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Is There “Junk” in Your Genome? Part 2

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January 19, 2012 Tags: Genetics
Is There “Junk” in Your Genome? Part 2

Dennis Venema. You can read more about what we believe here.

One of the challenges for discussing evolution within evangelical Christian circles is that there is widespread confusion about how evolution actually works. In this (intermittent) series, I discuss aspects of evolution that are commonly misunderstood in the Christian community. In this second of several posts on “junk DNA”, we explore how small, autonomous DNA sequences called transposons have shaped mammalian genomes for worse, and for better.

As we saw in the last post, only a small fraction of the human genome appears to be subject to selection (on the order of 5-6%). The rest appears free to mutate freely without consequence to mammalian biology, and as such constitutes good evidence that it performs no particular function. An additional line of evidence in favor of non functionality in the human genome is the observation that a large fraction of our genetic material is made up of what are known as mobile genetic elements, or “transposons.” These little snippets of DNA are well known and well studied in many organisms, including humans. So, what are they, and what are they up to?

Along for the ride, but looking out for number 1

Non-biologists are usually somewhat taken aback when they learn about transposons. Transposons are small segments of DNA inserted into in the genomes of many organisms that are little worlds unto themselves: they have a few genes that serve only to copy themselves and move themselves to new locations in a genome. That’s it! On the scale of biodiversity, transposons are less life-like even than viruses. They are the perfect parasites: using their host to provide resources so they can replicate themselves, and with a “lifestyle” so simple that replication is essentially its only feature. Their origins, like the origins of viruses, is somewhat of a mystery.

Despite their somewhat mysterious nature, transposon sequences make up a staggering 45% or more of our genome. That’s about 1.4 billion DNA base pairs of our genetic material that is recognizable as functional transposons or their mutated, fragmentary remains. Not surprisingly, nearly all transposon sequences in the human genome are not under selection – they are free to accumulate mutations. These mutations have no effect on us since they do not alter any function we require.

Rags to riches: converting transposons to functional sequences

Despite their parasitic nature, sometimes the host species can exploit transposons as a source of genetic novelty. The ability of transposons to copy and spread themselves around in genomes raises the intriguing possibility that they can acquire a function if they land in the right chromosomal area. While it is difficult (though not impossible) for a transposon to acquire a function as gene coding sequence (i.e. becoming a host protein product), it is comparatively easy for a transposon to pick up a function as a regulatory sequence: a segment of DNA that directs when and where a certain host gene product should be made. Transposons contain regulatory sequences for their own genes already, and these sequences can potentially interact with regulatory sequences in the host genome.

Perhaps a review of gene structure and function would be helpful at this point. Genes are portions of the long DNA sequences that make up chromosomes (each chromosome is one very long DNA molecule). As we have seen above, a good proportion of these sequences are either transposons or the defective fragments of transposons, as well as other DNA that is not under selection and is free to mutate. Interspersed in this sea of non-selected sequences are genes: segments of chromosomes that code for protein products that carry out functions within the cell: enzymatic functions, structural functions, and so on. These sequences stand out because they are subject to selection, and thus do not change at the same rate as sequences that are free to mutate (as we discussed previously).

Genes have a typical structure (obviously simplified here somewhat). First off, there is the actual DNA sequence that specifies the protein product sequence (the so-called “coding sequence”, shown in blue). This sequence is usually broken up into segments in mammalian genes, and these sequences are spliced together when the DNA sequence of the gene is transcribed into a “working copy” called mRNA – a short duplicate of the code that can be used by the cell’s machinery to actually build the specified protein.

In addition to the actual coding sequences, other sequences are needed to tell the cell when and where certain genes should be transcribed into mRNA. Every cell in an organism has the same genes in their chromosomes, but not all are transcribed. Using different genes in different combinations is what makes cells take on distinct roles – for example, cells in your small intestine need different genes (for absorption of nutrients) than do cells of the immune system (for fighting off pathogens). Regulatory sequences make sure any given cell type has the right genes transcribed and made into protein products. Some of these sequences are part of the mRNA transcript (shown in red), and others are not transcribed but only part of the chromosomal DNA sequence (such as the “promoter” region that directs the enzymes responsible for making the mRNA transcript (shown in blue).

