Junk DNA not refuted.

[Morat]

  I'm not blasting Souljah. I'm pointing out the honest truth. He posted an abstract, and made a claim about it. Someone came along, read the actual paper and disagreed.

   Souljah repeated his claim, refused to discuss the actual paper, and then started complaining about being attacked.

   He either needs to abandon the thread, or discuss the paper (or admit he won't or can't). As long as he hangs around in this thread, I'm going to remind him that he didn't read the paper, won't discuss it, and does nothing more than repeat himself despite having been shown wrong.

  The second he starts discussing Rufus' objections or admits he has no intention of doing so, things will change.

 

[RufusAtticus]

Originally posted by s0uljah
Exactly my point.

Care to discuss it? I have pointed out why the abstract is not saying what you think it is and that the paper does not show what you think it does. (Morat has nicely copied the meat of my comments to this thread.) Do you wish to actually address my comments?

 

[Morat]

  Actually, I think I'll be nice and step out. Perhaps Souljah will discuss it if I play nicer. Souljah, go right ahead. I am quite interested in hearing your discussion with Rufus, and promise just to lurk on this thread.

  I'll restrict myself to comments directed to others.

 

 

[Chris†opher Paul]

You can't <I>read</I> the primary literature, because you lack the education to grasp it.

Souljah, go right ahead. I am quite interested in hearing your discussion with Rufus, and promise just to lurk on this thread.

Bless you for your insult on my education Morat.&nbsp; Its alright, you simply don't know what you are talking about.

Anyway, you seem to be contradicting yourself.&nbsp; If you claim I can't read it, then why do you want me to read it and discuss it.&nbsp; (Since you assume I haven't read it)

 

[RufusAtticus]

Thanx, Morat. How about it Souljah? Do you wish to defend your interpretation of the paper and/or explain how mine is wrong? This is the science forum, we might as well discuss science.

Here is the repost of my full comments from the previous thread:
===============

Okay I read the Beaton & Cavalier-Smith paper over lunch and here are some brief comments.

The paper does not find a function in junk DNA. It is refered to as functional because the amount of DNA (primary plus secondary) has selectable effects on the phenotype of the cell. It isn’t some found function of secondary DNA, but rather a function for DNA period. Beaton & Cavlier-Smith (1999) is attempting to identify the selection pressures that lead to genome expansion. Thus anyone attempting to use this paper as evidence against evolution has a flawed argument. Basically, they are ignoring, either by deception or ignorance, the conclusions of the authors, which deal with the evolutionary aspects of genome size. This is readily apparent to just about anyone reading this paper. If anyone here, (s0uljah, npetreley, etc.) wants to contest my understanding of this paper, I invite you to get a copy and read it yourself. The paper is available free from the following link.

Beaton & Cavalier-Smith (1999)

This paper uses a class of related organisms that have two sets of DNA: one in the nucleus and the other in the “nucleomorph.” This is because these organisms are the result of a symbiotic fusion of a red alga with a biflagellate host, several hundred million years ago. The nucleus of the biflagellate host has been maintained, whereas the red alga has lost most of its DNA and nucleus. The nucleomorph is all that remains of the red alga’s nucleus. The morphology of these organism is a good argument against intelligent/common design, since the chloroplasts are inefficiently placed inside an extra membrane. Plants and algae don’t have this odd organelle-within-an-organelle configuration. If these creatures are the result of scient design, then it is not a very good one with respect to organization. Furthermore, the differences in chloroplast placement imply that the same scient designer is not responsible for plants/algae and cryptomonads, since there isn’t a common design there.

More info on cryptomonads:
http://www.wikipedia.com/wiki/Cryptomonads
http://www.talkorigins.org/faqs/evolution-research.html#endosymbiosis

Now back to the paper. Here is a section of the paper with discusses various attributes of secondary DNA. It is good background information for those who don’t want to read the paper.

Although it us widely assumed that mutational explanations, specifically the selfish DNA hypothesis, can explain the existence of so much non-Coding DNA (Maynard Smith & Szathmary 1997), comparative evidence strongly indicates that only a small fraction of secondary DNA in nuclei (e.g. most transposons) is simply genetically parasitic. A significant fraction of non-coding DNA, notably introns (Cavalier-Smith 1978, 1985d) and dispersed repetitive sequences (e.g. Alu repeats, L1 elements), is likely to be ‘selfish’ in origin (Cavalier-Smith 1985e), but is today predominantly not actively spreading genetic parasites. As ex-selfish DNA, their maintenance and persistence in the genome must be explain in the same way as other non-coding DNA. Most secondary DNA must be either neutral junk or functional.

