Saturday, January 27, 2007

Possible Pathways for the evolution of intracellular transport.

In his book “Darwin’s Black Box Behe made the claim with regards to the cellular transport systems that:
"A search of the professional literature and textbooks shows that no one has ever proposed a detailed route by which such a system could have come to be."

Some commenters here have argued that Behe is being intentionally deceptive they argue that there is an abundance of published material – shelf loads of it - that give a clear outline of how a pathway transporting a newly synthesized protein to an intracellular compartment could arise.

Some suggestions were given as to where I should start – (I acknowledge that they were probably hurriedly put together sources by scientists who are very busy doing more important work than arguing with me and I do appreciate the attempt to provide me with the references.)

http://www.mrc-lmb.cam.ac.uk/myosin/Review/Reviewframeset.html

This is sequence comparisons in the myosin superfamily looking at homologies between the different types of myosin molecules in different organisms.

http://www.pnas.org/cgi/content/full/103/10/3498
This is the attempted production of a phylogenetic tree comparing different types of myosin molecule.

The Richards and Cavalier Smith Nature paper is similar and suggests that the most primitive eukaryotes had three types of myosin from which all eukaryotic myosins come but that does not really help me.

This gives 111 delightful titles but not really what I am after. They are mainly phylogenetic trees and studies of sequence similarities. Behe accepts that there are an abundance of this kind of study.

What I am after is a simple step by step process whereby a single transport system from protein translation completion to function in a separate compartment can arise. It does not have to be a DVD of the process happening just a suggestion of some of the useful steps along the way.
I am thinking of the kind of thing that Matt Inlay produced in response to Behe’s Immunology chapter (here) or Nick Matzke’s response to the flagellum chapter ( here)


Tony’s scenario:
This problem concerns the way proteins are targeted to the mitochondria. These organelles (again, they’re shown in your diagram) are responsible for supplying a major fraction of the cell’s energy needs. They are distantly descended from free-living bacteria that began a symbiotic relationship with an early eukaryote. As part of that evolutionary history, mitochondria still retain a small genome which encodes a few of the proteins required by the organelle. However, over evolutionary time there has been a general drift towards more and more mitochondrial genes being transplanted to the nucleus. Mitochondrial proteins produced from such nuclear genes somehow have to get to their correct organelle. How do they do that? It turns out that such proteins contain, right at the start of their amino acid sequence, a so called ‘targeting signal’ made of about the first ten or so amino acids and which docks with import machinery in the mitochondrion. A mitochondrial gene newly transplanted into the nuclear genome must acquire this signal or it risks turning into a pseudogene. So how easy is it to acquire a functioning targeting signal? Some years ago a clever experiment was performed to find out. It’s a neat example of how our intuitive ‘gut feelings’ about these issues can lead us badly off-course. The scientists took a gene for a mitochondrial protein, then replaced its normal targeting signal with random DNA sequences sized to encode between about ten and thirty amino acids. They then determined what fraction of these random sequences acted as functioning mitochondrial targeting signals for the protein.What do you think the answer was? One in ten million? Or some other Dembski number perhaps? Actually, they got a remarkable 3 to 5%! Subsequent work with more truly random and uniformly-length sequences increased this estimate still further. Evidently, it’s almost ridiculously easy to evolve working targeting signals. One more point is worth making here. Because the results were so striking and the way the experiment was conducted was so elegant, this work is rather well known in the field. It was published in 1987 – almost ten years before Behe wrote his book. Yet he tells us with a straight face that no experiments have been done to address the evolutionary origins of protein traffic!


Tony’s point here is that the ID code for the mitondrial car park is pretty easy to forge. The fellow checking the ID’s is a pretty sloppy fellow and a great variety of ID sequences will do.

However let us imagine that this putative mitochondrial gene is the very first one to complete the journey into the cell’s genome. Let us also assume that the appropriate insertion of DNA occurs of the correct length and with the approximately correct sequence. Is this all that is required for the newly made protein to find its way into the mitochondrion? Is it just a single rough ID sequence that is needed or are other modifications required in the mitochondrial genome and elsewhere in the cell?

