DNA Has Another Shape

Not surprising:

For the first time, scientists have identified the existence of a new DNA structure never before seen in living cells.

The discovery of what’s described as a ‘twisted knot’ of DNA in living cells confirms our complex genetic code is crafted with more intricate symmetry than just the double helix structure everybody associates with DNA – and the forms these molecular variants take affect how our biology functions.

“When most of us think of DNA, we think of the double helix,” says antibody therapeutics researcher Daniel Christ from the Garvan Institute of Medical Research in Australia.

“This new research reminds us that totally different DNA structures exist – and could well be important for our cells.”

The new DNA component the team identified is called the intercalated motif (i-motif) structure, which was first discovered by researchers in the 1990s, but up until now had only ever been witnessed in vitro, not in living cells.

Now, thanks to Christ’s team, we know the i-motif occurs naturally in human cells, meaning the structure’s significance to cell biology – which has previously been called into question, given it had only been demonstrated in the lab – demands new attention from researchers.

At the end of Watson and Crick’s Nobel winning paper, there was a throwaway line about recognizing there was a possible alternative structure which was not helical, where the DNA strands were still connected, but instead of a pretty helix it was a more disorganized appearing parallel arrangement of the two strands.

The problem with a perfect helix for the length of the DNA is that the two DNA strands need to separate and be unspun, so the DNA machinery can access a single strand in order to read it and transcribe it into a single RNA-strand copy for actual use. Unspinning the helix, so the two DNA strands are separated and parallel would force that “spin” or “twist” into the remaining DNA on each side of the gene, in ways that would make the angles of the bonds difficult to maintain and which would create considerable stress on the structure.

Some hypothesized an enzyme clipped the DNA to release the tension of the twist, and allow it to temporarily unspin, and then it would be repaired afterward by another enzyme as the two strands sealed back together and the helix spontaneously formed. DNA does get damaged, and there are enzymes running around doing such repairs, so it was not that much of a stretch to think another enzyme might make a clip to facilitate gene reading, though it didn’t sit well with many. So it has been sort of assumed DNA would have more complex structures arrayed around, some of which likely will be related to transcription.

I stick this here, because it may relate to what we have looked at as epigenetics. Epigenetics is actually something different, specifically little molecules which affect transcription (usage) rates, by affecting how available the gene is to the DNA machinery. The principle is, if you use a gene a lot, or don’t use it at all, your gene will have little molecules attached or removed which will make it either easier and faster to use, or slower and more difficult to use. Since those changes are transferred to your offspring, if you lift weights to produce a lot of muscle for example, your children will come our of the womb producing more muscle because all those genes will be in high gear from the start. It is not a huge structural change, but rather just an increase or decrease in production of stuff in your kids based on what you needed or didn’t need in your life.

The gene structure (and thus the gene product) will not change (as far as we know, though I suspect there may be some relation between epigenetic status/usage and mutation rates), but the rate of production of the gene product will change. We probably see this in r/K with dopamine receptors and enzymes revolving around stress adaptation.

Since they say these little structures are seen forming and unforming, I could see where these may build up around genes that are transcribed often, and disappear around genes that are rarely used, or even have other effects, on gene exposure, thus functioning like the little methyl groups of epigenetics to alter transcription rates by easing the stress of burning off gene copies.

Food for thought about a mechanism affecting the expression of r and K, based on environmental variables, at the genetic level, and how complex the entire mechanism might be.

Tell everyone about r/K Theory, because the mechanism is key