Let’s look at the interpretation offered by the website in s0uljah’s post:

The new study is a stunning rebuttal to the evolutionary theories that attempt to discredit design and promote concepts such as "junk" DNA and "selfish" DNA.

What is interesting after I read this paper is that the above interpretation is found no where in the paper and is not supported by it. It takes a rather far stretch to justify the above interpretation using the actual study. In fact the paper has nothing to do with design, pro or con. It is only testing between three evolutionary theories, finding two insufficient to explain the observations. It confirmed that the third evolutionary explanation is the only one that explains the data. Since it shows that there is an explanation from evolutionary theory that stands up with all the data, it is amazing how the webpage can even claim that evolution has been discredited here. In no way has this paper supported any concept of design or anti-evolution beliefs.

The quote that the website offers up to support its claims is from the abstract of Beaton & Cavalier-Smith (1999).

Furthermore, the present lack of significant amounts of nucleomorph secondary DNA confirms that selection can readily eliminate functionless nuclear DNA, refuting 'selfish' and 'junk' theories of secondary DNA.

To a person who hasn’t read the paper carefully or even at all, the quote looks like it is saying that the authors have shown that there is no such thing as selfish or junk DNA. However, this is not this case, and the above quote is actually referring to the two hypotheses of why secondary DNA accumulates, not hypotheses of whether it does something or not.

Here are the three hypotheses:

1. Secondary DNA accumulates because it is junk and there is no strong selection pressure against it: the ‘junk’ hypothesis.
2. Secondary DNA accumulates because it is parasitic: the ‘selfish’ hypothesis.
3. Secondary DNA accumulates because the mass of DNA directly determines nuclear volume and the nuclear volume is under selection: the ‘skeletal’ hypothesis.

Using cryptomonads, the authors looked at ratios of cell volume to the size of the nuclear genome and the nucleomorph genome. What they found is that the size of the nuclear genome scaled up with the volume of the cell, but the size of the nuclemorph genome stayed relatively constant. If in these organisms DNA accumulated because of the first or second hypotheses, then the nucleomorph’s genome should be affected just like the nucleus’s genome. Because this doesn’t happen, the authors argue (probably correctly) that the first and second hypotheses cannot account for the observations. The authors then showed how the third hypothesis accounted for both the scaling of the nuclear genome and the non-scaling of the nucleomorph genome. (Read the paper for more information.)

What the authors didn’t do is show that there is no such thing as selfish or junk DNA, only that selfish or junk attributes of secondary DNA aren’t enough to explain why it accumulates. Because the webpage posted by s0uljah is claiming that they did the former, it is fundamentally flawed by depending on an erroneous interpretation.

But you don’t have to take my word for it; the paper is freely available online for you to read. If you have problems understanding the more technical aspects of the paper, I’ll be glad to discuss it. Please read the primary literature for yourself and post your comments in this thread.

 

[Chris†opher Paul]

Secondary DNA accumulates because the mass of DNA directly determines nuclear volume and the nuclear volume is under selection: the ‘skeletal’ hypothesis.

This is what the study supports, correct?

 

[RufusAtticus]

Yes.

 

[Chris†opher Paul]

Originally posted by RufusAtticus
Yes.

Right, and it supports the idea that secondary DNA is not pointless, correct?

 

[Sky]

Correct.

 

[RufusAtticus]

It supports the idea that the amount of DNA is not pointless. Secondary DNA does not have a special structural ability that primary DNA lacks. It is a natural property of DNA in eukaryotic nuclei, which appears to be due to historical constraints of evolution.

However, secondary DNA is still made up of junk regions, selfish regions, etc.

 

[Chris†opher Paul]

Originally posted by Sky77
Correct.

Right, so therefore, people claiming that non-coding DNA is "junk," ie, "not useful," then they are incorrect, which was the reason I posted that article in the first place.&nbsp; I have heard people on here claim that it is a sign of bad design, etc.

 

[Chris†opher Paul]

However, secondary DNA is still made up of junk regions, selfish regions, etc.

I don't understand how the paper supports that assertion.

 

[RufusAtticus]

Originally posted by s0uljah
Right, so therefore, people claiming that non-coding DNA is "junk," ie, "not useful," then they are incorrect,

The term "junk" does not perclude some usefulness. (Ask any auto salvage yard.)

which was the reason I posted that article in the first place. I have heard people on here claim that it is a sign of bad design, etc.

