Today’s DpSU is called Transposon Behavior Negates ‘Selfish Gene’ Theory.
It’s always a red flag when Creationists reference Dawkins’ The Selfish Gene. History has taught us that few read beyond the title – some may even stop at only its second word. Most criticism is therefore directed at the perceived implication that all life must be entirely selfish and meaningless, etcetera, instead of what the book is really about.
For anyone who doesn’t know, The Selfish Gene is really an explanation of how evolution works and altruism can arise if the gene is the chief unit of selection, rather than, say, a group. In other words, organisms can be nice to each other, even though all that matters is how successful the genes are. We shouldn’t talk about how a trait is beneficial to a group – if a gene can manage to profit in the long run with, shall we say, ‘antisocial’ behaviour (not sharing or some other activity that goes against the beneficial trait) then that trait is not going to get selected for, whatever the benefits for the group. That’s not to say that altruism can’t evolve – Dawkins covers that in depth. Bear in mind also this quote from Wikipedia’s article on the book:
In describing genes as being “selfish”, the author does not intend (as he states unequivocally in the work) to imply that they are driven by any motives or will—merely that their effects can be accurately described as if they were. The contention is that the genes that get passed on are the ones whose consequences serve their own implicit interests (to continue being replicated), not necessarily those of the organism, much less any larger level.
On a related note, I have done an (admittedly unscientific) test demonstrating that the book is much more interesting than a sermon, at least those boring presbyterio-methodist ones that I am used to.
Brian Thomas does, to his credit, stay closer to the actual topic of the book than most, due to the fact that the original allusion to the book comes from the paper that he is commenting on. The paper is Drosophila P elements preferentially transpose to replication origins from PNAS – the paper can be found in full here, as the PNAS site refuses to give up anything to the unpaying reader beyond the abstract.
The abstract of the paper reads:
The P transposable element recently invaded wild Drosophila melanogaster strains worldwide. A single introduced copy can multiply and spread throughout the fly genome in just a few generations, even though its cut-and-paste transposition mechanism does not inherently increase copy number. P element insertions preferentially target the promoters of a subset of genes, but why these sites are hotspots remains unknown. We show that P elements selectively target sites that in tissue-culture cells bind origin recognition complex proteins and function as replication origins. The association of origin recognition complex-binding sites with selected promoters and their absence near clustered differentiation genes may dictate P element site specificity. Inserting at unfired replication origins during S phase may allow P elements to be both repaired and reduplicated, thereby increasing element copy number. The advantage transposons gain by moving from replicated to unreplicated genomic regions may contribute to the association of heterochromatin with late-replicating genomic regions.
What that means, so far as I can tell, is that we have a transposon – a section of genetic code capable of upping and moving itself across the genome – that has ‘recently’ (i.e. around eighty years ago, which is recent enough to go unchallenged by the ‘you can’t do historical science’ creationists) entered the genome of everyone’s favourite small flying insect, D. melanogaster. This study shows that P – the name that they give the ‘transposable element’ – has a tendency to move to the origins of replication, the places where a chromosome begins to replicate. It should be mentioned that there are multiple origins on each chromosome – there seem to be thousands in the D. melanogaster genome, if I’m reading the paper correctly. P also has a tendency to insert itself at (a subset) of gene promoters.
The study authors do not pretend to know exactly why all this happens, but suggest that the choice of targets may relate to some kind of attempt to hitch a lift with the replication process – the normal system of movement of P is ‘cut-and-paste’, rather than ‘copy-and-paste’, and thus does not increase the number of instances of the element in the genome. Moving to replication sites may rectify that situation.
What has Mr Thomas got to say about this?
Are transposons trying to take over their host genomes, thus demonstrating the selfish behavior described by Dawkins?
The answer is no. These mobile genetic elements—also called “jumping genes” for their ability to move from place to place—don’t just randomly invade a genome. Instead, they are now well-known for inserting copies of themselves into very specific places on chromosomes. Most animals’ genomes are loaded either with recently acquired and active transposons, or with remnants of transposons acquired long ago.
