Let’s Hear It for Junk

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Hi! There's an interesting site which compares DNA to a programming language, take a look here. It's curious how the author seems to ignore the possibility of the system to have been 'created', and instead he recommends some Dawkins' books, like the blind watchmaker (a crap piece of work in my humble opinion). Fr3dY

Thanks Dave, I'll check it out. idnet.com.au

What is the evidence that these “endogenous retroviruses” are indeed “endogenous retroviruses”? Good question. I had to go looking for an answer as I took it for granted there were distinguishing markers of some sort. The presence of genes that code for viral protein coats appears to be the smoking gun. The viruses in all of us

Retroviruses differ from retrotransposons by the presence of at least one additional coding region, the envelope (env) gene, which codes for viral membrane proteins. Retroviral gag gene products have acquired the ability to be transported to the cell surface and to bud from the cell membrane, incorporating Env proteins during this process (Figs. 1 and 2C). Env mediates the binding of virus particles to their cellular receptors, enabling virus entry, the first step in a new replication cycle (Fig. 2D). Thus, the env gene adds to retroelements the ability to spread between cells and individuals (infectivity). The concerted action of Gag and Env proteins directing HERVs to budding and cellular export may exclude these sequences from the retrotransposition pathway. In addition, blocking of the receptor by secreted Env molecules may hinder re-infection of virus-producing cells (receptor interference) and re-integration of viral genomes. Both effects together could explain the limitations in copy number of HERV proviruses compared with other retroelements (Table 1). Proviruses of the HERV-H family, for instance, that have retained env-related sequences (12) are present in only 50 copies, whereas proviruses without the env gene exhibit a much higher amplification (see Table 1). Therefore, at first sight, elements with retrotransposon structure seem to be more prone to amplification than retroviruses, reflecting perhaps their different routes of replication: intracellular versus intercellular spread. Surprisingly, however, a moderate copy number of full-length proviruses is always accompanied by a considerable frequency of solitary LTRs (Table 1), suggesting that HERVs may indeed spread very efficiently either by infection or by retrotransposition. The subsequent formation of solitary LTRs by excision of coding sequences may indicate that an unrestricted increase of retroelements with an RT gene and LTRs would be detrimental. Truncation of the promoter sequences at the 5' ends of SINEs and LINEs may mirror a similar constraint. Alternatively, the latter may simply examplify insufficient reverse transcription starting from the 3' end of transcripts. Retroviruses may be seen as specialized mobile retroelements able to spread rapidly in a host population. Under the selective pressure of an extracellular exogenous life cycle, they take advantage of the plasticity inherent to RNA genomes. Endogenization of exogenous retroviruses can then be interpreted as an adaptation to the far slower evolutionary pace of the host.

DaveScot

DaveScot says "Endogenous retroviruses are trespassers that have vandalized the property, leaving a “Kilroy Was Here” kind of graffiti behind. The lifelong supply of primary oocyte (immature egg cells) is created before birth. They exist for as long as 50 years in humans in a state of suspended animation with meiosis halted at phase 1 anaphase (IIRC). There is no blood barrier during suspended storage. While in the state of suspended storage I propose that eggs can be infected by a retrovirus. Since the cell is dormant and there isn’t a lot of gene expression going on, the viral genes don’t get expressed in the way they would if they infected an active somatic cell. Furthermore I propose that the resumption and completion of meiosis deactivates the viral genes (maybe during crossover) so they are never expressed to form new virus particles. Remnants of germ cell viral infections take up some 8% of the human genome. It’s the presence of these endogenous retroviruses at the same loci in closely related species, but weathered differently in the amount you’d expect for the time the cell lines diverged, that I find as compelling evidence of common ancestry." What is the evidence that these "endogenous retroviruses" are indeed "endogenous retroviruses"? idnet.com.au

"The new stretches of genome start out as useless junk, but can later be fashioned through evolution into new on-off switches for genes." This is a statement of evidence free belief. It is necessary to interpret the unexpected discovery that what they previously said (by faith) was junk, is not in fact junk. idnet.com.au