It still is, as I elaborated in the original thread:
In fact, the paper is another example that historical constraint and not intelligent design guides evolution. It is still energetically wasteful to replicate secondary DNA. So then, why is that used as the solution to the nucleus size problem? Why didn't the designer just make a larger nucleus instead of relying on non-coding DNA? Why did the designer design it such that larger cells need larger nuclei?

Furthermore, the function they found is not just for junk DNA, it's for all nuclear DNA. Which brings up the question of why an intelligent designer would use junk DNA over coding DNA?

I don't understand how the paper supports that assertion.

Your original claim is that the paper overturns that idea that there exists Junk DNA. So I guess it is up to you to use the paper to show how. My above comments rest only on the obeservation that the paper does not support what you think it is. Or put it another way, the observation that you have still have not shown, using the paper itself, that Beaton & Cavilier-Smith (1999) is showing what you say it is. You made the original positive comment, the burden of proof is on you.

 

[Chris†opher Paul]

The term "junk" does not perclude some usefulness. (Ask any auto salvage yard.)

Ah, but it was used on these forums to demonstrate "bad" design. "Junk" is not a correct term, which is what bothers me.

Why didn't the designer just make a larger nucleus instead of relying on non-coding DNA? Why did the designer design it such that larger cells need larger nuclei?

Dunno, ask Him when you meet up, I'm sure it will be interesting to you, considering your expertise on the subject.

 

[RufusAtticus]

Originally posted by s0uljah
Ah, but it was used on these forums to demonstrate "bad" design.

Because it is energetically wasteful to replicated DNA that only acts as "filler." The sentient designer apparently designed bacteria better than humans in this respect.

"Junk" is not a correct term, which is what bothers me.

Why is not correct?

Dunno, ask Him when you meet up, I'm sure it will be interesting to you, considering your expertise on the subject.

You are offering this as an example of good design. Are you now not willing to defend that view?

You still haven't explained how the paper is showing that Junk DNA doesn't exist. Are you willing to do this, or do you now concede?

 

[Chris†opher Paul]

You still haven't explained how the paper is showing that Junk DNA doesn't exist. Are you willing to do this, or do you now concede?

Concede? This is not about me man, if I thought I was wrong I would gladly tell you that, and bow out.

Besides, I have clearly explained why I think that "junk" DNA doesn't exist, which is supported by that article. Its not "junk" if it is useful. It is actually non-coding DNA, not evolutionary "left overs" or something like that, which is the belief I was responding to by posting that article.

 

[RufusAtticus]

Originally posted by s0uljah
Besides, I have clearly explained why I think that "junk" DNA doesn't exist, which is supported by that article. Its not "junk" if it is useful. It is actually non-coding DNA, not evolutionary "left overs" or something like that, which is the belief I was responding to by posting that article.

The problem you are having is that you don't understand what junk DNA actually refers to. All junk DNA is secondary DNA, but not all secondary DNA is junk DNA. Junk DNA only refers to those sections of the genome for which the sequence doesn't matter for its existance. The sequence is effectively neutral. This does not mean that the DNA has no use, or wasn't selected. In fact, the origin of junk DNA and in fact a significant fraction of secondary DNA lies in evolutionary history. They are left overs of parasitic DNA, as the paper states:

A significant fraction of non-coding DNA, notably introns (Cavalier-Smith 1978, 1985d) and dispersed repetitive sequences (e.g. Alu repeats, L1 elements), is likely to be ‘selfish’ in origin (Cavalier-Smith 1985e), but is today predominantly not actively spreading genetic parasites.

So when you claim that Junk DNA is no longer Junk DNA if it shows some function, you are making a big mistake.

You seem to be arguing that the existance of so much Junk DNA is the result of intellegent design. If so, why is it such an ineffecient design? You have been claiming that this paper shows a use for Junk DNA, and thus it can't be used as an example of bad design. Yet you neglect the fact that it is still a very ineffecient use and not too great a design. So in fact, this paper doesn't help your position one iota.

 

[chickenman]

souljah, the real problem you have is that it isn't only the "amount" of DNA that is the same between humans and chimpanzees - the sequence is homologous as well. The function this paper ascribes to secondary DNA is one that doesn't depend on the sequence. Thus, the secondary DNA is still very powerful evidence for evolution

 

[Chris†opher Paul]

If I "have a problem understanding" and if we want to rely on authorities and "experts", let's actually rely on authorities, shall we?