35 Comments:

Anonymous Anonymous said...

I don't know of any nice popular-level web articles on the evolution written for the consumption of those too impatient to go to the library to do the relevant research. I think the system just isn't as sexy as the flagllum, immune system, etc.

But to even be serious on this topic you would have to look up the intracellular transport systems in eukaryotes (not just yeast or something, but several basal eukaryotes), as well as whatever intracellular transport systems bacteria and archaea have. Then do a comparative analysis and see what if any components are novel to eukaryotes, how much of the system was preexisting in prokaryotes, etc.

In the end it will all be a piece of the more general question of the origin of eukaryotes, on which there is quite a bit of literature at PubMed.

9:49 pm  
Blogger Tony Jackson said...

Andrew,

You’ll never get a single review or paper that addresses all your questions in one sitting. Break the problem down into bite-size pieces otherwise you’ll just get indigestion. ‘Bite-sized pieces’ in this context still means major research areas in their own right that would easily be the source of many PhDs.

We’ve already seen how easy it is to evolve targeting signals. But a newly transplanted organelle gene has another problem: it also has to acquire functioning control sequences (so called promoters and polyadenylation sites), otherwise it won’t be expressed in it’s new home. How does that happen? If your intuition tells you it's impossible (as I’m sure Behe would argue), then again you’d be wrong.

Here’s a recent paper that shows how: Stegemann, S and Bock, R: “Experimental reconstruction of functional gene transfer from the Tobacco plastid genome to the nucleus”. The Plant Cell, vol 18, pages 2869-2878 (2006).

Plant cells contain an organelle called the chloroplast. It’s where photosynthesis takes place. Like mitochondria, chloroplasts are also derived from free-living bacteria that began an endosymbiotic relationship with an early eukaryote ancestor of plants. Like mitochondria, there has been a similar tendency for chloroplast genes to transfer to the plant nucleus over evolutionary time.

The scientists had previously demonstrated the transfer of chloroplast DNA into the plant nuclear genome as an ongoing process. This in itself was a pretty result.

By clever use of a screening assay, they now detected multiple independent examples where a newly transferred gene evolved new functional control regions and was expressed. Moreover, they were able to determine the exact mutational changes to the DNA sequence surrounding the gene that lead to this acquisition. As most molecular biologists would have predicted, there were multiple different ways in which the chloroplast gene became reactivated.

This is a neat piece of work for several reasons. Firstly, the experimental set up is elegant. Secondly, it shows that it is perfectly possible to design experiments to study these evolutionary questions and thirdly, it exposes yet again the utter nonsense behind Andy McIntosh’s claim that random mutation and natural selection can’t ‘create new information’.

10:10 pm  
Blogger Smokey said...

Andrew wrote:
"Some commenters here have argued that Behe is being intentionally deceptive..."

Yes, but you have the reason wrong.

"... they argue that there is an abundance of published material – shelf loads of it - that give a clear outline of how a pathway transporting a newly synthesized protein to an intracellular compartment could arise."

Andrew, are you spectacularly dishonest or just spectacularly incompetent? Here are three major points you need to consider:

1) I wrote, very clearly, that such an outline does not exist, because the whole thing is too complex to put in one volume. Therefore, your claim that I or anyone else said that there was a "clear outline" was patently false.

"...of how a pathway transporting a newly synthesized protein to an intracellular compartment could arise."

2) Erm, Andrew, "intracellular transport" is a couple of orders of magnitude more than transporting newly synthesized proteins to a single intracellular compartment. Your problem is that you are basing your challenge on Behe's sophomoric description. Again, YOU ARE AFRAID TO DISCUSS EVIDENCE. Your faith is laughably weak.

"Some suggestions were given as to where I should start –..."

But you didn't start at all.

"This is sequence comparisons in the myosin superfamily looking at homologies between the different types of myosin molecules in different organisms."