What we seem to be discovering, is that what makes a human different from a mouse is not to be found in the coding DNA. The problem still seems to be a certain mindset that insists the difference must be found in the DNA at all. Both sides here seem to accept the premise. Is what makes a human different from a mouse to be found in the DNA at all? I predict, that even if it is found that the reasons for differences are not found in DNA, this will still pose no problem for the Darwinians. I also find it intersting every time someone points out similarities in non-coding regions as evidencd for common ancestry. Every single instance of this is yet another nail in the coffin of the underlying premise, which is that the differences are due to differences in DNA. Mung

Matthew Tan: "And this should show up in the descendant where the egg-DNA is longer sperm-DNA by the same amount of retroviral DNA. Is this the observed data?" Perhaps the oocytes, in a state of suspended animation, are not vulnerable to viral attack. The whole purpose of a virus attack is for the virus to use the cellular machinery of the host to replicate itself. But if that cellular machinery is in hibernaton, perhaps there is an immediate way for the virus to detect that, hence, no need to protect the oocytes via the mechanism employed to protect the sperm cells. PaV

dave, "that last bit of compelling evidence of common ancestry", and the egg "can be infected by a retrovirus". I don't understand you here. If only the egg and not the sperm is infected by retroviral DNA, then the egg-DNA will have more nucleotide bases than the sperm-DNA. And this should show up in the descendant where the egg-DNA is longer sperm-DNA by the same amount of retroviral DNA. Is this the observed data? And how do we know that these are retroviral infection of DNA in the first place? Suppose hypothetically, the common ancestor of primate does not exist, and the DNA of the first humans, chimps, gorillas, etc. just happen to have these same DNA sequences, at the same loci, which are weathered over time (or unchanged over time, whatever the case maybe). If our starting point is common ancestry, then we take it as evidence of common ancestry. If our starting is not, then we take it as non-evidence. MatthewTan

MatthewTan "What do you think about the hypothesis that retroviruses inserted their DNA sequences into the common ancestor of primates, and these inserted sequences have been repeated in all primates - supposedly an evidence of common descent?" It might work. As a Computer Science person, however, everything looks like a computer so I'm inclined towards the "compiler hypothesis" WinstonEwert

Atom re; shared errors I tend to agree that a lot of junk DNA has undiscovered purpose with undiscovered methods of modulation encoding data. Even if every single one of the 3 billion base pairs in a human genome were exploited to encode data it seem incredible it's enough to define the structure of a human. I suspect that a great deal of heritable information is epigenetic and lies in the structure of the cell itself. Ostensibly the cell comes from an unbroken line of cells going back billions of years where the arrangement and fine detail are passed along through all that time. This then adds trillions of molecules to the potential information storage space. But back to the point of junk DNA. Endogenous retroviruses, which aren't really mistakes but rather more are trespassers that have vandalized the property, so to speak, leaving a "Kilroy Was Here" kind of graffiti behind. The graffiti sometimes gets inducted into some meaningful task but most often it just weathers away over millions of years until it's no longer recognizable; having no function it isn't kept up very well. These remnants of germ cell viral infections take up some 8% of the human genome. It's the presence of these at the same loci in closely related species, but weathered differently in the amount you'd expect for the time since the cell lines diverged, that I find as that last bit of compelling evidence of common ancestry. If common design instead of common ancestry then the designer seems to be using an existing species in situ as a template for the new species and that essentially makes common design and common ancestry effectually the exact same thing. In a private discussion group one objection raised was how germ cells get infected so often without compromising the germ cell's ability to grow into a healthy adult. Mammals were the focus, particularly primates. In the case of sperm cells it does seem unlikely. There's a blood barrier in sperm cell storage that inhibits viral infection and they don't remain alive long - either being used for their intended purpose or being disposed of within days of creation. Mammalian egg cells are a whole different story. The lifelong supply of primary oocyte (immature egg cells) is created before birth. They exist for as long as 50 years in humans in a state of suspended animation with meiosis halted at phase 1 anaphase (IIRC). After puberty at monthly intervals one or several come out of suspended animation and complete the process of meiosis to become ready for fertilization. There is no blood barrier during suspended storage. While in the state of suspended storage I proposed they can be infected by a retrovirus but since the cell is dormant and there isn't a lot of gene expression going on the viral genes don't get expressed as they would in an active somatic cell. Furthermore I proposed that the completion of meiosis deactivates the viral genes (maybe during crossover) so they are never expressed to form new virus particles. In that manner the new bit of viral graffiti gets passed along to the next generation but it rarely if ever compromises the germ cell in the process. DaveScot

