Of what benefit is the helix in DNA

Cite? Sure you’re not thinking of RNA viruses? All(?) life uses RNA, but the RNA is transcribed from a DNA genome.

It’s speculated that earlier life used nucleic acid chains other than those based on deoxyribose (several candidates have been proposed besides RNA), but all present-day bacteria have DNA genomes.

Just to restate my point about the fact that there is a burden of proof for the (to me) implausible notion that the helicity of DNA is an evolutionary adaptation:

It’s obviously true that DNA has many cool and complex properties and interactions with proteins that are all intrinsically related to its helical structure. But that does not speak to whether the helix was itself originally an adaptation. Whether the helical structure is an adaptation or chance or an incidental side-effect of other required properties of the molecule, if a helix is what’s there, the molecular machinery will evolve around it. And, of course, the helical structure itself can be tweaked and fine-tuned by natural selection making subtle changes to the polymer, even if the existence of the basic helical form were not originally an adaptation.

DNA obviously emerged by natural selection as a polymer that has all of the important properties to carry the genetic information. But it seems to me that helicity was unlikely itself be one of those important properties. Helicity is the natural 3-d structure that tends to occur by default in almost any polymer that has the requisite properties, i.e. twin annealing polymer strands with base units all arranged in the same orientation (on each individual strand), since any bond angle other than “dead straight” between each repeating unit gives a progressive rotation up the backbone. There would certainly be natural selection for a polymer that can form a stable (and perhaps compact) structure of some kind, but it seems to me that a helix is the most natural form that such a stable structure would take given the other requirements for the molecule.

My mistake … the virus RNA uses the host cells’ DNA for genetic transcription … now I have a belly-ache …

nm, I’ve just realized I can’t remember what happens with dsRNA virsuses, let me get my facts straight and repost this more coherently

Most RNA viruses either synthesize proteins directly from their RNA, or first replicate it to get an opposite-sense messenger RNA. Retroviruses do synthesize DNA from RNA — they don’t use the host’s DNA per se, but they do attach their own generated DNA to the host’s chromosomes; these proviruses are then automatically passed to new cells’ chromosomes during the cell’s mitosis.

Exactly. There are tons of examples of helical macromolecules. For example, polypeptides tend to form either alpha helices, or beta sheets which are rarely perfectly flat (I hesitate to say “never”, because biology…). Most dramatically, amyloid fibrils are formed from extended beta sheets, and have a helical structure. Off the top of my head, most ordered protein filaments are also helical: collagen, actin, tubulin, myosin, etc. I believe there are plenty of helical carbohydrates as well.

Across the entire kingdom of life, plants and animals with bloated genomes tend to be the exception. There are lots of eukaryotes with compact genomes, and prokaryote genomes are extremely compact. E. coli only has 12% of non-coding DNA in its genome, and much of that is composed of well-defined regulatory elements. At least on the scale of individual bacteria, there is selection for a compact genome if only because DNA is expensive to make, and replication speed is a limiting factor in cell division.

More generally, there must be some selective pressure against growing genomes even in animals. Otherwise, if selfish genetic elements like transposons were allowed to increase unchecked ever generation, we’d have damn near infinite genomes. IIRC transposable elements comprise about half the human genome, and about 1% of those elements are active. If we assume that the active transposons manage to copy themselves once per generation, in round numbers that would add 10 million base pairs. With purely linear growth, the human genome would double in only 300 generations.

I’m aware of several active mechanisms that suppress transposon mobilization and insertion, particularly in the germ line. This implies that there is positive selection for mechanisms that keep genome bloat in check.

But none of this has to do with simple linear compactness of DNA.

I certainly agree that it’s true for organisms such as bacteria with short generation times, rapid DNA replication is a limiting factor, so there is selection for a compact genome.

But the primary reason for RNAi suppressing transposon activity is not to limit the size of the genome, it’s to prevent potentially harmful mutagenic insertions. So I think it’s less clear that limiting the size of the genome per se is particularly important in (say) mammals. But it’s a complex issue, and obviously a contentious point just how much of the non-coding material has any function, and could be removed without any loss of information.

In any event, as you say, linear compactness in the genetic material is not a relevant factor.

Good point.

I wonder if there’s any evidence for selection against the growth of more benign “junk” elements, like variable number tandem repeats. I have a vague recollection that chromosome break points are commonly in tandem repeat regions… So perhaps more/longer VNTRs would lead to less stable genomes, and a higher frequency of gametes with screwed up chromosomes.

