Side Comments on Durston

H ( X f( t )) = -∑ P ( X f( t )) log P ( X f( t ))

Hi Kirk
I sent you a facebook message. I assume you got it since you are here :grinning:

The above is the equation that is in discussion. First can you describe it precisely. Second can you show why you think it is a valid equation. I need an education on the differences in FSC and Functional information.

Bill, we will get to that once everyone is on the same page re. some basic principles of functional information. There may be some discussion on one or two of them before we can move on to address my method of estimation.

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Sounds good Kirk. Great to have you here.

In respect of turning up in a genome? The crux of “calculating” functional complexity and related concepts is how rare proteins that may have a function in some biological context are in sequence space. I guess we could say that new functional sequences are more likely to be modifications of existing proteins. Doesn’t tell us what else is out there.

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A great example of how Durston’s method fails.

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Can someone point me to this paper? I’m not finding any citations or links to it.

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It looks like this is the thread the discussion will take place. When you have time could you take Kirk’s original post and explain the points where you agree and disagree.

Thanks! Ideas sparking here - what is a sufficient, minimal, and complete statistic to estimate function!

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Already done on the main thread.

Cancer is not possible without a fully functional cell as a starting point. It certainly can be the result of a change of genetic information but that information has to exist prior to it being changed.

How is it determined if the change is due to loss or gain of information?
Your answer to this is new function but I would challenge you that the function you think is new already exists but may be dormant in a mature cell.

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Evolution also is only possible with a fully functional cell as a starting point.

All changes require information to specify. All changes.

That is exactly what we think in evolutionary science. That the function is dormant in pre-existing proteins and DNA, and that is how evolution is able to work. That is how life can evolve, because random sequences are stores of dormant functional information. The term is: exaptation.

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I’ll comment here, rather than in the main thread.

I’m skeptical of all of these information arguments.

As Durston describes it, he is measuring functional information based on the function of protein production. So he sees duplication as providing little additional information, since the same proteins are being produced.

From my way of looking at it, functional should be in terms of biological function – the ability of the organism to prosper and perhaps to deal with a change in environment. If duplication happens to enhance that biological viability, then could be a very important functional change.

I’m left with the concern that the argument is over a mathematical model, without a convincing accompanying argument about the applicability of the model. I’m reminded of Zeno’s paradox on the impossibility of motion.

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Or more specifically, function should be described in terms of fitness, as you describe in the latter portion of your post.

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I got it but what I have observed from the experiments I have researched is that what is happening in cancer is breaking of existing function by mutation or low levels of vitamin d and enabling embryo functions that should be dormant in normal healthy mature cells.

These are pathways such as the WNT and Hedgehog that are active in embryo development. Things we observe like runaway cell division, vascular growth and immune suppression are all regulated differently during embryo development then in mature cells.

There are thousands of papers in pubmed that show these embryo pathways are activated during a cancer phase. Some of the activation I have observed is due loss of regulation of the ubiquitin system.

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Yes, but how does the cancer “know” how to turn that pathway on? With functional information. How much? Well, we can quantify it.

I may be wrong but I don’t think Kirk would disagree with this.

The pathway in mature cells is normally down regulated. This is generally done by the activation of the destruction mechanism in the ubiquitin system. For example if the destruction mechanism is disabled because of a mutation then the embryo pathway is turned on. If you look at some key oncogenes they are mutations in this pathway which disable the destruction of transcriptional proteins.

So in the case I have observed so far the proteins lose function that normally down regulate embryo pathways. This can be by mutation or lack of vitamin d. Mutation in the case of providing a reliable destruction mechanism and vitamin d in the case of expressing an embryo pathway down regulator.

I repeat, we can quantify the amount of information required to acquire these new functions.

Do you consider a mutation that causes a normal cell to operate differently new information or a loss of existing information?

In the case of cancer I have observed it is probably a mutation that stops a protein from binding properly.

In the case of cancer the results are often very bad so how do you justify that this is new information?

These are my current thoughts. I would like to see how the discussion goes at this point as I am very interested in the different types of information and their relevance to biology.