So, what happens when a transposon inserts into the regulatory sequence of a gene? In many cases, this mutation (the insertion event) will cause a problem (perhaps the gene is no longer transcribed in the right way, for example). In some cases, however, the gene can tolerate such an insertion. Regulatory DNA is more able to accept changes than is coding sequence DNA, so it is quite possible that an insertion may not harm the function of a gene.

In some cases, sequences from the transposon can participate in the regulation of the neighboring gene. If these changes are beneficial, as they sometimes are, then the transposon sequences involved in regulation come under selection. Some parts of the transposon mutate away beyond recognition, and the useful bits remain since they, now being under selection, are not (as) free to mutate. The end result is a gene that has co-opted a fortuitous event (a transposon insertion) and, through mutation and selection, honed it to serve a new function (altered regulation of its product). This is an example of exaptation, the conversion of one function to another through mutation and subsequent selection. In this case the old function (a “self-serving” transposon) has had a portion of its sequence exapted to become part of the host regulatory DNA.

Recent work comparing 29 different mammals has shown there are about 280,000 examples of exapted transposon fragments in mammalian genomes. Despite this large number, the absolute fraction of human DNA that falls into this category is tiny: of our 3 billion base pairs of DNA, only about 7 million are the detectable remnants of exapted transposons. The vast majority of transposon and transposon fragments in the human genome (as we mentioned, totaling around 1.4 billion base pairs) are not under selection and are free to mutate without affecting any function.

The genomic recycling bin

So, transposons are at once a good example of non-functional DNA in genomes (indeed, nearly half of our own genome is made up of them), and an example of how evolutionary processes can convert non-functional DNA into functional DNA through mutation and selection. While I did not discuss exapted transposons in my previous series, this is another clear example of how evolution can produce novel information within the genome: by “recycling” small amounts of its junk to produce new functions. Note well, however: the fact that a small fraction of transposons have been exapted into functional sequences does not “confer” functionality on all transposons. We see the signs of selection on only a tiny minority, and even then typically only on fragmentary remains.

In the next installment of this series, we’ll examine another form of non-functional DNA present in genomes: processed pseudogenes.

For further reading

International Human Genome Sequencing Consortium, (2001). Initial sequencing and analysis of the human genome. Nature 409, 860-921. http://www.nature.com/nature/journal/v409/n6822/full/409860a0.html

Lindblad-Toh, K., et al. (2011). A high-resolution map of human evolutionary constraint using 29 mammals. Nature 478, 476-482. http://www.nature.com/nature/journal/v478/n7370/full/nature10530.html

Dennis Venema is professor of biology at Trinity Western University in Langley, British Columbia. He holds a B.Sc. (with Honors) from the University of British Columbia (1996), and received his Ph.D. from the University of British Columbia in 2003. His research is focused on the genetics of pattern formation and signaling using the common fruit fly Drosophila melanogaster as a model organism. Dennis is a gifted thinker and writer on matters of science and faith, but also an award-winning biology teacher—he won the 2008 College Biology Teaching Award from the National Association of Biology Teachers. He and his family enjoy numerous outdoor activities that the Canadian Pacific coast region has to offer. Dennis writes regularly for the BioLogos Forum about the biological evidence for evolution.

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HornSpiel - #67233

January 18th 2012

Fascinating. Thanks for the insights. I am intrigued by two things. The fact that transposons, like viruses can add relatively long snippets of code into functional areas of the genome, and that apparently mammals have a lot of these.

My question is if does this make an animal with a relatively large number of transposons more adaptable to changing conditions than organisms that might not have as many transposons? It seems tro me that if variations involve larger bits of already functional code, there there will be potentially greater diversity and therefore survivability for the species.