That is just brilliant. Are you claiming that it doesn't show you detailed evolutionary pathways for these molecular motors that play critical (often essential) roles in intracellular transport pathways?

"...but that does not really help me."

Why not? Because you couldn't bring yourself to abandon Behe's red herring and discuss real evidence?

"Let us also assume that the appropriate insertion of DNA occurs of the correct length and with the approximately correct sequence."

Andrew, you're ignoring the evidence again. Tony pointed you to evidence clearly showing that THERE IS NO SUCH THING AS AN "APPROXIMATELY CORRECT SEQUENCE."

Your faith is weak, so you simply misrepresented it.

"What I am after is a simple step by step process whereby a single transport system from protein translation completion to function in a separate compartment can arise."

And I showed you the detailed evolutionary tree for critical motors in many of these processes.

Again, Andrew, your assumption that Behe knows what he is talking about has caused you to make an absurd assumption: that there is a single transport system that targets newly-synthesized proteins.

There are hundreds. It wasn't designed. The multiple pathways came about from duplication of the genes encoding proteins that function in them, including the myosins that you completely disregarded.

2:35 am  
Blogger Tony Jackson said...

You need to get away from thinking about these structures in terms of man-made objects. Remember, the text-book diagrams that illustrate some pathway or other (and that you have reproduced here) are highly simplified abstractions that emphasise some aspects of a mechanism but ignore many others for the sake of clarity.

Go to this website:

http://mgl.scripps.edu/people/goodsell/illustration/cell

It’s run by David Goodsell, a scientist who is also a talented artist. His paintings depict the inside of cells at molecular dimensions, with the macromolecular components drawn to accurate scale and at the correct density. See how crowded it is! Now imagine each and every one of the proteins in the painting, shimmering and twisting, bending and tumbling, crashing into each other again and again and again and you get a better idea of what it must be like.

Advances in technology now mean that we can see some of this ‘single molecule’ action ourselves in living cells. In the case of clathrin-coated vesicles, you don’t see the smooth orderly transformation implied by the diagrams. Rather, you see individual clathrin molecules binding and falling off the pit; you see some pits start to form only to collapse suddenly and still others that form inactive dead-end complexes. This isn’t like any mousetrap I know.

Behe sometimes talks about the cell as factory. This analogy is also muddleheaded. As you’ve pointed out, secretory proteins first assemble in the endoplasmic reticulum. Most proteins that don’t fold correctly are destroyed at this stage before they’re transported further. What fraction of a newly synthesised protein do you think gets degraded in this manner? If you think in terms of factories, you’d probably guess at a very low number. Well, this has now been measured for the case of a chloride channel, and the answer may shock you: between 50 and 70% of this newly made protein fails to assemble correctly and is destroyed. Of course this number may vary from protein to protein, but even so. Imagine a car factory where 70% of the cars coming off the production line are defective and are sent straight to the scrap yard – not even British Leyland in the 1970’s was that crazy!

We need a better analogy, one that doesn’t pander to ID prejudices. Try this, from the Molecular Biologist Sydney Brenner:

“…it is easy to show that [cellular] regulation works on the basis of locally controlled anarchic demons bound together only by a global property of resource partitioning in which greed is punished by death. There is no master controller, or single supervisor or monitor, as some might once have assumed, based on intuitive experience of man-made machines”.

10:00 am  
Blogger umbjm said...

Andrew,

Since you seem to like mail/delivery service analogies, let me offer Tony's point in that form.

Behe wants you to think that everything is addressed and simply taken to the right place, like your mail is when the system is working.

If we use a mail analogy for intracellular transport of vesicles, your mail carrier (a molecular motor like the ones you claimed weren't relevant, or just plain diffusion) carries a small bundle of mail from house to house, ringing the doorbell and asking if the mail is yours. Is this intelligent?

Moreover, many times after you tell the mail carrier that the mail is not yours, he still returns to your house with the same bundle of mail to ask you again.