By Jaan Suurkula M.D.

Presently, only the function of a few percent of the DNA is known, the rest has been believed to be "junk". The most exhaustive knowledge is about the genes responsible for the bodily structures, the structural genes, which are the simplest part of the system. But the knowledge about the most important part of this system, the regulator genes, is incomplete. The genetic code language of these genes is only partially known.

More than 95 percent of all DNA, was called "Junk DNA" by molecular biologists, because they were unable to ascribe any function to it. They assumed that it was just "molecular garbage". If it were "junk", the sequence of the "syllables", i.e. the nucleotides in DNA should be completely random.

However it has been found that the sequence of the syllables is not random at all and has a striking resemblance with the structure of human language (ref. Flam, F. "Hints of a language in junk DNA", Science 266:1320, 1994, see quote below). Therefore, scientists now generally believe that this DNA must contain some kind of coded information. But the code and its function is yet completely unknown.

It has been reported that the sequences of this unknown DNA are inherited and that some repetitive patterns in it seem to be associated with increased risk for cancer. Also, the DNA has been found to mutate rapidly for example in response to cancer. It has been speculated that this DNA may contribute to the regulation of cellular processes. Haig H. Kazazian, Jr., chairman of genetics at the University of Pennysylvania has recently found reasons to suspect they may be a key force for the development of new species during evolution. He thinks this DNA may be essential for increasing the plasticity of the hereditary substance.

Such observations have spurred an extensive research into "Junk DNA" in recent years, some of which is briefly presented below.



Recent studies
Various important roles of "Junk DNA" have been discovered in recent years.

Some studies have found that noncoding DNA plays a vital role in the regulation of gene expression during development (Ting SJ. 1995. A binary model of repetitive DNA sequence in Caenorhabditis elegans. DNA Cell Biol. 14: 83-85.), including:

development of photoreceptor cells (Vandendries ER, Johnson D, Reinke R. 1996. Orthodenticle is required for photoreceptor cell development in the Drosophila eye. Dev Biol 173: 243-255.),
the reproductive tract (Keplinger BL, Rabetoy AL, Cavener DR. 1996. A somatic reproductive organ enhancer complex activates expression in both the developing and the mature Drosophila reproductive tract. Dev Biol 180: 311-323.), and
the central nervous system (Kohler J, Schafer-Preuss S, Buttgereit D. 1996. Related enhancers in the intron of the beta1 tubulin gene of Drosophila melanogaster are essential for maternal and CNS-specific expression during embryogenesis. Nucleic Acids Res 24: 2543-2550.).
Over 700 studies have demonstrated the role of non-coding DNA as enhancers for transcription of proximal genes. This includes a/o:

eosinophil-derived neurotoxin (EDN) and eosinophil cationic protein (ECP) (Tiffany HL, Handen JS, Rosenberg HF. 1996. Enhanced expression of the eosinophil-derived neurotoxin ribonuclease (RNS2) gene requires interaction between the promoter and intron. J Biol Chem 271: 12387-12393),
the variable region of the rearranged immunoglobulin mu (IgM) gene (Jenuwein T, Forrester WC, Fernandez-Herrero LA, Laible G, Dull M, Grosschedl R. 1997. Extension of chromatin accessibility by nuclear matrix attachment regions. Nature 385: 269-272.; Nikolajczyk BS, Nelsen B, Sen R. 1996. Precise alignment of sites required for mu enhancer activation in B cells. Mol Cell Biol 16: 4544-4554),
the alpha-globin gene (Bouhassira EE, Kielman MF, Gilman J, Fabry MF, Suzuka S, Leone O, Gikas E, Bernini LF, Nagel RL. 1997. Properties of the mouse alpha-globin HS-26: relationship to HS-40, the major enhancer of human alpha-globin gene expression. Am J Hematol 54: 30-39),
the activin beta A subunit gene (Tanimoto K, Yoshida E, Mita S, Nibu Y, Murakami K, Fukamizu A. 1996. Human activin betaA gene. Identification of novel 5' exon, functional promoter, and enhancers. J Biol Chem 271: 32760-32769).
Over 60 studies have demonstrated the role of non-coding DNA as silencers for suppression of transcription of proximal genes. Such silencer genes include a/o:

