Oolon Colluphid

Hi David

That is a very good question, especially to ask yourself. It is no small problem. In humans, for example, there is a family of junk DNA called Alu sequences, about 300bp long, that are repeated some million or so times, and this one family alone accounts for about 5% of our DNA. Those are ‘moderately repetitive sequences’. But they’ve got nothing on ‘satellite DNA’. I imagine they’re called this because of the astronomical number of repeats. In Drosophila fruitflies (one of the best studied organisms, genetically), there are three little pieces of DNA, just seven (IIRC) bp long. They do not code for anything, even if they had the appropriate codons. And these three bits are repeated eleven million, 3.6 million and 3.6 million times each. They make up 40% of the fruitfly’s total genome.

There are a variety of evolutionary explanations... but I’d be fascinated to hear why you think a creator-designer would include this feature in organisms’ makeup. After all, using more materials than is necessary is not usually thought of as good design.

As far as geneticists are concerned, the only point to junk DNA is that it’s great for helping to determine phylogenies -- that is, what’s related to what.

DNA is passed down lineages. Naturally, members of a population will have very similar DNA, even the ‘junk’. Now, since exons are the bits that make bodies, they are open to natural selection, so not all mutations get passed on. But mutations in introns can accumulate randomly, since they usually make no difference. If a population becomes divided eg geographically, their DNA, junk and all, carries on down the separated lineages. Since they’re no longer mixed by sex, the random changes in the ‘junk’ will accumulate still, but different ones in each lineage. Thus the similarities and differences between the junk DNA of (assumed for loads of other reasons) related organisms can be used to sort out (often complicated -- why should that be?) phylogenies. Sorry, more for you to read, but you ought to study <a href="http://www.talkorigins.org/faqs/molgen/" target="_blank">this article</a>. I posted that link before. I guess you missed it.

In fact, by measuring the differences and calibrating from a known fossil ancestor, these accumulated changes can be used as a ‘molecular clock’ to date evolutionary divergences. Does the clock work? Well, it makes testable predictions. For instance, palaeontologists used to be convinced, on the basis of the available fossils, that Ramapithecus, at around 22mya, was the last common ancestor of humans with the African apes. In the late 60s and early 70s, Sarich and Wilson, who developed the clock method, calculated that the last common ancestor was much more recent than that. They were ridiculed and ignored by palaeontologists, who are not geneticists. But gradually, as more and more fossils were found, their date of around 4mya has become more and more accepted. (Ramapithecus, it seems was an ancestor of orangutans.) The fossils vindicated the clock. And vindicated a molecular approach to ancestry.

Of course comparative genetics would work for this, since it’s dealing with the actual DNA patterns that are passed down lineages, rather than interpretation of fossils.

The same methods that can determine if a child belongs to father X rather than Y, or who committed a crime, when used comparatively, clearly show relationships between individuals, families, populations... and species, genera etc. If evolution were wrong, it wouldn’t work. And if it weren’t a useful tool, it wouldn’t be so widely used.

While investigating junk DNA, try looking up pseudogenes. You’ve been told of it before, but I’m still interested to hear your explanation: why did this creator of yours choose to give humans a broken version of the gene that makes vitamin C in most other mammals. Thus condemning those without adequate diets to scurvy. And also gave a pseudogene broken in the same way to chimpanzees and gorillas, which for so many other reasons are thought to be our nearest relatives.

Cheers, Oolon

[Edited for silly transposon ]

[ January 23, 2002: Message edited by: Oolon Colluphid ]</p>

Asha'man

Ok, I've been trying to lurk on this thread and learn something interesting, but am starting to get overwhelmed. This stuff is really amazing.

However, I think it is time to turn the "argument from incredulity” around. An Intelligent Designer did this?!? Maybe it is just me, but this is starting to sound like an amazing Rube Goldberg mechanism, and I can’t imagine a competent designer coming up with this and then calling it “good.”


Sorry for my interruption, please continue with your technical discussion....

Quetzal

Congratulations Asha'man! You've inadvertently stumbled upon the biologist's Argument from Personal Incredulity! To wit: I can't believe any "intelligent" Designer could possibly have actually built something this half-baked.

bluefugue

Are you calling my brain "half-baked"? I resemble that remark!

[ January 22, 2002: Message edited by: IesusDomini ]</p>

davidH

Sorry I haven't replied in so long but I was revising for exams and I needed all the time I could get!

Thanks for all the info. I've learnt a lot (though no where near everything!!)

Right, there's one thing I really need to get straight here. A yes or no answer would be good.
Are introns necessary for the cell to be able to produce proteins?

As Yellow3 pointed out - when they removed the introns and insected the DNA into a vector something happened and the vector didn't produce the correct protein(or anything at all). - Not sure on this, I'm offline and going by memory.
The one base change in haemoglobin intron wrecks the whole structure.

When I said that from this am I correct to assume that intron isn't junk, people said that that was faulty and I couldn't assume that.

I would like to see some evidience that a mutation in an intron doesn't cause damage. You have said that a mutation in it doesn't cause problems, yet is there any proof to back up this assumption? (-I'm not being awkward, I just want to know if there is any.)
If there is no proof then I will go with the evidience I now have, if there is proof then I will weigh them together and see.

Oolon, you ask me for answers to the vit. C problem - I can't answer that because I have nowhere near enough knowledge of genetics to suggest anything. - Ask one of the others here and see if they would know what would happen if we could produce vit C.

I'll pose some questions that would need to be answered if I knew enough.

