Too much UV light and your DNA’s no longer right! Here’s a quick primer on what’s called a PYRIMIDINE DIMER. These occur when strong bonds form between DNA letters that are on top of each other, messing up how they bond with the DNA letters that are across from them, and they’re one of the reasons why you should not shine UV light on or in people.
DNA is made up of NUCLEOTIDE building blocks that link together using a generic backbone and unique nitrogenous bases (usually we just call them bases) (A, T, G, or C). These bases stick out from the backbone and they can form (individually) weak bonds with bases on other strands of DNA that have the “opposite” letter (A to T and G to C).
DNA likes to form double helixes where you have 2 strands running opposite directions and each of the bases bonds to a complementary base on the other strand. To accommodate all these BASE PAIRS (the between-strand contacts) they adopt a spiral-staircase-like shape.
You know in Harry Potter where the 1st years get warned to watch out for the trick staircases, because they like to move? Well, the rungs of these staircases can come apart because those INTERSTRAND bonds are all weak. This is important because it allows us to unzip it to make copies.
But the railings of the staircase stay together because they’re connected by strong COVALENT bonds. What’s the difference? Molecules interact through their electrons. (molecules are made up of atoms and atoms are made up of smaller parts – positive protons & neutral neutrons that hang out in a dense core & negative electrons that whizz around them).
Atoms “own” a certain number of electrons, but this isn’t always the # they’d like to have. So they can share with each other – when 2 atoms share a pair of electrons (each donating 1) you get a COVALENT bond. Electrons “live” in homes called orbitals and in a covalent bond, the electrons actually “renovate” and “move in together” but in a non-covalent bond they just “hang out together”
The only COVALENT bonds between nucleotides *should* be between their generic backbone – these are formed when the DNA was put together – so after the strands are made, it should all be weak (non covalent) bonds from then out. These weak bonds can form between bases on different strands of DNA – BASE PAIRING. And this is the kind of bond we usually think of.
But there are other weak bonds taking place. In that double-helix ladder of DNA, the rungs of the ladder actually interact with one another through what we call BASE STACKING. I picture it kinda like hovercrafts. You have the disc-y part and that’s like the flat base you see. That’s made up of “normal” covalent bonds we call sigma bonds, where 2 atoms link up by each sharing an electron with the other. But then above and below you have “extra” shared electrons hanging out in pi bonds. When you have such “resonance sharing” occurring in rings like this, we call the ringed thing “aromatic.” The consequence here is that, even though it looks like the bases are pretty far apart, their electron clouds are closer together and they can sync up. And, if the lighting’s just right (more like wrong) electrons can move.
Light is made up of packets of energy called photons and different types of light have photons with different amounts of energy. These photons travel as waves. When you shine light on something it’s like streaming pennies and nickels and dimes of free energy money for molecules in its path, but the molecules have to have the right “slot size” in order for them to accept these coins. The “slot size” in the case of molecules is the difference in energy between the places in that molecule where electrons are allowed to live in and this depends on what the molecule is and what’s around it.
If a photon comes along that is just right, the molecule will absorb it and one of its electrons will “jump up.” But just like when you jump up, you can’t stay up there forever and the electron has to give back that extra energy. A lot of the time it’ll just kinda fizzle out and slide back down, giving off that extra energy as heat. Boring…
But some molecules, FLUOROPHORES, instead of fizzling non-dramatically will release that energy as a new photon, but with lower energy (they do lose some of it in those more boring ways so they can’t give it all back). More interesting… This, for example is how the DNA-staining dye ethidium bromide (EtBr) works – it intercalates between the DNA bases (wedges in between the bases like a slab of butter between your pancakes in a stack), then absorbs UV light when we stick it on a UV tray and gives out visible light. We often use this or similar fluorescent dyes to stain bits of DNA that we separate by size using agarose gel electrophoresis (basically we make a gel mesh out of agarose sugar and then use electricity to send DNA pieces through it, with the longer pieces getting tangled up more and thus traveling slower).