If some of the mail is yours, you accept the bundle, even though not all of the mail is yours. Sometimes you can give mail for others back to your mail carrier, other times you meet your neighbors and might (only might) be able to transfer the mail correctly.

Would anyone in his right mind call this an intelligently-designed mail system, even if most of the mail was eventually delivered to the correct recipient?

In fact, wouldn't all of us be ranting about the stupidity of such a mail system?

4:46 pm  
Blogger Tony Jackson said...

Ha! Nice one umbjm!

6:16 pm  
Blogger Andrew Rowell said...

Tony,

Thanks for the ref to the Steggeman and Bock paper.

1x10 ^-14/15 for transfer and activation in somatic cells.

They acknowledge that the antibiotic selection may increase the mutation rate.

The transfer and activation in the germline cells would be an extremely rare but not impossible event.

However I do not see how this solves your problem at all.

10:27 pm  
Blogger Andrew Rowell said...

Tony,

You said: "it exposes yet again the utter nonsense behind Andy McIntosh’s claim that random mutation and natural selection can’t ‘create new information’. "

By no means. The real information here is that stored in the control regions of the upstream gene and the conserved essential amino acid positions in the transferred gene. This has been merely shifted sideways... it has not been created.

10:29 pm  
Blogger Andrew Rowell said...

Tony,
Re: http://mgl.scripps.edu/people/goodsell/illustration/cell

They are superb!

10:39 pm  
Blogger Andrew Rowell said...

Tony,

I am not convinced that your problems with the cells analogy with human activity really destroy the argument.

Of course there are real differences but that does not destroy the reality of the analogy. DNA is still a real digital code. Transcription and translation are real and useful analogies.

Just because the molecular interactions are random and low efficieny does not destroy the argument to design when these inefficient and random interactions are harnessed to actually make the thing work.

10:45 pm  
Anonymous Lay Person said...

Most of the material here is way over my head but I found the mail analogy posted by umbjm very useful. However as a complete biochemical lay person I don't think that "random" or "low efficiency" to use Andrew's words mitigate against design as all physical manufactured machines are less than 100% efficient and RAM computer memory works on a random access principle. Reviewing this and other blogs and the reasoned arguments being put forward by both sides I do feel some exposure at schools/colleges to the ideas of ID has been well and truly made. Fascinating stuff and thanks to all who take the trouble to post.

12:54 am  
Blogger Andrew Rowell said...

umbjm,

Re - stupid mail system idea.

Of course the analogy with a mail system has its limitations and of course we would not use such a system with our mail. However the limitations of the analogy do not destroy its usefulness. There is real selectivity going on here and the messy address systme is sufficiently specific to work. There are real targeting systems and it is the origin of these that I am interested in.

11:53 am  
Blogger Andrew Rowell said...

Smokey,
Tony pointed you to evidence clearly showing that THERE IS NO SUCH THING AS AN "APPROXIMATELY CORRECT SEQUENCE."

Ok there are some sequences that work and others that do not. I was calling the working group "correct" is that ok?

12:03 pm  
Blogger Smokey said...

Andrew wrote:
"Of course the analogy with a mail system has its limitations and of course we would not use such a system with our mail. However the limitations of the analogy do not destroy its usefulness."

Andrew, I am pointing out that Behe's analogy is PATENTLY FALSE, not merely "limited." Please stop misrepresenting my position. Doing so is dishonest and un-Christian.

"There is real selectivity going on here..."

Agreed, and there is selectivity in my analogy. However, Behe claims that the selectivity is specificity. That's why his analogy is fraudulent and dishonest.

"... and the messy address systme is sufficiently specific to work."

Ah, but:
1) Behe doesn't portray the address system as messy, because he is ignorant/dishonest/both.
2) No one would describe such a system as intelligently designed, because intelligent people can easily offer a better one.
3) The only rational conclusion is that the designer of this system (God) is an idiot.

"There are real targeting systems and it is the origin of these that I am interested in."

