Just a note that I have put up a new post at Panda’s Thumb in response to a post by Eric Holloway at the Discovery Institute’s new blog Mind Matters. Holloway declares that critics have totally failed to refute William Dembski’s use of Complex Specified Information to diagnose Design. At PT, I argue in detail that this is an exactly backwards reading of the outcome of the argument.
Commenters can post there, or here — I will try to keep track of both.
There has been a discussion of Holloway’s argument by Holloway and others at Uncommon Descent as well (links in the PT post). gpuccio also comments there trying to get someone to call my attention to an argument about Complex Functional Information that gpuccio made in the discussion of that earlier. I will try to post a response on that here soon, separate from this thread.
Among other issues, the
in the 
in functional information is a cumulative 
, not the probability of one outcome. Unlike the 
‘s in Shannon’s formulas
The uncontrolled proliferation is a consequence of the expression of the viral copy of Src (v-Src), which is a homolog of the gene that is native to our cells. No additional mutations in the host genome are necessary, as far as I am aware.
Care to answer the question?
Corneel,
I think you have pointed out that information can be transferred to a genome through horizontal transfer. A legitimate point, however cancer does not usually form with a single mutation. There is initiation and then a process that follows which is something that could be measured as a reduction in FI.
Joe Felsenstein,
I agree, but can you compare subtracting the number of functional bits from the total number of bits?
The answer is right there in Szostak’s first paper.
That accumulation of functionally-equivalent sequences is what I understand Joe is referring to.
I’m not sure what in that explanation is not clear to you. Perhaps it is the math? Do you suffer from Mung’s syndrome?
Good thing you did not see my earlier post which brought up objective morality.
What I’m saying is that it’s not inherent in nature. We may decide on a space of configurations that is real. We may define a function of the configurations in terms of some physical measurement we may make on them. But the functional information defined in terms of the configuration space and the physical measurement were not “out there,” waiting to be observed.
The reason that functional information can be applied in many dissimilar contexts is that it’s an abstraction of ours, not some particular property of entities in nature. It’s something that is intended to aid us in explanation of physical systems. But functional information has no existence independent of the investigator who defines it.
I’m very tired, and struggling with this. Hopefully this helps someone, if not you.
Over and out.
BruceS,
In this case I suffer from you answering a question I asked Tom English 🙂
The viral genome is a sequence that is associated with high functional information. Yet when it inserts into a host genome you perceive that as a reduction in FI*.
How is that possible?
Because the former is only functional from the point of view of the virus, not from that of the host.
*(I’d say that the reduction occurs during integration and NOT during the process that follows)
Very helpful. Thanks, Tom.
Corneel,
No, I don’t. Please re read my answer. I agree that information has been laterally transferred into the genome. To get from there to cancer requires additional genetic change which is probably a loss of FI.
How did you estimate that probability?
No lateral introduction of a viral genome here:
Has Rupert experienced an increase or a decrease in FI?
What process did you go through to decide?
Follow up question will be:
Ubj pna lbh fubj gung lbhe qrsvavgvba bs /abezny/ vf bowrpgvirL
You have just added 12 bits of functional confusion.
You have just subtracted 24 bits of functional confusion.
According to he law of conversation of functional confusion you owe us 12 bits.
If we defined function as producing cancer the cell gained functional information. Furthermore, if we specified function as producing cancer we’d have an increase in specified functional information.
O. That is a surprise. I did not understand that you perceived the insertion of the viral genome to be an increase in FI. So according to you the oncovirus is not contributing to the subsequent development of cancer, because that requires a loss of FI? Did I understand correctly?
If you cannot see that the virus is a pathogen working against the interests of the host, then there is nothing to gain for you from my example. I suppose it does cheer you up everytime you get influenza, right?
I have difficulty understanding all those emoji thingamajigs; perhaps my deficiency means I am somewhere on the internet-autism spectrum.
I’ll take it as a good-natured request to butt-out, and so will slink off into the night. Or at least into Eric’s thread.
BruceS,
The emoji was to say that what you did was usually fine but in this case I was particularly interested in Tom’s response as he has spent a lot of time on this subject.