And there’s another option, sometimes, an electron can jump up and, before it has a chance to fall back down, it gets “caught” by another molecule. It’s kinda like a coordinated trapeze act. It can only happen if the molecular players are exactly in the right place at the right time. It may sound really unlikely, but this can happen when you have 2 pyrimidine residues (Ts or Cs) next to each other on the same strand (so they’re stacked on top of each other in the helix) and you hit it with UV light.
UV light has photons with a really high energy (which is why we can’t see it – it’s outside of the visible light range that our eyes can detect). These photons are like the right coins for T & C, so they get absorbed – an electron jumps up and – thanks to that base stacking, there’s another electron’s home right above it. So it moves in. This leads to new COVALENT bonds being formed between these bases.
Unlike the weak bonds between the DNA strands that can melt apart, these covalent bonds are “stuck” and they can cause problems during copying. These dimers most frequently form between 2 thymines -> thymine dimers and our cells can *usually* detect the bulge and fix it, typically through something called nucleotide excision repair. This involves cellular quality control recognizing that the DNA has an awkward bulge due to the dimer, cutting out a short stretch of DNA encompassing the dimer, and then filling back in the removed letters using the second strand as a template.
If the problem doesn’t get fixed before it’s DNA copying time, the copiers (DNA Polymerases) just do the best they can to “guess” what the stuck letters are – for T-T dimers, they usually get it right, writing the complementary letters A-A. But, for dimers of cytosine (C-C), they’re more likely to mess up, and write A-A instead of G-G. Now, when this new strand gets used as a template for making more copies of the strand with the dimer, instead of C-C, that strand will read T-T. And this mutation will get passed on to all the daughter cells made from this cell. If the mutation is in a key regulatory molecule, it can lead to uncontrolled cell growth (cancer).
So it’s really important that we use caution if we have to work with UV light. Take, for example, when we’re exposing our EtBr (or another other fluorescent dye, like DAPI, the dye in the EZ vision stain our lab uses) -stained DNA gels on a UV tray. We *want* the dye to absorb the UV light and give it back to us as light we can see. We DON’T want the DNA bases absorbing that light and forming dimers – in our gel or in our cells. So we scan our gels in a shielded box and, if we want to recover the DNA, we limit its exposure.
This is why red lights went off in the brains of molecular biologists and biochemists across the country as they heard people talk about shining UV light on/in people as a treatment for Covid-19, the disease caused by the novel coronavirus SARS-Cov-2.
SARS-Cov-2 is a single-stranded RNA virus. It has RNA instead of DNA, but that doesn’t mean it’s out of the woods in terms of UV damage. Like DNA, it can also form pyrimidine dimers (but instead of having thymine it has uracil (U)). And UV light can even get the viral RNA’s backbone to break. And, unlike our cells, the virus doesn’t have all that repair machinery to fix the damage. So UV light *can* kill the virus – ON SURFACES. If you shine UV light on an infected person, the person’s skin will take the damage, the light won’t get inside far enough to hurt the virus. And by surfaces I mean tables and stuff, not skin – please don’t try to disinfect your skin with UV light. It’ll hurt you, not just the virus, because UV light isn’t picky…
And it’s not just any UV light – sunlight contains 3 main types of UV light – UVA, UVB, & UVC. The most virally-damaging is the most energetic type, UVC. This type of light is blocked by the ozone layer, so we don’t get it from sunlight (though UVA & UVB can also do damage hence sunscreen). So when people use it as “germicidal UV” they have to do so using UVC lamps. These lamps aren’t all created equal – they give off light with different intensities, so for the weak ones you’d have to hold the light really close to something you’re trying to disinfect for a really long time in order to give it a large enough dose of radiation to get it clean. More on this in yesterday’s post: https://bit.ly/2VFK1v4