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Sup Seq Squad, Hi, it’s Maddie. I have never been a very linear writer. By that, I don’t mean that I struggle with writing from point A to point B (although I guess that could be up for debate, too). Rather, picture a graph where x is time and y is words written. If you were a linear writer, your graph would look like this:  If this is you, I envy your process. Teach me your ways. The way I write often feels a lot more like this:  And I'm probably underestimating the time spent flatlining. As a biology person and a Setphen Jay Gould superfan, looking at this extremely unscientific graph screams “punctuated equilibrium” to me (the theory that evolutionary innovations don’t happen at a constant rate, but rather “speeds up” or “slows down” depending on factors like scarcity and environmental pressure.) If you average it out, I (sort of) end up in the same place as the linear writer, but the difference is what the process feels like. Being able to sit down and have a fully formed story pop out of my head like Athena emerging from Zeus is awesome. But the rest of the time, wanting to write but feeling incapable of it is a form of torture I wouldn’t wish on my worst enemy. This has always been how I wrote, even in high school and college. I used to believe I just had something wrong with my work ethic — that those moments when I tried and failed to put pen to paper were indicative of not trying hard enough. I realize now that’s not the case, and I’ve learned to work with the way I write rather than try to tame it. My passion for writing is a bit like a deer, in that Andrew Cuomo and Bill DeBlasio could kill it by putting it in captivity. All this to say: here are 1,000 words I wrote about mpox the other night. It was quite easy to sit down and write it, and I hope you enjoy reading. And I’m grateful to this site for giving me an outlet for the cathartic part of writing without the banging-my-head-on-the-desk part. Read on to see what my talented colleagues are up to! Send the newsletter to a friend, or consider subscribing to a paid tier. 1 Retweet = 1 Happy Maddie. What we’re working on: Max: Last week a video I wrote went live on TED-Ed. It's about the weird history and chemistry behind Kevlar. I've also been working on some other scripts and writing about bugs. Don't ever hesitate to reach out with any ideas for stories you'd like to see! Dan: I’ve been working on a reflective piece about the biological and evolutionary nature of death. It’s really uplifting. Let’s take a sneak peek! Maddie: Kim is out living her best life in Brazil. I’m not sure what I want to be mad about next! Probably dengue. What we’re reading: Max: Aside from Maddie's great mpox piece, one story that stood out to me was "Climate change is messing with city sewers — and the solutions are even messier" from Angela Ang at Grist. Major cities like New York and Boston are hustling to redesign their sewer systems. Both currently have "combined" sewer systems where stormwater overflow and sewage commingle and, during big rains more common with climate change, dump back into the human environment together. Boston is separating the combined system primarily with new pipe. And New York is trying to manage rainwater better. One cool idea suggested as part of a larger suite: "sunken basketball courts that can capture stormwater in the event of heavy rain." PS about fiction: I finished Never Let Me Go this weekend. Then I watched the movie. Both wrecked me in their own ways. Idk why I do this to myself. Maddie: This NYT piece on the “New Brunswick neurological syndrome of unknown etiology.” What does it mean when a governing body decides that a disease is or isn’t “real”? Or alternately, when a doctor goes against the medical establishment, falling into quasi-paranoid thinking? Lots of questions raised with not many clear answers. I also watched “Mystery Men,” which is a great movie. Dan: Normally in this section I’d mention something light and readable, a book or magazine article. Today let’s talk a little about this new piece of primary literature. It appeared in Science last week. It’s called “Compensatory mutations potentiate constructive neutral evolution by gene duplication.” Let’s see what the science group chats were saying about it: The question the paper addresses is quite knotty. Proteins often don’t perform their functions on their own, but exist as pieces of a larger protein complex that can have dozens or hundreds of individual units. Importantly, those units frequently do not function on their own. Some estimates suggest that upwards of 30% of all proteins (in available databases) exist in superstructures like this. But if the function of a complex depends on its individual subunits, and the subunits themselves are inactive when not part of a larger structure, how does each of those subunits evolve to fulfill that structure’s function? This could be straightforward if all the subunits were identical (a situation called a “homomer”). If you need to build a brick shed, all you need is a bunch of identical bricks. But most complexes aren’t like this, instead being made up of different proteins encoded by different genes (a “heteromer”, the -mer suffix denotes something made up of units, like a polymer). If you’re still following along, here’s the twist: many multi-unit protein complexes exist in one species as a homomer, made up entirely of identical subunits, and in another species, performing the exact same function, as a heteromer, a mix of units, some of which are the same as the original homomer units and some that are completely different. How does this heterogeneous mix of proteins, arising and evolving independently of each other, maintain its original function? It’s like trying to get two Lego pieces to fit together nicely without knowing what the other looks like, or that it even exists. The answer, according to the researchers from the Université Laval in Quebec City, is that, in a simple system of two proteins, as each protein mutates to facilitate the creation of a heteromer, the mutations in both compensate for the mutations in the other. If a mutation in protein A allows it to form a heteromer with protein B while simultaneously destroying its ability to create the function of the full complex, protein B will mutate in a way that both allows for the creation of the larger structure and restores the function of that structure. Each hand washes the other, as they say.
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