But now I’m just pulling WAGs out of thin air, so I’ll bow out before I make too much of a fool of myself.

There was an old essay by Isaac Asimov, pointing out that organic chemistry is possible, in large part due to the flexibility of the carbon atom. The bonds can give, a little, bending away from the ordinary geometry, so that large constituents (what is the name for a part of a molecule?) can attach without getting in each others’ way.

If the carbon atom was rigid in its geometry, a lot of really complex molecules couldn’t form.

functional group, or just group; sometimes moiety

Watching the videos of DNA folding, intuition tells me a helix structure more easily/naturally folds/wraps. If it was a straight ladder, it seems like there is increased complexity and more rigidity to the different ways it can be folded and brought together.

So, is it possible that some of the pressure to arrive at and/or retain a naturally occurring helix structure is due to simpler folding?

You’re watching a set of molecular machinery that has been exquisitely refined over a timeframe of the order of a billion years for the specific purpose of compacting helical DNA. Of course it does it well.

I don’t really see how you can claim to have good comparative intuition about how compacting might have evolved over a similar timeframe for a hypothetical non-helical molecule.

Again, an adaptive hypothesis requires that there must have existed variant helical and non-helical structures upon which natural selection acted. I think it’s a mistaken notion that any non-helical variant ever existed, because it would be quite awkward and unnatural to construct one from organic subunits.

The essential flaw in the OP’s question that has led this thread astray is that an essentially two-dimensional “flat ladder” is somehow a more natural default state, with the implication there must be a reason for the helix. The converse is true. In a 3-d world, the helix is the natural default state for this type of polymer, and a flat ladder would be unnatural.

No doubt natural selection acted on variation among alternative helical structures to fine-tune the properties. But I’m skeptical that variation among molecules that possess the important topological characteristics of the DNA double-stranded polymer ever encompassed any non-helical structures. The burden is really upon those who propose an adaptive explanation for the helix as opposed to a non-helix to propose what an alternative non-helical polymer might have looked like.

Here’s a question: Is the twist the same for every base? That is to say, if I had a strand of DNA that just consisted of AAAAAAAAAAAAA… (with, of course, the corresponding Ts on the other strand), would that have the same twist as a strand of just GGGGGGGGGGGGG (and corresponding Cs)? If they do have the same twist, or close to it, then that might suggest that there’s some benefit to having that particular twist angle, but if they’re not, then it seems much less likely.

Yes, it’s the same. The backbone that determines the angle is made of the sugar-phosphate part that’s identical in every nucleotide. And the A-T and G-C base pairs are each formed from one smaller and one larger base, when paired up the two pairs are very similar in size and shape, so a different sequence does not change the overall helical shape.

This raises the question of how sequence-dependent protein binding to an annealed helix of dsDNA can occur. There are two grooves around the helix between the backbones, where the bases are somewhat exposed. So proteins can bind to DNA in either a sequence-dependent or sequence-independent manner, depending which part of the structure they contact.

[QUOTE=Chronos;19Ω95984]
…If they do have the same twist, or close to it, then that might suggest that there’s some benefit to having that particular twist angle, but if they’re not, then it seems much less likely.
[/QUOTE]

It certainly seems credible that an arrangement where the overall structure is not sequence-dependent has advantages. Many handling tasks are not sequence-dependent, so it’s an advantage to be handling just one consistent overall shape. To make a crude analogy, you don’t want the size of your flash drive to change when different files are saved on it, or it won’t fit in the slot!

And the presumed advantages of having the twist be sequence-independent are why I said “might suggest”, there, because that’s a perfectly good alternate explanation. Of course, “that part of the molecule is the same” is an even simpler perfectly good alternate explanation, which I didn’t properly appreciate.

Orderly packing tends to be more volume efficient than random packing.

You could say the same about any particular round of the DNA packaging sequence. Why was the solenoid stage necessary? It’s only a factor of N over the previous stage. The answer is that the stages are multiplicative and if you lose a factor of 2 in one place, then you need to gain it somewhere else.

It’s difficult to coil a stiff ribbon. Actually, just try to coil a thick extension cord without using the “over under” method–it becomes tangled almost instantly. A molecule that’s already coiled just becomes a little more/less coiled with each larger twist.