PNG - #67234

January 19th 2012

There is some evidence that this might be the case, going all the way back to Barbara McClintock’s work in plants, where she found that transposition seemed to be triggered by stress conditions, suggesting that transposons might be a mechanism of stress induced changes in the genome. Presumably here and there a transposition or accompanying rearrangement might produce some useful change in the genome of a single plant that would then be under positive selection. There’s been a fair amount of speculation about it, but I’m not sure how the idea stands at the moment.

Organisms have a lot of mechanisms to keep the expression of transposon sequences, and hence their transposition, under control. The repression is relaxed somewhat during early development in mammals and in some tumors, and it is possible that repression is relaxed under some stress conditions in some species as a sort of evolutionary “Hail Mary” pass. When all else has failed, try some genome rearrangement. It’s an interesting idea, but I don’t think that it has been “proven.”

Another thing I want to point out is that it is certain that there is some sequence in the genome that is not conserved with any other species but is nonetheless functional. There is bound to be some functional sequence that is species-specific - there has to be if different species are different. On a percentage basis, it may not be very large, and some of it is just individual base pairs or short bits of sequence that are specific to the function of that species. This is just to point out that, while conservation is very useful for analysis, it isn’t the ultimate criterion of functionality. I just happened to read about 7 TRIM genes which are human specific. They are conserved in the sense that they are similar to all other TRIM genes in many species, but those specific genes have no orthologs in other species, and there are undoubtedly some regulatory and RNA gene sequences that are species-specific as well. Some of them might not even have paralogs in other species, if they are completely new genes. There is some evidence for such things.
Jon Garvey - #67235

January 19th 2012

It’s a question of Mike Gene’s ducks and rabbits, isn’t it Hornspiel?

“Selfish” and “parasites” (not to mention “junk”) are loaded terms rather redolent of Dawkins’ highly gene-centric view of evolution. Since the organism’s structured use and manipulation of the genome as a “mere” database is becoming more recognised in the light of epigenetics etc, is that the most helpful way of looking at things?

Transposons’ origins are uncertain, and the “selfish” view sees them as ex-viral parasites. But supposing one sees them instead (and maybe even viruses, come to that) as primarily eukaryotic developmental mechanisms - the way evolution itself has evolved towards greater variety and adaptability? It seems there is good evidence (from Barbara McClintock onwards) of transposons being a major source of innovation. Should one see that as the occasional fortuitous exploitation of a parasite that generates junk, or as the development of a raw-materials resource that requires evolutionary refinement to select what is useful?

At root that’s a metaphysical distinction - but with consequences, just as the gene-centric view arguably held back research on other cellular mechanisms of development and evolution for a number of years.

For the theistic evolutionist, too, there is surely a difference between a “disease” process that can occasionally be mitigated and a biological progression purchased at the cost of a bigger genome. The former speaks “undirected” and the latter “teleological”.

KevinR - #67238

January 19th 2012

“Their origins, like the origins of viruses, is somewhat of a mystery.”

I’m always amused that evolutionary biologists make the observation that such a small fraction of the genome appears to be active and hence the rest should be junk or leftover from some evolutionary ancestor.
Have they really explored the whole lifecycle of the genome - from inception to death of the organism [ in this case human beings ] involved to know exactly that the rest of the genome is not being used somewhere. Do they know exactly how each and every part of the body forms and functions that they can rule out any functionality from the “junk” part of the genome?

Furthermore, in the quotation, they admit that they don’t know where the transposons come from, so just how can they be sure they know exactly what they’re there for?

The idea of junk is now being overtaken by new discoveries for that part which doesn’t code for anything - an example is that part of it plays a role in regulating gene expression or other functionality in the cell. Just because the evolutionary biologists have not yet discovered the use of the rest of the genome does not give them the authority to make evolutionary statements about it. They just have no clue what it’s there for.