Corneel,
Contribution is not the issue. The issue is the total cascade of events leading to cancer not just the initial shove or some effect in the middle of the causal chain. To get cancer you need the following.
-Replication of cancer stem cells
-Disabling of DNA repair
-Disabling of apoptosis
-Up regulation of vascular growth
-Down regulation of immune response
-Disabling or protein destruction
You are clearly not talking about nucleotide sequences any more. Where is the information encoded if not in the genome?
Corneel,
I am not sure I understand your question. Genes are clearly involved in all the process I mentioned however not exclusively.
Well, I’m not sure what “cancer stem cells” are, but I will happily stipulate that “To get cancer, you need cancer cells replicating.” Not really news, that.
As to the rest, you are incorrect, in some cases rather obviously so.
By way of illustration, Rupert’s cancer does involve “disabling of apoptosis”, but it does not need “up regulation of vascular growth”, and actually has elevated DNA repair mechanisms.
Any thoughts on Rupert’s FI?
Sorry for the necromancing, but I noticed that you have consulted the oracle at UD, and that he confirmed what everybody has been telling you: cancer is associated with an increase in FI where your function is the growth rate of cancer cells (or something along those lines).
Did this enlightening insight in any way affect your judgment of Kirk Durston’s refusal to accept that cancer involved a gain of functional information?
I had not seen gpuccio’s opining on FI and cancer. Thank you, Corneel, for the link.
I guess he doesn’t realize that he just gave away the store. Bcr-Abl fits all the criteria for a massive undesigned injection of FI into the genome. It is only when you discover its provenance that the IDist will declare that it doesn’t count. This is problematic for a test that is supposed to detect provenance.
So much for FI then.
That still leaves FEE, FO and FUM.
DNA_Jock,
If you define loss of cell regulation as function.
Which gpuccio does:
That was Corneel’s point in linking to gpuccio’s comment.
DNA_Jock,
The reality is the cell is using information it already has no matter how you define function. There really is no argument here but if anyone can create one out of thin air its you 🙂
colewd,
Very interesting. Thanks for replying, Bill.
But the reality is that two people you hold in high regard produced clearly contradictory statements. Let us for a moment accept that the cell is using “pre-existing information” (which is nonsense, because completely novel arrangements are produced, such as the fusion protein that DNA_Jock alludes to). Then still gpuccio and Kirk Durston espouse two mutually exclusive viewpoints:
– gpuccio (correctly IMO) identified carcinogenic mutations as gains in FI with function defined as contributing to the persistence and profileration of cancer cells.
– That collides head-on with Kirk Durston’s refusal to accept that the loss of p53 protein function qualifies as an increase in FI.
In my mind, you need to weigh the strength of both arguments and choose one side, declaring the other nonsensical. Since you seem to rely quite heavily on the pronouncements of authoritative persons, I am very interested how this psychological experiment turns out 😉
Corneel,
Taken out of context maybe but in reality they did not contradict each other. Gpuccio was making a general theoretical claim and Kirk a specific claim. If you look at specific claims and understand the cancer mechanisms they fall toward the empirical argument Kirk made based on P53 mutation and disabling apoptosis. The apoptosis mechanism already existed in the cells and mutations leading to cancer simply disabled it.
Corneel,
This is a theoretical construct as when you look at specific examples of why cell division elevates the mutations are loss of function. Could cancer theoretically create a couple of functional gain mutations, sure, but there is no evidence I am aware of it has. I was hoping Jock would pull a rabbit out of his hat 🙂
Bluster and ignorance is rarely a compelling argument, Bill. Here’s your rabbit.
In this thread, I have already pointed you to [“Rupert’s”] Bcr-Abl more than once, and asking you whether you view it as an increase or decrease in FI (and asking you to justify your answer…)
I’ll add EML4-ALK to the list. Same questions.
EGFR variant III, OTOH, looks like a loss-of-function to me. What do you think? Why?
In all cases, gpuccio reckons these can be viewed as increases in FI, and Kirk insists that they cannot.
