Given my research background with DNA, I was very intrigued when I read the portion of the Baird text that mentioned UV-B-induced mutations of DNA sequences (pg. 33-34). I’m sure we’re all aware that one of the effects of chronic UV radiation exposure is skin cancer, so DNA mutation probably isn’t all that shocking to read about. What was interesting, though, was how the DNA is mutated. Take a look at this picture!
Here’s a more chemical view of what the mutations can look like; keep in mind, these are bases that are staking along the phosphate backbone, not bases across the strand from one another:
As can be seen in the picture above, the two major products of UV mutation are 6,4 photoproducts and cyclobutane pyrimidine dimers (CPD), respectively. CPD mutations only occur when UV radiation strikes a sequence with consecutive pyrimidines (C’s or T’s) and induces the formation of covalent linkages. Despite the fact that CPDs are usually recognized by DNA repair enzymes, mutation correction is not 100% efficient, so these damaged sequences can persist. That’s one of the reasons why chronic exposure to UV-B radiation is so dangerous.
I personally thought it was interesting to get a little more of an in-depth look at what a depletion of the ozone layer can lead to on the molecular level. Ozone isn’t particularly good at absorbing radiation at 300 nm, which is the wavelength that wreaks the most havoc on DNA, but a little is better than nothing!
If any of you are interested, here’s a link to a Web Book that has a bit more of a mechanistic approach to showing DNA mutation by UV radiation.
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