Then Behe's phony analogy won't help you. Nor will demands for complete histories, when you can't produce even a smidgen of a history from your own position.

"Ok there are some sequences that work and others that do not. I was calling the working group "correct" is that ok?"

No, it's not, because it is presumptive. The data Tony cited showed that it is trivially easy to get random sequences to work.

This alone demolishes all of the hooey that Dembski has ever written.

6:13 pm  
Blogger Tony Jackson said...

Andrew: “Thanks for the ref to the Steggeman and Bock paper.”

We’ve got you reading real papers. That’s progress….

“They acknowledge that the antibiotic selection may increase the mutation rate.”

They controlled for that – read the materials and methods section.

“The real information here is that stored in the control regions of the upstream gene and the conserved essential amino acid positions in the transferred gene. This has been merely shifted sideways... it has not been created.”

Um.. originally the gene was inactive. Then it acquired a specific promoter – that’s ‘new information’ in the genome isn’t it? And in each of the reactivated examples, the precise molecular changes leading to reactivation was different, reflecting different DNA rearrangements around the gene.

New genes and new gene regulatory regions arise by DNA rearrangement, large and small. That’s just how it works. Accept it, and get on with your life.

“Re: http://mgl.scripps.edu/people/goodsell/illustration/cell They are superb!”

Yes, they are beautiful aren’t they? But remember, even these paintings are simplified abstractions. Goodsell is careful for example to omit all the ions, small molecular weight compounds (glucose, amino acids etc) and of course water itself. If he didn’t, his paintings would be an utterly impenetrable mess.

Recently, I’ve been working with some colleagues who use a method for directly visualizing single protein molecules on the surface of live cells. It’s awesome chaos there with the molecules in constant Brownian motion, and I assure you there are absolutely, positively no mousetraps.

7:22 pm  
Blogger Andrew Rowell said...

Smokey,
You said:
"Behe's analogy is PATENTLY FALSE, not merely "limited." "

I am not sure I agree. You would presumably be happy with the transport system analogy - if not then what sort of terminology are you going to use? The whole area of study is full of transportation system terminology.

Behe was writing for a popular level audience and these sort of analogies do convey some truth. They help to get people interested in the systems.

10:01 pm  
Blogger Andrew Rowell said...

Smokey,
"2) No one would describe such a system as intelligently designed, because intelligent people can easily offer a better one. "

Are you saying that you could engineer an improved transport system for a cell that would be guaranteed to increase efficiency?

10:03 pm  
Blogger Andrew Rowell said...

Smokey,
You said:
"Ok there are some sequences that work and others that do not. I was calling the working group "correct" is that ok?" No, it's not, because it is presumptive. The data Tony cited showed that it is trivially easy to get random sequences to work. This alone demolishes all of the hooey that Dembski has ever written. "

From Tony's description at best only 5% of random pieces work. It is very sloppy but there are obviously some kind of rules that determine which sort of amino acids work and which dont- The correct ones work and the incorrect ones don't.

This alone does not demolish all that Dembski has written. 5% of random sequences does not make a fully functional transport system.

10:09 pm  
Blogger Andrew Rowell said...

Smokey,
"You correct your gross misrepresentation of my explanation as to why Behe's demand is a red herring: http://idintheuk.blogspot.com/2007/01/possible-pathways-for-evolution-of_27.html"

Smokey I did not intend to misrepresent anything you said. If I did in fact misrepresent you then I ask your forgiveness however I am not clear on exactly what I did which upset you.

I have spent about 15 minutes trying to work it out... can you help or just give me the benefit of the doubt for the moment?

10:37 pm  
Blogger Andrew Rowell said...

Smokey,
"You address my accurate analogy for intracellular transport in the same thread. If you disagree with it, you must cite data from the primary literature that support Behe's sophomoric analogy."

Your analogy is closer to reality but Behe's analogy was focused on the origin of the selectivity of the entire system. It functions at the popular level to arouse interest in how such a system might arise. It is the multiple rounds of labelling and recognition that Behe is interested in.

