Malmesbury

https://malmesbury.substack.com

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it's no biology lab

I'm afraid you're overestimating how well biologists follow the safety procedures. I wouldn't be surprised if we all had fluorescent bacteria in our guts.

Oh, that's a really good point. Actually, it might be common for chemists to work with panels of related molecules, while in clinical trials they only work with one purified drug candidate. This makes it less likely for them to discover things by accident. Surely a piece of the puzzle!

Sure, all these stories totally sound like urban legends, but the sweeteners are out there and I don't see how they could have been discovered otherwise (unless they were covertly screening drugs on a large number of people).

That's a great question, this is totally mysterious to me. There are a lot of examples of people putting thaumatin in transgenic fruits or vegetables (and somehow in the milk of transgenic mice because there's always one creepy study), but I don't know why it hasn't been commercialized. It sounds like superfruits would make a nice healthy alternative to palm-oil-and-chocolate-based comfort foods. Maybe it's a regulatory problem?

That sounds exciting! I hadn't seen Elisabeth's comment, I just wrote a reply. Do you think there are modifications I should make to the main text to clarify?

That sounds plausible, but I've not looked into the empirical research on that topic so I can't tell you much more! 

(Sorry I missed your comment)

Here by "reproduce" I just meant "make more copies of itself" in an immediate sense (so reproductive fitness is just "how fast it replicates right now"). For example, in Lenski's long-term evolution experiment, some variants were selected not because they increased the bacteria's daily growth rate, but because they made it easier to acquire further variants that themselves increased the daily growth rate. These "potentiating" variants were initially detrimental (the copy number of these variants decreased in the population), and only after a long long time they took over the population. So, according the definition of reproductive fitness I used, they lead to a lower reproductive fitness – the reason they were eventually selected for is not that they're good for reproduction, but that they're good for evolvability. Of course, you can say that eventually they increased in copy number, but that would be defining "reproduction" in a different way, that I find less intuitive.

Now, is that other definition (how gene copy number increases over the long term) what evolution ultimately selects for? I'm not sure. To quote Kokko's review on the stagnation paradox:

"Trees compete for sunlight and attempt to outshade each other, but when each tree consequently invests in woody growth, the entire forest must spend energy in stem forming and—assuming time or energy trade-offs—will be slower at converting sunlight into seeds than a low mat of vegetation would have been able to. Every individual has to invest in outcompeting others, but the population as a whole is negligibly closer to the light source (the number of photons arriving in the area is still the same). This is why in agriculture, externally imposed group selection to create shorter crops has improved yields."

She gives other examples. In these cases, the number of individuals tend to decrease over time, even in the long run. 

You're right. Honestly I wouldn't be able to talk about this in detail because this is getting far from the things I know best (full disclosure, my own research is on bacteria). The few papers I've cited give some general patterns, and my general point was "things can go in many different ways depending on the specifics, and even the well-known Bateman principle isn't universal".

That's unfortunately all can do: there's a whole world of things to say about how sexual dimorphism actually develops in metazoans, but it takes years of learning to get a deep understanding of what's going on.

Definitely post the papers you're thinking about! If you feel like making a new post about that, I can't encourage you enough to do it. This post was by far my most successful, so it looks like a lot of people are interested in the topic. I'm sure many people would enjoy your contribution (at least I would).

As for the Red Pill thing, I kind of regret mentioning it – I just thought it was funny, but it's not really that funny or useful. Maybe I should edit it out.

What do you mean by curating? So far I've tried to answer the questions and objections when I saw them, are there some I've missed? (Obviously I don't pretend to be able to answer everything). Also, do you think there are some clarifications that I should add to the main text?

I would guess that when organelles are inherited from both parents, the traitor organelle is disadvantaged by its burden on the host, but advantaged by it's ability to be the predominant organelle in the offspring. If the cost-benefit is favourable, then the traitor organelle will take over. OTOH, if only one parent transmits the organelle, the advantage disappears but the burden remains. So I'd expect that it makes it more difficult for traitor mitochondria to invade. Hopefully that makes sense!

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