I can safely predict that in  another decade or so, Dr Venema and his associates will not want to be associated with anyone who talks about junk in the genome. It will be anathema.

Ashe - #67247

January 19th 2012

Doesn’t look that way. Recently it has been shown that MEIs segregate in what appear to be a neutral fashion in the genome, which suggests that imuch of the genome the specific sequence does not have a large impact on fitness, as these regions can tolerate the absence or presence of often long mobile elements, whereas in coding regions, there is an almost complete absence of MEIs. 

PNG - #67242

January 19th 2012

Actually the origins of some transposons are pretty clear. Alu elements are derived from 2 tandems copies of the 7SL cellular RNA gene. This RNA is part of the signal recognition particle which targets translation complexes containing secreted proteins to the endoplasmic reticulum. SVA elements are a combination of an Alu element, a fragment of an endogenous retrovirus and a VNTR (variable number tandem repeat sequence. The origins of LINE elements and LTR-containing elements (endogenous retroviruses and related elements) are much further back - there are LINE elements in yeast species - and hence less certain.

Kevin seems to think that he can just consult his theological biases to answer scientific questions. The history of that kind of reasoning is not very encouraging. The whole geocentrism thing comes to mind, as well as the church fathers who were certain that because the OT seemed to assume that the earth was flat, the Greek finding of a spherical earth must be wrong.


Jon Garvey - #67244

January 19th 2012


I guess it’s overwhelmingly likely that RNA viruses themselves originally derived from cellular elements (where else does RNA come from than cells?). So it still seems relevant to ask if they somehow developed as “parasites”, losing their cellular components as unnecessary, or whether they could have developed as transposons and then “escaped” as parasitic gene-transfer agents.

KevinR - #67334

January 23rd 2012

So have you explored the whole life cycle of the genome from inception thru to death so that you can definitely state that those pieces of “junk” has not been used somewhere?

PNG - #67349

January 24th 2012

Actually, the expression of genes and the binding of transcription factors as well as chromatin structure, which has a large role in determining whether the nearby DNA can be transcribed, have been characterized in a large number of cell types. Those large scale analyses are included in estimates of the amount of the genome that is functional. As Ashe pointed out, there are other indications that large gene deserts have no sequence-specific function, such as the fact that they tolerate new insertions of large transposons. lncRNAs, which are involved in controlling expression of some genes, may by a generous estimate span 10-15% of the genome in their total length, but like protein coding regions a large majority of their sequence is introns. The possible function of the large gene deserts is limited by the fact that they are highly repetitive. What do you do with millions of copies of transposons when there are only 30,000 or so genes at the most?

Perhaps a more fundamental point is that the assumption that the organism is designed (which I believe as a theological matter) implies exactly nothing about how much of the genome is functional. I really don’t understand why some people are so concerned about this. You can believe that God assembled Adam by hand 6000 years ago and that implies nothing at all about how much of the genome is functional. It might strike human engineers as inelegant or wasteful, but I can’t see any reason that God should care what they think. Nature is full of apparent waste (think of all those sperm that get to do nothing useful at all) - so what if the instruction book has a million pages of gibberish if the other pages are amazingly beyond anything we could have imagined?
HornSpiel - #67246

January 19th 2012

Lots of interesting technical insights here, but not something that really addresses the issue of “Junk DNA” being a lightning rod for ID criticism of evolutionary theory (which they insist on calling Darwinism).

So my question: Is “Junk DNA” a misnomer? If so what would be a better short description?

PNG - #67248

January 19th 2012

“Junk DNA” is probably an unfortunate bit of slang, but I don’t know what else to suggest. “Selfish DNA” may be more to the point, since most individual transposon insertions don’t serve any purpose to the cell. A few of them later acquire some function, or at least some fragment of their sequence does, as Dennis pointed out. All viruses, DNA and RNA based, certainly arose from cells. I don’t see any other possibility since they can’t do anything apart from cells, and transposons could be an intermediate in that process. Of course lots of viruses don’t usually insert into chromosomes, so they presumably have a variety of histories. 