E4Rupert
DNA_Jock,
Again, Kirk is making a specific claim gpuccio is not. If you want to claim that the cancerous protein you identified is creating new FI go for it but this is a detailed argument that will take lots of research. The first basic question is how the mutation identified is initiating elevated cell division in a mature cell. I will look again and see if this question has been studied. If not you need a new rabbit 🙂
No, Bill.
As I explained to you previously, any of these mutations can be viewed as an increase, or as a decrease, in FI, depending on the definition of ‘function’ that the individual choses.
Separately (and also explained to you), claiming that these changes in FI cause any cancer is a category error.
DNA_Jock,
Yes, you have made these assertions yet your arguments are not ready for prime time.
What do you mean by a “cause of any cancer is a category error”? Who created the standard here?
BTW what appears to be going on is the merger of the two genes you have identified are causing the cell cycle gene BCR to be caught in the on position. So how would you position this as a gain of FI given the white blood cell has lost regulation?
Clearly they are not using the same definition of “function” and FI depends on how you define function. So there’s nothing contradictory about it.
ETA:
Precisely.
gpuccio acknowledged that the FI in cancer could be viewed as either increasing or decreasing, depending on what you decide to be the function. In the functional information thread @PS, Kirk Durston (like Bill) was incapable of seeing that the loss of p53 function could be interpreted as an increase in the FI of a cancer cell.
Those are definitely contradictory statements, Mung.
Corneel,
He demonstrated this based on loss off specificity of sequence which is germane to the FI definition. In the case of cancer sequence specificity was less critical then in the healthy cell for P53. Can you make argument here that challenges Kirk’s math?
In all the cases Jock has brought we see loss of cell regulation due to receptor proteins stuck in the on position vs being regulated by ligands. How can you argue that loss of regulation is a gain of function? Even from the cancer perspective (rapid cell division is good) if the specificity is lost then FI is lost.
Good grief, colewd, I have already explained this to you on this thread!
If we define function as “promotes cell division” (and Corneel and gpuccio agree with me that we can) then loss of function of p53 represents an increase in FI.
BY DEFINITION.
and
[Emphasis in original]
For completeness, here is my illustration of why you cannot claim that the cancer is due to the change in FI.
colewd,
Have considered the possibility that you explanation could be wrong?
I agree in this strict definition this is possible. So what?
Does it take more functional information to operate a normal cell or a cancer cell. The answer is a normal cell and that is what is critical. You can lose functional information of a normal cell and form a cancer cell starting from a normal cell.
Corneel’s error is that Kirk was defining function not as speed of cell division but as P53 function.
Lovely, Bill.
And, as promised, here is my follow-up question:
Ubj pna lbh fubj gung lbhe qrsvavgvba bs /abezny/ vf bowrpgvirL
rot13 –>
How can you show that your definition of “normal” is objective?
🙂
No, silly. Kirk’s error was to refuse to see that Kirk’s definition of function was NOT the only one possible, as gpuccio (and now, belatedly, you) recognize.
One man’s increase is another man’s decrease.
DNA_Jock,
It can go from a zygote to a mature human on its own. Kicks ass over a cancer cell 🙂
DNA_Jock,
Straw man alert 🙂 You have to fn kidding me if you don’t think Kirk realizes this.
Really? Kirk seemed pretty resistant to the idea that cancer might be associated with an increase in FI when JS and J Mercer were wiping the floor with him on Peaceful Science.
Your definition of ‘normal’ seems rather subjective, and your estimation of what a zygote can do “on its own” seems rather optimistic.
😮
Heh.
Let’s replay that part, shall we?
[emphasis mine]
I sense some perspective missing here, don’t you?
“No, removing that wheel clamp from your car will not affect its speed, because then it doesn’t DO anything, you know”.
Corneel,
From the perspective of the car it does something but not from the perspective of the wheel clamp as it goes from active to inactive. Again, Kirk’s analysis was from the perspective of P53’s function.
DNA_Jock,
It will win the race every time over a cancerous Zygote.:-) Most the world will accept an objective explanation of how a “normal” cell behaves and a cancerous cell will miss the cut.
All kidding aside thanks for the two citations they are very valuable.