10:44 pm  
Blogger Andrew Rowell said...

You perform Tony's homework assignment.

Hmmm it is getting late.

Please Sir can I have an extention of the deadline?

10:45 pm  
Blogger Andrew Rowell said...

Tony,
They controlled for that – read the materials and methods section.
I was going on this from the discussion:
"As some antibiotics, including streptomycin, which was used in our screen, are known to have mutagenic effects (Balashov and Humayun, 2002), it is possible that, in our experiments, evolution of a functional nuclear aadA gene was additionally accelerated by screening for antibiotic resistance. "

Are you saying that they had controlled for this and then mentioned it anyway?

10:52 pm  
Blogger Smokey said...

Andrew wrote:
"I am not sure I agree. You would presumably be happy with the transport system analogy - if not then what sort of terminology are you going to use? The whole area of study is full of transportation system terminology."

You're missing the point by a mile, Andrew. If I use all the terms of Behe's analogy accurately, MOST-not all-of the vaccine gets to the right address. Some gets sent back to the factory. Some gets sent to where it isn't needed. Some gets sent to the town dump and is buried or destroyed. The system is incredibly inefficient.

Let's review what you wrote in your post:

"1. The delivery of urgently needed vaccine to an area of the country where there is an outbreak of a highly infectious viral disease. If the correct vaccine arrives at the correct location then lives can be saved- if not lives will be lost. Behe then imagines a film director making a film called “epidemic” in which the vaccine labels get muddled – This situation is similar to the situation inside a cell he argues when the transport system breaks down- death is the result."

This analogy doesn't begin to describe the system accurately. The mechanisms that "read" the "labels" normally make lots of mistakes--they are merely "correct" more often than they are "wrong."

The analogy is fraudulent because Behe claims that the system is specific, when in reality, it is only selective. If you don't understand this important difference, please read up on it before responding. Evolution has no problem producing selectivity, and biology is full of it. Design produces specificity, which is rare (usually illusory) in biology.

"Behe was writing for a popular level audience and these sort of analogies do convey some truth."

No, it conveys a falsehood. There is absolutely no truth in his analogy.

"They help to get people interested in the systems."

Hardly. Are you interested enough to read the primary literature?

"Are you saying that you could engineer an improved transport system for a cell that would be guaranteed to increase efficiency?"

In a heartbeat. Tony could too. We'd make the "labels" specific instead of selective.

"From Tony's description at best only 5% of random pieces work."

Only? That's a huge proportion. It demolishes Dembski's thesis.

"It is very sloppy..."

That's the point that Tony and I have been trying to make. Behe is deceiving you by claiming that the system isn't sloppy.

"... but there are obviously some kind of rules that determine which sort of amino acids work and which dont- The correct ones work and the incorrect ones don't."

That's circular.

"This alone does not demolish all that Dembski has written. 5% of random sequences does not make a fully functional transport system."

It suffices for a critical step. Do you think other critical steps are this sloppy, or are they as improbable Dembski claims them to be?

"Smokey I did not intend to misrepresent anything you said. If I did in fact misrepresent you then I ask your forgiveness however I am not clear on exactly what I did which upset you."

Thanks, that's good to know. Try rereading the parts I excerpted below.

"I have spent about 15 minutes trying to work it out... can you help or just give me the benefit of the doubt for the moment?"

Try rereading my detailed explanations:
2) Behe's analogy "the vaccine labels get muddled" describes the normal state of compartmental labels. He wants you to think that it's digital like DNA, when in fact, the labels are entirely fuzzy and partially redundant. For example, many of the "bubbles" go the wrong way as well as the right way.

3) It's also not IC, because of the redundancy. Most homozygous null mutations in the "labeling" components--Rabs, SNAPs, SNAREs, etc.--aren't lethal.

And no, there wouldn't be a single review of the "evolution of intracellular transport," because the subject is too complex to fit in a single paper. There aren't even any single reviews of the MECHANISMS of intracellular transport, because that is too complex as well.