I don’t think it makes sense to refer to transposons as a developmental mechanism, since a developmental mechanism is something that happens during the development of every individual. There are programmed genome rearrangements in some species - in mammals the antibody gene rearrangements are an example, and it is interesting that the RAG proteins that direct this are apparently related to transposon proteins. But transposition in general is not a regular developmental mechanism - it isn’t targeted to specific sites and it doesn’t happen in all cells on a particular differentiation pathway. Is it a designed evolutionary mechanism? As Jon pointed out, that is a metaphysical question, and science has no way to get at it. Modern science got started when people set aside the interminable arguments about teleology of the scholastics and started concentrating on the things that are decidable by observation and experiment. It seems to me that the ID movement is based on an insistence that we reintroduce these undecidable arguments to science. My prediction is that it isn’t going to happen, although the arguments will go on on internet forums and will be just as interminable as those of the old scholastics.

Since Kevin is making “safe” predictions, I will make a prediction, although I wouldn’t venture to call it safe. Within a couple of decades, when functional elements have been mapped out more thoroughly and the technology for assembling large pieces of DNA is better, someone will make a streamlined mouse chromosome of no more than 15% of the normal length, with the non-functional stuff left out, and when substituted for the normal chromosome it will make a perfectly normal mouse. Part of my basis for predicting that is that it is fairly routine now to make mini-genes with the introns left out. When you make a knockout allele in a mouse and find certain phenotypes, you have to replace the gene and see if it complements the phenotypes to make sure that they didn’t come from some other mutation that occurred during the process. This is typically done with mini-genes that include all the known regulatory elements and the coding exons fused together. This usually works - it did on the mouse version of the human gene I worked on. These minigenes are often a small fraction of the size of the normal gene - introns comprise over 30% of the human genome, while the functional sequences amount to a few percent. Our gene was 1.7 million bp, but was replaced with a mini-gene that was a few thousand bp. So, I won’t call my prediction safe, but, unlike Kevin’s it is based on a lot of evidence.
Jon Garvey - #67263

January 20th 2012

“Modern science got started when people set aside the interminable
arguments about teleology of the scholastics and started concentrating
on the things that are decidable by observation and experiment.”

PNG, I think that’s a questionable point, not to mention actually wrong - have you read James Hannam’s “God’s Philosophers” (cited at BioLogos before)? It shows just how well science was getting on before teleology began to be excluded, particularly after Darwin.

But granting the point for discussion’s sake, science needs to be meticulous in not making statements about teleology when it is claiming to avoid them scrupulously. “Non-coding DNA” is a scientific decription, as is “transposon”.

But “junk” is a metaphysically anti-teleological statement, actively denying both present function (risky and arrogant, and mistaken in at least some cases) and possible purpose (playing at the scholastic without the necessary philosophical grounding).

“Selfish” is a pure anthropomorphism which has already proved substantially inadequate when applied to genes, and which is in any case a statement of teleos which, I granted you above, has no place in science. One should avoid metaphysics altogether, or else allow a plurality.

beaglelady - #67270

January 20th 2012

At the end of the day it doesn’t matter what we call it. The fact that humans have  the “mutated remains of the vitellogenin gene” (for egg yolk production) speaks for itself.

See “Signature in the Pseudogenes Part 2” on this site.

PNG - #67348

January 24th 2012

All that is meant by “selfish” is that the fact that a segment of DNA can make additional copies of itself in a genome is sufficient to explain its spread in the genome and in a population. It doesn’t have to do anything functional for the organism in order to spread. We use anthropomorphic metaphors and other metaphors in science as shorthand, not as philosophical constructs.