True, but it’s at least suggestive. Already being a helix reduces the load on higher-level coiling mechanisms.

Until we know more about how DNA/RNA came about, and in particular the competing replicators, I don’t think we can really speculate as to whether the helix was an accident or a selected-for feature.

I was not suggesting a disordered alternative. There are many orderly ways to pack things.

No, it’s a quantitative argument. I don’t concede that a helix necessarily confers twofold compaction over unspecified hypothetical alternatives, but for the sake of this argument let’s stipulate that it does. A factor of ~2 is small compared to the total amount of compaction required. The other compaction mechanisms achieve around 5-10-fold compaction at each stage. Since there are some species with much larger genomes out there, it appears that the other compaction mechanisms are not close to their limit, so the gain or loss of a factor of 2 in compaction is not significant and does not affect fitness.

In fact, DNA is extremely rigid, like a stiff rod. It is one of the most rigid biopolymers known to exist.

I really don’t think that an analogy with coiling an extension cord really grants much insight into what kind of cellular compaction mechanisms could plausibly evolve over a billion years for helical vs hypothetical non-helical polymers.

No, the existence of a helix per se is not suggestive of anything adaptive if a helix is the most natural form for a polymer that has the topological properties that we know are certainly important for the genetic material: two annealed strands, a repeating orderly structure with all the subunits in the same orientation (on each strand); and biological building blocks, in which 180-degree bond angles are rare.

It’s not like we know nothing about abiogenesis. RNA is the only known molecule that can catalyze its own replication. And recent experiments show that nucleic acids can arise spontaneously and fairly easy under conditions plausible for the early earth…
http://www.sciencemag.org/news/2015/03/researchers-may-have-solved-origin-life-conundrum

To be clear, I am not for a moment arguing that many of the the particular characteristics of the specific type of helix that we find in DNA are not adaptive. And the fact that life has subsequently exploited many neat properties of the helix is beside the point.

What I’m arguing against is the notion that a helix was ever selected over a non-helical variant, since that is the key requirement for any hypothesis that a helix per se is an adaptation.

Abiogenesis is a speculative field, but we do know some things, and the laws or physics and chemistry have not changed in a few billion years. I do think the reasonable default hypothesis is that helicity is not per se an adaptation but simply a natural property of any polymer with the requisite properties to be the genetic material. And that the burden is really upon someone who proposes otherwise to suggest a plausible non-helical alternative biopolymer that might arise naturally under fairly simple conditions, and that has all the other required properties for the genetic material but is non-helical and (say) inferior in compaction.

You said you don’t get any volume advantage from a helix: that’s incorrect, because you have to consider packing efficiency, and nested helices do pretty well in this regard. There may well be other solutions to the problem, but nested helices is what we got.

Or these species may just have large nuclei, and for whatever reason this doesn’t impose a great cost.

In any case, the selection criteria that led to DNA are obviously gone by now. No new replicator could hope to compete, so even if there were some more efficient molecule, it could never get a foothold.

That factor of 2 may have been very important early on, when the replicators weren’t much more than a xNA strand in a molecular bubble. They didn’t have the extra coiling machinery at that point, so an extra factor of 2 might have allowed some of the replicators a genomic advantage.

But it is at least equally flexible in all directions. Whereas a flat ladder would be even more rigid in one dimension, and less in the other. To coil, it would have to use the over-under method, requiring more support molecules. Simply coiling it along the flat implies a twist along the whole length–completely impractical (unless, of course, the molecule is already twisted).

Maybe xNA is the only plausible replicating molecule. If so, the twist is indeed just a convenient side effect. But I think it’s way too early to conclude that.

I agree that that’s the criteria, but I don’t think there’s more than the barest hint of evidence of it. Even if completely untwisted replicators are unlikely based on bond angles, that still doesn’t say much about why xNA is as tightly twisted as it is. A loose twist is probably just as likely as a tight one, but perhaps the latter had an advantage early on.

Why would a flat ribbon be difficult to coil? I’ve seen coiled flat ribbons plenty of times. Just look at a roll of tape.

Related question: why exactly was it so significant when Watson, Crick and Franklin discovered the double helix structure? Did it tell us something about how DNA functions?

A roll of tape is coiled evenly using a machine. But without a machine, things don’t coil evenly. Try rolling toilet paper up after a cat or child pulls it off the roll.