Nice to see creationists acknowledging the existence of genetic ‘remnants’ for once, but that’s not the point here.
A Carnegie Institution for Science news release reported:
What many P insertion sites share in common is an ability to function as starting sites or “origins” for DNA duplication. This association between P elements and the machinery of genome duplication suggested that they can coordinate their movement with DNA replication.
Somehow, these transposons “know” exactly where to insert themselves. And although they “remain highly ‘infective’ today,” they eventually stop “jumping” into new places in the fruit fly genome through inherited mechanisms of protein truncation and “piwi-interacting RNA” complexes. In other words, they eventually stop because of well-designed components in the host cell that interact very precisely with the transposons.
Or it could stop because the species has been (naturally) selected for mechanisms that help individuals deal with transposon invasions. Methinks he doth jump to ‘design’ too fast.
Since their discovery, evolutionists have been trying to work transposons into an overall evolutionary scheme of genetic development. The study authors asked, “Does a selﬁsh drive to increase copy number by replication timing inﬂuence the evolution of genome organization?” They briefly discussed why this might be true, without addressing the glaring reasons why it could not possibly be true.
The full paragraph that that quote is from continues:
Such a connection might rationalize the nearly universal observation that heterochromatic regions replicate late in S phase and are enriched in transposons. Any late-replicating region might ex- perience elevated transposition, leading over time to its acqui-sition of heterochromatic properties. This tendency also may be used to regulate transposition. piRNA clusters are located in heterochromatin (12) where presumably they replicate very late in S phase. Such locations might increase the chance that transposons will integrate within these large transcription units and generate repressive piRNAs. In sum, by gaining insight into why a specific transposon moves nonrandomly, we may have begun to glimpse mechanisms that have profoundly influenced the evolution of metazoan genomes.
Let’s see those reasons, shall we?
First, transposons target specific sites. If they were truly “selfish,” they should show no preference for location, but would invade the genome anywhere they could to increase their own numbers. But if they were created by design to serve a particular purpose, transposons might be inserting themselves into these specific sites for a biologically significant reason, such as gene regulation or DNA stabilization. But this possibility was not even mentioned in the PNAS study.
Why, “If they were truly “selfish,”” should they “show no preference for location, but would invade the genome anywhere they could to increase their own numbers”? As I mentioned above, this preference may well be how they replicate, and thus a transposon sequence that had a strong bias of landing in such sections would far out-compete a version that did not – natural selection at work. And I’d guess that the reason why potential functions of P is left out is the total lack of evidence on hand.
Also, the transposons’ copy numbers are controlled and eventually stopped by inherited cellular mechanisms that seem to “understand” exactly what the transposon is doing. If the transposon is selfishly competing with the genome in order to survive and reproduce, as Dawkins described, then why does the transposon interact with its host genome in a cooperative manner that fits like a hand in a glove?
There was a whole chapter in The Selfish Gene on the subject of Game theory – how, for example, everything isn’t ‘zero sum’, i.e. it is possible in many situations in real life for you to benefit as well as your ‘opponent.’ Life: not a game of chess.
So yeah – he got nothing.
Genes do not behave “selfishly”—in fact, most genes on earth are plant genes that serve largely selfless roles.
The link for this is to an eleven-year-old Acts and Facts article, The Unselfish Green Gene. Creationists have the ridiculous idea that plants are our selfless servants. This misconception deserves an article on its own – one more for the list. *sigh*
And even “jumping genes” do not exhibit signs of selfishness. Genes do not struggle against one another, but at almost every level have been found to mesh with coordinated, well-planned precision to perform tasks that serve their larger organisms. And that behavior could only have resulted from deliberate engineering by a superior Designer.
Brian Thomas really needs to read up on this stuff a bit more. I don’t think he gets it.