Behe is misleading you.

---

I'm saying that it's a red herring. A "detailed route" would fill dozens-to-hundreds of textbooks.

It's a red herring because there are plenty of papers that describe and discuss the evolution of the families of COMPONENTS of these systems. These are enormous gene families with partially-overlapping functions, which makes no sense in design terms. IOW, one never sees this sort of complexity in designed machines.


"Your analogy is closer to reality but Behe's analogy was focused on the origin of the selectivity of the entire system."

No, mine shows how it the entire system works (fuzzily) in the cell. Behe claimed specificity, which is not there.

"It functions at the popular level to arouse interest in how such a system might arise."

It deceives lay people because it portrays selectivity as specificity.

"It is the multiple rounds of labelling and recognition that Behe is interested in."

Is it? I thought that he was just interested in selling books. I know that he has completely lost interest in doing experiments in his lab.

"Please Sir can I have an extention of the deadline?"

There wasn't one on my part. I would hope that you would put significant time into it, as it is very, very informative.

Here's another on the Web:
http://udel.edu/~mcdonald/evolhw2.html

12:49 am  
Blogger Tony Jackson said...

Andrew: “Are you saying that they had controlled for this and then mentioned it anyway?”

Ah.. a very revealing comment. It’s called being scrupulously honest and bending over backwards to imagine all the possible ways your experimental set-up might be inadequate. It’s one of the hallmarks of a good scientific paper.

“You perform Tony's homework assignment. Hmmm it is getting late.”

I very strongly suspect that Smokey already knows the answer. I very strongly suspect that you and Antony don’t.

6:36 am  
Blogger Andrew Rowell said...

Tony,
In the materials and methods section it is made clear that false positives were screened out by using two anitobiotics but no corrections have been made for a possible increased mutation rate as a result of the presence of the antibiotics.

The point is however that this is a rare event in somatic tissue and the requirement for it to occur in germ line material further reduces the probabilities. Moreover this is reduced still further by the requirment for the working address sequence (5% of random 5-10 base insertions... but how often do these occur randomly in the correct place?) On top of all this there is still the infra structure to recognise the address system which must already be in place... or have I completely misunderstood the situation?

9:39 am  
Blogger Andrew Rowell said...

Tony,

With regards to the production of new information...

The situation in this paper is the capture of an upstream promoter and control region usually by a deletion.

Thus the promoter of another gene has been stolen and combined with the coding sequence of the new gene. It is a reshuffling of already available information no the creation of new information.

9:48 am  
Blogger Steven said...

This statement from Behe is irrelevant.

“Darwin’s Black Box Behe made the claim with regards to the cellular transport systems that:
"A search of the professional literature and textbooks shows that no one has ever proposed a detailed route by which such a system could have come to be."

Even if this is correct and no such literature has ever proposed such a system this does not mean it won't be discovered in the future or that someone can't discover it.

If ID creationism lasts it will eventually be in the far corners of sub atomic particles and theories of conciousness.

Not just a god of the gaps but a god of ever increasingly smaller gaps.

9:12 pm  
Blogger Smokey said...

Andrew,

If I have been immunized or exposed to measles and you have not, does my immune system have information yours lacks?

If we both have been exposed, do our immune systems have the same information? IOW, do they make the same antibodies and T-cell receptors specific for measles?

9:13 pm  
Blogger Andrew Rowell said...

Steven,

You are assuming that there are no real gaps. The gap between life and non-life has not narrowed with further research it has broadened into a huge gulf. With a persistent gap you can either presuppose naturalism and as a statement of faith say this gap will certainly be closed one day or you can start thinking about alternatives.

7:32 am  
Blogger Andrew Rowell said...

Smokey,

I had a long and useful discussion with Matt Inlay on the Immune system ending here with links to the previous posts.

If you could do what he did with immunology with regards to the intracellular transport system then I think we would be making progress.

7:40 am  
Blogger Smokey said...