And its seems apparent that when you leave behind Aristotelian ideas of an object “seeking its natural place” and start thinking about the geometrical shape of orbits, the speed of the object as a function of where it is in its elliptical orbit, the fact that Jupiter has moons that follow elliptical orbits around it, that you have set teleology aside and settled for finding out what mathematical functions the measured variables fit. You have in a sense settled for less - you have set aside the question of why in a teleological sense, but you have focused on a class of questions that can be answered with quite a bit of certainty, with enough work. It seems apparent that that was an essential part of the development of modern science. People didn’t stop thinking about teleology on one particular day - there was a long overlap in the two ways of thinking, but as long as God isn’t giving interviews about why He chose the physical laws that He did, the teleological questions seem to remain just questions without answers that everyone can agree on.
HornSpiel - #67355

January 24th 2012

Nicely put. I would like to have those like links on these pages.

Douglas E - #67252

January 19th 2012

One person’s junk is another person’s treasure!  So, perhaps junk is not such a bad word if we remember that an awful lot of junk has uses that are not easily identified.  Junk is not the same as trash, so since we are pretty much stuck with the term, perhaps we should emphasize that although we have labelled it junk, that does not rule out the possibility of usefulness

HornSpiel - #67256

January 19th 2012

Thanks for your replies guys.

Absolutely Douglas. Maybe evolution works better when there is a junk yard of old parts lying around.

However, it occurred to me that there is a lot we need to learn before we can say in any theoretical sense exactly what this DNA is about. So perhaps a better name for it wold be Mystery DNA reflecting our lack of understanding of it.

One reason I like this name is that science wold be well served if it expressed a bit more humility. It would be great to see scientists admit that they don’t know everything about their chosen field. I think it would actually increase public trust.

beaglelady - #67259

January 19th 2012

Maybe evolution works better when there is a junk yard of old parts lying around.

Exactly, because evolution can only work on what is already there. It can’t go back to the drawing board as human engineers do.

One reason I like this name is that science wold be well served if it
expressed a bit more humility. It would be great to see scientists admit
that they don’t know everything about their chosen field. I think it
would actually increase public trust.

They actually do admit what they don’t know. 
Please watch this short clip:

btw, I’m not crazy about the name “mystery DNA” because mystery has a religious connotation and is not the same as scientific ignorance.  It might be confused with  God-of-the-Gaps thinking.   The mystery of faith deepens with knowledge, but ignorance retreats.

Douglas E - #67282

January 20th 2012

Vestigal comes to mind, but is also not without some problems.  However, some of the so-called vestigal organs of the past - thymus, tonsils, appendix - upon further study, turned out to have important functions.

beaglelady - #67290

January 21st 2012

Vestigial doesn’t mean without any function at all. It simply means reduced function.  But why do dogs, goats, and cows have dew claws? Why do our wisdom teeth more often than not have to be extracted since our jaws are not big enough for them? Why do whales have vestigial hind limbs embedded in their bodies? And so forth…

Douglas E - #67299

January 21st 2012

Well, the Wiki clears it up for us

“Although the term serves a purpose in many gross phenotypic
characteristics, vestigial has probably little applicability to DNA
sequences, be they genes or non-coding sequences. Noncoding DNA
has become a revealing example for vestigiality. Many types of
noncoding DNA sequences have been found to have biological functions.
Some sequences, however, have no known biological functions and are
often referred to as “Junk DNA”.”

HornSpiel - #67313

January 21st 2012

Thanks for the link. Even better: Check the <a href=“http://www.scientificamerican.com/article.cfm?id=what-is-junk-dna-and-what”>sources</a>

Although very catchy, the term “junk DNA” repelled mainstream
researchers from studying noncoding genetic material for many years.
After all, who would like to dig through genomic garbage? Thankfully,
though, there are some clochards who, at the risk of being ridiculed,
explore unpopular territories. And it is because of them that in the
early 1990s, the view of junk DNA, especially repetitive elements, began
to change. In fact, more and more biologists now regard repetitive
elements as genomic treasures. It appears that these transposable
elements are not useless DNA. Instead, they interact with the
surrounding genomic environment and increase the ability of the organism
to evolve by serving as hot spots for genetic recombination and by
providing new and important signals for regulating gene expression.

