Gpuccio: Functional Information Methodology

There are many things to say, and many interesting issues to be anwered in the comments that have been offered here. I am really not sure where to begin.

So, let’s begin at this last statement of yours, hoping that it can help me clarify a few things about FI and its measurement.

First of all, it should be clear thatr all the information we are discussing here is in digital form. That reakky helps, because it is much easier to measure FI in digital form. However, we need to know the reral molecular basis of our functions. That’s why I rarely discuss fossil, morphology and similar issues, and stick rather ot protein sequences. It’s the only way to begin to be quantitative about FI.

Even so, it is not an easy task.

I will just remind here that FI is defined as the minimum number of specific bits that, to the best of our knowledge, are necessary to implement some explicitly defined function.

You will find more details about my definitions of design and FI here:

Defining Design

and here:

Functional Information Defined

These are, indeed, the first two OPs I wrote for UD. I like to have my definitions explicit, before going on.

Now, very briefly, FI is usually measured directly as the rate between the target space and the search space, as defined by the function. The measure is completely empirical, and it must be referred to some definite system and time window. The purpose, of course, is to possibly infer design fro some object we are observing in the system.

We infer design if we observe that some object can implement a function, explicitly defined, hich implies at least 500 bits of specific FI. This is a very simlified definition, and we may need to clarify many aspects later. For the moment, it will be a starting point.

But, of course, those 500+ bits of FI must arise in the system at some time, and must not be present before. IOWs, we need the appearance of new complex FI in the system, to infer a design intervention.

So, just to be brief, I believe that none of the three examples you offer is an example of new complex FI arising in a system. I will briefly discuss the first two, avoding for the moment the example of viruses (I am not really expert about that, and I may need some better clarifications about what you mean).

So, the first point. You say: " There is more than 500 bits of FI differing between individual humans".

Well, the point is not if there is such a difference. The point is: what is the origin of such a difference?

Let’s see. The basic reference genome and proteome are rather similar in all human beings. The FI there is more or less the same, and we can wonder how it came into existence. Much of it comes, of course, from “lower” animals, but some of it is human specific. In all cases, according to my theory, complex FI arose as the result of design, in the course of natural history.

Then there are the differences. Of course humans are different one from the other. There are many reasons for that.

First of all, the greatest part of that difference is generated in the course of human procreation. We know how the combination of two different genomes (father and mother) into one generates a new individual genome, with the further contribution of recombination. That is a wonderful process, but essentially it is a way to remix FI that is already there, in a new configuration. The process is combinatorially rather simple. I don’t see how it should generate new FI.

I will be more clear. We would observe new FI if some individual, for some strange reason, received a new complex protein capable of implementing a new function, a protein which did not exist at all before in all other humans. Let’s say a new enzyme, 500 AAs long, that implement a completely new biochemical reaction and has no sequence similarity with any other previous protein. That would be new FI. Or the addition of a new function to an existing protein by at least 500 new specific bits, as some new partial sequence configuration which did not exist before.

These are the things that happened a lot of times in the course of natural history. The information jumps. But there is nothing like that in the differences between humans.

There are also differences due to variation. Mainly neutral or quasi neutral variation, which generates known polymorphisms, or simply individual differences. The online Exac browser is a good repository of them.

And there are the negative mutations, genetic diseases.

Nothing of that qualifies as new complex FI.

Let’s go for the moment to the second point. You say:

“We see more than this amount of FI develop in the evolution of cancer”.

I don’t think so. Could you give examples, please?

What we see in the evolution of concer is a series of random mutations, most of them very deleterious, that in some cases confer reproductive advantage to cancer cell in the host environment. But those mutations are combinatorially simple. They are usually SNPs, or deletions, duplications, inversions, translocations and so on. Simple events. Many of them, but still simple events.

We are exactly in the scenario described and analyzed by Behe in his very good last book. Simple mutations affect already existing complex structures, altering their previous functions in sucvh a way that, sometimes, a relative advantage is gained. For example, a cell can escape control, and start reproducing beyond its assigned limits.

I will just give an example. Burkitt’s lymphoma is caused, among other things, by a translocation involving the c-mych gene, a very important TF. The most common event is a 8-14 translocation. The event is very simple, but the consequences are complex. However, the change in FI is trivial.

A single frameshift mutation can easily cancel a whole gene and its functions. Still, the molecular event is very simple.

FI arises when more than 500 specific bits for a new function appear. That is about 116 specific AAs. Do you know of any cancer cell where a completely new and functional enzyme appears? That did not exist before?

Well, that’s enough for the moment.

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