The architecture of a self-healing multi-fault-tolerant system (like biology) will be radically different than the computer systems architectures we are familiar with. If one builds a self-healing architecture, it is wise to store spare parts and blue prints in totally unrelated places. I've not given up on the idea that one of the uses of junk DNA is for spares. By the way, we barely understand how to build self-healing architectures. Once engineers begin to explore the art of building self healing, we will probably have a better conception of junk DNA. Salvador scordova

WinstonEwert, interesting idea with the compiler. I do have an issue with people saying "shared DNA errors" when we're not even sure what a lot of DNA really does ( See "junk" DNA) and are kinda clueless on a lot of details of the genetic program. We understand some things, but are not close to knowing every level of function. It wouldn't surprise me if the "errors" were actual codes on a different level of abstraction. We'll see, I guess. Atom

MatthewTan: "Perhaps spiritual rather than mechanical? That’s why the “dynamic” transposons are there - spiritual remote control system through which the angels of God work through to bring about evolution and miraculous healings!" I like the idea! Anyway, I like to think that the spiritual-material axis is more a continuum than a dichotomy, and so, at some level, our dynamic transposons must benefit of some form of "mechanical" control, at least just to realize some "repetitive" functions in a more efficient way (just as we do with computers). As I have said many times, I don't really care if our "angels of God" (take it as a brilliant synonim for "designer(s)) work their transposonic wonders on already existing hardware (common descent), or on "ex novo" hardware through already existing code (uncommon descent). What's the difference? The really important problem is: what is the code? what is the information? how is it practically implemented? (at least for the part we can observe, and therefore analyze scientifically?). gpuccio

WinstonEwert "alleged shared copying errors" What do you think about the hypothesis that retroviruses inserted their DNA sequences into the common ancestor of primates, and these inserted sequences have been repeated in all primates - supposedly an evidence of common descent? MatthewTan

gpuccio "it is almost certainly mechanical and algorithmic at the level of lower implementation." Perhaps spiritual rather than mechanical? That's why the "dynamic" transposons are there - spiritual remote control system through which the angels of God work through to bring about evolution and miraculous healings! MatthewTan

PaV, thanks for the link. I have always been a fan of non coding DNA. In particular, I am fascinated by transposons, probably the most elusive, and atv the same time dynamic, part of the genome. I completely disagree with the common view that transposons are useless, or egoist, or negative parts of the genome. Indeed, they are probably one of the main mechanisms of control of the procedures. The only problem is that we don't understand anything of how the control, of which so many are beginning to speak, is coded and "controlled". In other words, as I have often said, we don't know the code for the procedures, for the software itself. It should be in the non coding DNA, introns and transposons have certainly an important role, but who understands the code, who understands the general plan? I am sure that non coding DNA is going to surprise us ever more. And yes, explaining the procedures, explaining the controlling code, in terms of RM + NS will certainly be much more difficult than trying to explain the gross effectors (the protein genes). But we should not despair: darwinists' resources of creativity are immense! WinstonEwert: About God's compiler: I certainly agree, though I prefer to speak of designer(s), to stay consistent with the ID approach. Whoever designs the code, and however he does it, at some point he must implement the information in a physical code (let's say DNA). And, certainly, some form of "mechanical" compiler is reasonably used at that level, be it a biochemical-biophysical system or something else. So yes, although the generation of information is certainly not mechanical, not algorithmic and not deterministic at the higher level (conscious, intelligent action), it is almost certainly mechanical and algorithmic at the level of lower implementation. gpuccio

This inclines me to think that God used a compiler to produce the DNA. It is a "hypothesis" which I've been thinking about in relation to such things as shared genetic information and alleged shared copying errors. Both, I believe, could be seen in the products of compilers. If we have essentially a shared library of protiens which the compiler uses and adapts for individual products then this sort of things seems very natural. WinstonEwert

Thanks for the link PaV - I'll add it to my arsenal. It is just so sad to see these guys never give up. And guess what else. This week's issue of science has another profound statement to make about (variable) evolution: "Researchers are discovering the intricacies of relationships in which one organism sometimes influences the evolution of another and sometimes doesn't" So it sometimes affects and sometimes doesn't - wow startling. jpark320