1. Does the broken down version of the Vit C play no part in any reactions of the body? - Are you sure about this? ie. sufficient evidience.

2. How would our bodies (presently) respond if the gene were to suddenly become fixed and Vit C produced? - Would there be anything to regulate Vit C production? - Is an overdose of Vit C dangerous? - If the gene was fixed how fast would Vit C be produced? - Would it alter pH of blood?
(Vit C is absisic acid?? - not sure if this is right but I think it is an acid.) How does an increase (large amount)of Vit C affect body functions? If we did produce it would anything else in our bodies have to change?

3.Why is Vit C present is some fruit anyway? -Is it essential for the production of the fruit?

4.Where is Vit C (half) produced?

5.In the DNA structure coding for the Vit C gene is the sequence just incomplete? Is there something blocking the whole sequence? Is the correct enzyme not present?

For me anyway all these factors and probably many more would need to be considered before the question could be answered.
However please answer the questions on the genetics that I asked above first.

Some of you are asking how I'm going to use introns and all to prove God etc. You miss the point. I am open minded. Before I make my judgement on evolution I have to take into consideration all the facts.
I have to trust what you tell me to be true because I couldn't prove everything that you tell me.
Because to write off evolution straight away even when I haven't got a good understanding of it would be wrong.
So I'm putting everything into the balance.

And isn't evolution due to genetics? I think this has a big part to play so I'm trying to understand it all.

(Oolon I haven't read that link yet - I'll read it when I post this.)

theyeti

No.

theyeti

theyeti

David, you should first read the article that Oolon linked to before asking these questions. Most of them are answered there. I will try to answer them breifly, but I make no claim to be an expert on vitamin C. Also, I'm just going from memory here.

1. Does the broken down version of the Vit C play no part in any reactions of the body? - Are you sure about this? ie. sufficient evidience.

As sure as we can be. The gene has what is known as a "nonsense" mutation (IIRC). This is where one of the codons in the middle of the gene is turned into a "stop" codon, and the resulting protein is severly truncated, and thus useless. It's hard to imagine how such a gene could have a function, even if there had been no studies on it. One thing's for sure, it does not have the primary function of making vit C, as it does in non-primate mammals.

2. How would our bodies (presently) respond if the gene were to suddenly become fixed and Vit C produced? - Would there be anything to regulate Vit C production? - Is an overdose of Vit C dangerous? - If the gene was fixed how fast would Vit C be produced? - Would it alter pH of blood? (Vit C is absisic acid?? - not sure if this is right but I think it is an acid.) How does an increase (large amount)of Vit C affect body functions? If we did produce it would anything else in our bodies have to change?

This is actually several questions. First, it's ascorbic acid. Secondly, the gene itself doesn't make it, it just provides an enzyme to catalyze the final step in a pathway that makes it. Third, yes, you can get too much vitamin C. Fourth, I doubt too much (within reason) would lower your body's pH (you're probably thinking of citric acid, which is a much stronger acid). I don't know how the gene is regulated -- that would make a big difference in whether or not it could be overproduced. If this step in the pathway is not rate determining, it probably wouldn't matter, since the other steps have presumably retained their regulation. In most cases, the worst thing that happens from not regulating a gene is that you waste protein. The gene as it now stands probably has a busted promoter, in which case it wouldn't work even if you fixed the nonsense mutation.

If your idea here is that the gene was never good for making vitamin C, then you're using faulty reasoning by comparing what would happen if the gene were fixed now. The event that broke the gene goes back many millions of years to the beginning of the primate lineage, and the gene has accumulated many mutations since.

3. Why is Vit C present is some fruit anyway? -Is it essential for the production of the fruit?

Fruit has one purpose and one purpose only: to spread the seeds of the plant by encouraging you to eat it. You may as well ask why fruits have sugars, because it's the same reason. By giving you nutrition, the plant rewards you for doing it an invaluable service. And some have speculated that the plant actually "enslaves" you in this way. By overproducing vitamin C, ancestral tropical fruits managed to make ancestral primates dependent on them, thereby ensuring that a ready and willing population of primates will always be around to disperse their seeds.

4. Where is Vit C (half) produced?

Huh?

5. In the DNA structure coding for the Vit C gene is the sequence just incomplete? Is there something blocking the whole sequence? Is the correct enzyme not present?

To clear it up, the gene codes for an enzyme. That enzyme is disfunctional because it is severly truncated (i.e. cut short). It is truncated because of a nonsense mutation in the DNA that turns a codon into a "stop" codon somewhere in the middle of the sequence. It is the same nonsense mutation that renders the gene disfunctional in all primates. In guinea pigs, it is a different mutation. This is why it is striking evidence of common descent.

theyeti

tronvillain

I seem to recall that the one base change in the haemoglobin intron wrecks the whole structure because the intron is not removed from the RNA transcript.

theyeti

Sorry, after looking through the article, I see that it's a frameshift mutation, and not a nonsense mutation. Either way, the same argument holds. There are lots of these kinds of psuedogenes, and here's the relevant paragraphs on them and their mutations.

So it's not just the Vit. C bit you have to deal with, it's a whole bunch of 'em.

theyeti

[ January 24, 2002: Message edited by: theyeti ]</p>

Dr Rick

A single base pair substitution is the cause of sickle cell anemia, but the hemoglobin is fuctional under most circumstances and the substitution occurs within the exon. Other hemoglobinopathies such as the thalassemias are often due to mutations in promoter or enhancer sequences. Some of these hemoglobins can be functional and compatible with survival.