Andrew,

I don't see that you made any progress. You completely missed Matt's point, and didn't respond to his pointing that out.

Moreover, that discussion isn't pertinent to my questions about information, which go to the heart of your claims about rearrangement not creating any new information.

Why not just answer my questions?

5:09 pm  
Blogger Andrew Rowell said...

Smokey,

Sorry you think that I made no progress at all with teh immunology issue. I am not sure that Matt Inlay would agree with you. I tried pretty hard.

Sorry I misunderstood where you were going with your questions.

The Immune response is a good example of a system which produces new genes by reshuffling sections of DNA and then using (as I understand it) specially raised rates of mutation to fine tune the binding site.

However it does not produce new genes which can be inherited (as I understand it.)

So in answer to your questions on measles.
1. Yes
2. No
Check mate - I concede the point. I will be more careful in my use of no new information ideas in the future.

5:41 pm  
Blogger Smokey said...

Andrew wrote:
"Sorry you think that I made no progress at all with teh immunology issue. I am not sure that Matt Inlay would agree with you. I tried pretty hard."

I just didn't see any evidence that you recognized that the issue is not whether something is IC, but whether something that is IC can arise by RM+NS+drift. If you do, that's inconsistent with your recent offering of Behe as an authority on anything but the (IMO boring) biochemistry of histones.

"The Immune response is a good example of a system which produces new genes by reshuffling sections of DNA and then using (as I understand it) specially raised rates of mutation to fine tune the binding site."

Exactly. This occurs in real time, and none of those are directed (most rearrangements result in gibberish and the cells carrying them die). Now, if God designed the immune system this way so that we have a nearly infinite capacity to generate incredible amounts of information in weeks, what does that say about the claim that rearrangement and selection can't produce an organism over billions of years?

"However it does not produce new genes which can be inherited (as I understand it.)"

Well, they can't be inherited by the progeny of the human carrying them, but they are inherited by all the descendants of that cell (a clone).

"So in answer to your questions on measles.
1. Yes
2. No
Check mate - I concede the point. I will be more careful in my use of no new information ideas in the future."

I'm impressed. Thanks for being forthcoming. If you're interested, there's a very interesting recombinational mutant in mice, WldS (the S is a superscript), whose positive effects can't be explained by a reductionist approach, despite numerous attempts.

7:16 pm  
Anonymous Sparky said...

"Plant cells contain an organelle called the chloroplast. It’s where photosynthesis takes place. Like mitochondria, chloroplasts are also derived from free-living bacteria that began an endosymbiotic relationship with an early eukaryote ancestor of plants."

Is there any direct evidence? Certainly not for Mitochondria… please consider the following.

Genomics and the irreducible nature of eukaryote cells.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=16709776

"it exposes yet again the utter nonsense behind Andy McIntosh’s claim that random mutation and natural selection can’t ‘create new information’."

How so? How do we prove the mutations are random? How do we know natural selection played a major role?


Still I feel I am missing something. Where is the plausible, detailed, step by step pathway for intracellular transport? I was referred here by tony from "Inside the Cell" but I don't see it.

9:16 pm  
Blogger Tony Jackson said...

sparky: "Is there any direct evidence? Certainly not for Mitochondria… please consider the following.

Genomics and the irreducible nature of eukaryote cells.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=16709776a"

Um... sparky, did you read this paper you quote by C. G. Kurland et al., rather than just skimmed the abstract? Be honest now...

The Kurland paper addresses the question of the origin of the eukaryotic nuclear genes. It's been suggested that they originated as a fusion between archaea and bacteria, but Kurland argue on the basis of large scale genomic and proteomic data that that's unlikely.

In other words, they're doing science - testing hypothesis against the data.

The origin of the mitochondria is a different question. There’s very good evidence that mitochondria arose as a result of an endosymbiotic relationship between a primitive eukaryote and some sort of bacteria.

In fact, if you actually read the Kurland paper, you'll find references to some of the evidence supporting this theory.

9:38 am  

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