Wojciech Makalowski, Penn State
Jon Garvey - #67324

January 22nd 2012

But it’s still mainly junk, though…

Dennis Venema - #67249

January 19th 2012

Hi PNG  -

You’re right that the origin of some transposons is known - I should have made that more clear in my attempt to gloss the entire field in one sentence for a non-specialist audience. 

Some virologists, however, do not share in your certainty that viruses must be derived from cells. Recent work has advanced the hypothesis that they may actually be rooted in the tree of life before the last universal common ancestor (LUCA), and thus parasitic remnants of replication strategies tracing back towards the RNA world. Hypotheses only, but interesting ones, and with some experimental support. 

PNG - #67347

January 23rd 2012

It would be interesting if that was the case, but the main point is that viruses and transposons can’t replicate without the assistance of something that can replicate. Bob Shapiro said to me 25 years ago that, having worked with RNA for years, he was pretty sure there never was a naked replicating RNA and I’m inclined to agree. RNA is just too unstable for it to work. If there was an RNA world, that RNA was enclosed in and protected by something, so functionally I would say that was a cell of some sort. Maybe some viruses are descended directly from a more primitive replicating form, but it doesn’t change the basic point.

PNG - #67350

January 24th 2012

In honor of junk, here is a poem by that title, a modern attempt, and quite a good one, at alliterative Old-English poetry. The first few lines are a quote from a real Old English poem, but, don’t worry, the rest is in modern English.


by Richard Wilbur

Huru Welandes                   
  worc ne geswiced
monna aenigum
  dara de Mimming can
heardne gehealdan.

(Truly, Wayland’s handiwork - the sword Mimming which he made - 
will never fail any man who knows how to use it bravely.)

An axe angles
       from my neighbor’s ashcan
It is hell’s handiwork. 
    the wood not hickory
The flow of the grain 
    not faithfully followed.
The shivered shaft
    rises from a shellheap
Of plastic playthings
    paper plates,
And the sheer shards
    of shattered tumblers
That were not annealed
    for the time needful.
At the same curbside 
    a castoff cabinet
Of wavily warped 
    unseasoned wood
Waits to be trundled 
    in the trashman’s truck.
Haul them off! Hide them!
    The heart winces
For junk and gimcrack
    for jerrybuilt things
And the men who make them
    for a little money
Bartering pride
    like the bought boxer
Who pulles his punches,
    or the paid-off jockey 
Who in the home stretch
    holds in his horse.
Yet the things themselves
    in thoughtless honor
Have kept composure
    like captives who would not 
Talk under torture. 
    Tossed from a tailgate
Where the dump displays
    its random dolmens,
It’s black barrows
    and blazing valleys,
They shall waste in the weather
    toward what they were.
The sun shall glory 
    in the glitter of glass chips,
Forseeing the salvage
    of the prisoned sand,
And the blistering paint
    peel off in patches,
That the good grain
    be discovered again.
Then burnt, bulldozed,
    they shall all be buried
To the depth of diamonds
    in the making dark
Where halt Hephaestus
    keeps his hammer
And Wayland’s work
    is worn away.

Jon Garvey - #67351

January 24th 2012


It’s funny you should quote that, as it treminds me of this ancient fragment found stuffing the cover of an Anglo-Saxon manuscript, which seems very apt:

The Ruined Genome

...the unwritten writing - ruined runes
Weird thrust them forth, words without speech.
Strong once were the cells where genes jostled,
Thronging to fine forms and well-wrought wonders.
Came days of plague; the venom of virus,
Death gripped genome - function failed.
High halls filled with the fallen; stocked with the slain,
Scarce the spliced sequences now - junk mouldereth all…

Seems like they had it all sussed in the Dark Ages…

PNG - #67360

January 25th 2012

Excellent. Very prescient of the old bard.

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