apolipoprotein A-II gene (Bossu JP, Chartier FL, Fruchart JC, Auwerx J, Staels B, Laine B. 1996. Two regulatory elements of similar structure and placed in tandem account for the repressive activity of the first intron of the human apolipoprotein A-II gene. Biochem J 318: 547-553.),
the osteocalcin gene (Goto K, Heymont JL, Klein-Nulend J, Kronenberg HM, Demay MB. 1996. Identification of an osteoblastic silencer element in the first intron of the rat osteocalcin gene. Biochemistry 35: 11005-11011),
the 2-crystallin gene (Dirks RP, Kraft HJ, Van Genesen ST, Klok EJ, Pfundt R, Schoenmakers JG, Lubsen NH. 1996. The cooperation between two silencers creates an enhancer element that controls both the lens-preferred and the differentiation stage-specific expression of the rat beta B2-crystallin gene. Eur J Biochem 239: 23-32).
Some studies indicate that non-coding DNA regulate translation of proteins. This includes a/o


the Lipoprotein Lipase gene (Ranganathan G, Vu D, Kern PA. 1997. Translational Regulation of Lipoprotein Lipase by Epinephrine Involves a Trans-acting Binding Protein Interacting with the 3' Untranslated Region. J Biol Chem 272: 2515-2519)
glutathione peroxidase and phospholipid-hydroperoxide glutathione peroxidase genes (Bermano G, Arthur JR, Hesketh JE. 1996. Role of the 3' untranslated region in the regulation of cytosolic glutathione peroxidase and phospholipid-hydroperoxide glutathione peroxidase gene expression by selenium supply. Biochem J 320: 891-895),
the luteinizing hormone/human chorionic gonadotropin receptor gene (58. Lu DL, Menon KM. 1996. 3' untranslated region-mediated regulation of luteinizing hormone/human chorionic gonadotropin receptor expression. Biochemistry 35: 12347-12353),
the thyrotropin receptor gene (Kakinuma A, Chazenbalk G, Filetti S, McLachlan SM, Rapoport B. 1996. BOTH the 5' and 3' noncoding regions of the thyrotropin receptor messenger ribonucleic acid influence the level of receptor protein expression in transfected mammalian cells. Endocrinology 137: 2664-2669),
the interleukin 1 type I receptor gene (Ye K, Vannier E, Clark BD, Sims JE, Dinarello CA. 1996. Three distinct promoters direct transcription of different 5' untranslated regions of the human interleukin 1 type I receptor: a possible mechanism for control of translation. Cytokine 8: 421-429)


Conclusion
The idea that a major part of our DNA is "garbage" ignored the fact that a key feature of biological organisms is optimal energy expenditure. To carry enormous amounts of unnecessary molecules is contrary to this fundamental energy saving feature of biological organisms. Increasing evidence are now indicating many important functions of this DNA, including various regulatory roles. This means that this so-called non-coding DNA influences the behavior of the genes, the "coding DNA", in important ways. Still there is very little knowledge about the relationship between non-coding DNA and the DNA of genes. This adds to other factors making it impossible to foresee and control the effect of artificial insertion of foreign genes.




--------------------------------------------------------------------------------


JUNK DNA- May Not Be Junk After All
(Quoted from Gene exchange no 2, 1996)

In another reminder that we may not understand the full ramifications of genetic engineering, Science magazine recently reported new work on the function of genetic material*. Scientists have long been puzzled by the fact that fully 97% of the DNA in human cells does not code for proteins and appears to consist of meaningless sequences. The possibility that this apparently useless DNA has some as yet unknown function continues to tantalize scientists.

The Science article reports on a paper suggesting that the non-coding 97% of the DNA, commonly referred to as junk DNA, might have a function. The authors of the paper employed linguistic tests to analyze junk DNA and discovered striking similarities to ordinary language. The scientists interpret those similarities as suggestions that there might be messages in the junk sequences, although its anyone s guess as to how the language might work. * F. Flam, Hints of a language in junk DNA, Science 266:1320, 1994.

http://www.psrast.org/junkdna.htm

 

[Chris†opher Paul]

Here is some more info I found...

"Until recently, researchers maintained that 97 percent of human DNA was repetitive and useless. After mapping the entire human genome, researchers at Celera and the international Human Genome Project believe that actually about 98.5 percent is repetitive -- but they no longer think it's junk. "

http://www.wired.com/news/technology/0,1282,41750,00.html

It is still energetically wasteful to replicate secondary DNA. So then, why is that used as the solution to the nucleus size problem? Why didn't the designer just make a larger nucleus instead of relying on non-coding DNA? Why did the designer design it such that larger cells need larger nuclei

No offense, but many other experts disagree with you on this "wasteful," "bad design" viewpoint.