the activation of an intrinsic gene.

If the gene is present, but not switched on, you can detect the presence of the gene by Southern blotting. Basically you make a probe which will "stick" specifically to a sequence of the gene in question. You then take the DNA of the organism in question, seperate it out on an agarose gel then apply your labelled probe and see if it sticks. That detects the presence of the gene.Alternatively you can use specific primers and attempt to amplify the gene in question using PCR. If the gene isn't present, there's no template for PCR to copy from so you get no product at the end.

Well, if you look at the DNA directly you can see where the mutation is and so what it's affecting, whether it's in protein-coding DNA or something else.I'm not sure why you think it matters, can you expound on this? Well, there aren't bacteria using it for something else. Well, yes it does. Why do you think it doesn't?If gene X is switched on as a consequence of environmental stimulus Y, then you'd see the whole bacterial culture switching on gene X in the first generation exposed to stimulus Y. Genes controlling cell division, natch. I can't find the full text of the relevant articles, just abstracts, but I don't think the researchers did look at the DNA, that's why I gave it as an example of something that one could deduce wasn't gene switching by other means.The original experiment was done, so to speak, by accident. Dinoflagellates (single-celled predators) got into a culture of chlorella (single-celled prey), which was not what the experimenters wanted to happen. It was lucky for them they didn't just throw it out, but investigated what was going on.One way chlorella can avoid predation is simply to get too big for the dinoflagellates to eat, and this is what happened.Now, my reasons for thinking that this wasn't gene switching are as follows:* The change was not immediate and universal.* The first change was that cell division was interfered with to such an extent that big blobs of as many of a hundred cells were formed. This has the advantage that the chlorella couldn't be eaten; it has the disadvantage (one presumes) that the cells on the inside would find it difficult to acquire nutrients. The chlorella then tended towards an eight-celled form which was still too big to eat but in which every cell was on the outside of the cluster. Wouldn't gene switching jump to this form immediately?* This never happens in the wild. Why not? Because in the wild chlorella is not just preyed upon by single-celled predators such as dinoflagellates. A clump of chlorella is too big for a dinofalgellate, it's a tasty meal for a fish. Why would chlorella have a genetic switch just to cope with conditions only met with in the laboratory?* When the eight-celled forms were transferred to an environment without dinoflagellates, their descendants continued to have the eigth-celled form. Now, this would be something unique in gene switching --- a gene which can be turned on, but can't then be turned off, and is inherited stuck in the on position.So I think this is a good example of what I'm talking about --- in this case, even if we don't directly look at the DNA, it seems safe to conclude that we're looking at the results of mutation.

Why would it matter if it did something else before? What matters is if a mutation causes the protein to do something new and novel. In the case of the nylon bug, the insertion of a base created a new start codon in an alternate reading frame. The new enzyme was capable of digesting nylon which was lacking in the bacterium prior to the mutation.

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When pOAD2 plasmids encountered nylon by-products, an insertion of T indicated by an arrow in the 3rd row of a proved advantageous, for this insertion silenced the PR.C. coding sequence by creating the T-G-A chain terminator; at the same time, the newly emerged A-T-G created a new coding sequence from an alternative open reading frame, which happened to specify a polypeptide chain with 6-AHA LOH activity for degradation of nylon byproducts.
http://www.ncbi.nlm.nih.gov/...345072/pdf/pnas00609-0153.pdf

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If bacteria with identical genomes are exposed to the same stimuli then they will have almost the exact same reaction. The fact that these new phenotypes only occur once in every million+ cells strongly indicates a mutation and not gene switching.

Currently being edited.Edited by dan4reason, : No reason given.

As both a biologist and a computer systems analyst, information is simple.As far as Shannon information is concerned, any change is a loss of information, i.e., the message sent is not the message received.But biological information is not subject to the rules of communication theory. The definition of biological information that I learned some decades ago is this: the number of bits required to represent a genome. Any change in the number of bits required to represent the genome (a novel mutation, + or -), is a change in information.The requirement for a new function is a boondoggle. It is another case of an unreasonable creationist demanding the biologists use his definition of information by using a definition that no one but creationists use.

I think it's the other way round.The acquisition of new functions is precisely what adaptive evolution is all about, and asking to see it happening (in appropriately small quantities) is a perfectly legitimate request. Dragging the language of information theory into the discussion is the boondoggle, unless at some point creationists propose to do any actual math with it.Edited by Dr Adequate, : No reason given.

Sure it is. At heart communication theory is just thermodynamics. This is only true for that portion of communication involving the sending of a message. Creating your message set is also part of communication theory, and in biology where received messages become part of the message set mutations have a tendency to expand the message set, i.e., increase the amount of information that can be communicated.The easiest way to see this is to consider the example of a population with a certain gene that possesses 3 alleles. The amount of information about this gene that can be communicated to the offspring during reproduction is log₂ 3 = 1.58 bits. If an individual in this population experiences a mutation in this gene that creates a unique new allele, then this gene now possesses 4 alleles, and the amount of information communicated during reproduction is log₂ 4 = 2 bits. Yes, this is the real problem.--Percy

One common theme that I run across in discussions with creationists is that they define "new information" in such a way that evolution does not need to produce it in order for evolution to occur. In fact, using the creationist definitions evolution actually needs to produce a loss in information in order for complex life to evolve. Why? Any mutation is considered to be a loss in information, or at most no net change. What we need to do, IMHO, is challenge the contention that evolution requires an increase in information as defined by creationists.For example, pick any stretch of homologous DNA for humans and chimps. Ask them which differences represent an increase in information. I have yet to find a single creationist that is capable of determining which differences represent an increase or decrease in information. It just shows how meaningless the creationist argument is.