Sun, Sand, and Damaged RNA
By Katie Pratt on July 12th, 2012
Some of you might have noticed the irregularity of my Mind the Gap posts of late. But fear not, I’m back! I defended my PhD a couple of weeks ago after having only 3 weeks to finish writing the thesis, so things got a little crazy. Crazy awesome: I’m now Katie PhD, for real!
One of the bonuses of defending in the summer is that a lot of the ensuing celebrations took place outside in the sun, which for a Brit like me also meant several rounds of sunburn. Fortunately I keep a stash of aloe in the fridge for just such an occurrence to calm the red and the itchy, and I promise I wore sunscreen.
So it was with a two-day-old sunburn that I was cruising the interwebs looking for a paper to blog when I stumbled upon a study that implicated damaged non-coding RNAs in triggering the immune response to UV-damage. Having spent the last few years working on non-coding RNAs, I was (nerd alert) pretty excited, and printed myself a copy of the Nature Medicine paper.
Disclaimer: several mice were sunburnt in the making of this paper.
While it’s been known for some time that sunburn is an immune response to UV irradiation, the molecular trigger for this response has been a bit of a mystery. To address this question, Bernard and colleagues began by using a cell culture system that, like the cells in our bodies, responds to UV irradiation by producing several cytokines. They found that lysates from these irradiated cells could trigger a similar response in non-irradiated cells, but that this effect was lost if the lysates were treated with RNase. Injecting similar lysates into the ears of living mice, with “sunburn” only observed if RNA was present, further corroborated the idea that it was UV-damaged RNA that was causing the immune response.
Next, using a high throughput RNA sequencing approach, they found that there were changes in the structure of particular regions of snRNAs (non-coding RNAs involved in several nuclear processes, including mRNA splicing), and that these changes were likely candidates to activate ______ and produce the observed cytokine release. Sure enough, injection of UV-irradiated U1 snRNA induced “sunburn” in wild-type mice, but in ______ knockout mice the researchers saw no response.
These data open up a number of avenues for downstream applications, including the use of damage non-coding RNA as a biomarker for UV-induced damage and the development of alternatives to the phototherapeutic treatments used in several skin disorders.
Unfortunately, it would appear that the authors have no immediate plans to develop a super-sunscreen or anti-sunburn drug. I guess my fair-skinned compatriots and I will just have to stick to the old sunscreen and aloe combination for now.
Katie Pratt is a postdoc in Molecular Biology at Brown University. She has a passion for science communication, and in an attempt to bring hardcore biology and medicine to everyone, she blogs jargon-free at www.katiephd.com. Follow her escapades in the lab and online on Twitter.
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About the winner: Bryan is a researcher at the University of Calgary studying the microbiology of the cystic fibrosis lung. He’s particularly interested in mechanisms of Pseudomonas aeruginosa strain competition and “superinfection”.
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