Malmesbury
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?
There is way too much serendipity
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!
Not quite, if it’s less efficient at doing the normal mitochondria work, it puts a big burden on the cell, who is then less likely to reproduce.
Thank you for spotting this, I fixed it.
It’s not so much the different types in themselves that prevent competition, but having multiple types make it possible to have a mechanism that forces all organelles to come from only one pre-selected parent. If all organelles come from the female, then a rogue mitochondria cannot take over by making more copies of itself or by poisoning other mitochondria, because the only way to make it to the next generation is to be in the female gamete, period. In other words, there’s not much an organelle can do to increase in frequency, aside from improving the overall fitness of the organism. Does that make more sense?
The n°1 reason why I said not mention fungi is that I’m absolutely not a mycologist and I wouldn’t be able to talk about them. So I greatly appreciate that you do it! Typically, I had never heard of glomeromycota, despite them apparently being involved in symbiosis with 80% of plants. I like to think that I have a decent understanding of the living world, and then I’m constantly reminded that I don’t, and probably nobody does...
According to this paper, the “root” factor is how much effort each parent invests in caring about offsprings, as in some species the male is the primary caregiver. But that’s really hard to measure and check empirically, so they instead measure “the maximum number of independent offspring that parents can produce per unit of time”, and they find very good agreement with which sex faces the most intense competition.
On notable exception is the hippocampus, where the males both face intense competition and invest more resources in the offspring. Because of course it had to be hippocampi.
The “random sampling” that causes genetic drift is applied once every generation, asexual or not, so the optimal number of types depends on the ratio of generations that are asexual vs sexual. The Constable & Kokko paper has a mathematical model to quantify how many asexual generations you need for 2 being the optimum, and it turns out that most isogamous species are well into that regime.
That being said, you’re entirely right when you ask “why is the equilibrium 2 instead of 3 or 5 or different for different species?” – Constable’s model and empirical data is only for isogamous species like baker’s yeast. It seems plausible that our isogamous ancestors were in the same regime, and then anisogamy evolved and kind of locked us into a 2-types configuration. But that’s mostly speculation, I don’t think we have any clear empirical data that confirms this hypothesis. That’s still open to investigation.
Another thing I didn’t mention is that the organelle-competition hypothesis naturally leads to 2 types, so it could simply be that.
The Talk: a brief explanation of sexual dimorphism
In their book on social dominance, Sidanius and Pratto make a relevant point: first, they cite a bunch of audit studies where researchers send fake resumes to employers, and find a marked bias against employing African American. Then, they point to Gallup polls asking people whether African American face any discrimination, and almost half of African-Americans themselves say they don’t. Same for discrimination in justice or housing. So, when the book was published back in the 90s, many black people didn’t believe in racial discrimination, even though it affected them personally in their life.
This means that people’s perception of discrimination is not so much influenced by lived experience, but by what the dominant ideology is at a particular time. Back in the 90s, racial discrimination wasn’t emphasized in the dominant discourse, so people thought it wasn’t very important. In that case, standpoint epistemology just entrenches the dominant beliefs.
Another example: today, there’s a vast body of research showing large discrimination against men when applying for housing. If you’ve ever applied for a place to rent, this has affected you personally favourably or not. But were you aware of it? If you did an online survey asking men what discrimination they face, how many of them would bring up housing discrimination? They don’t know about it, because the dominant ideology doesn’t talk about it.
I see this as a critical failure of standpoint epistemology (and the “lived experience” approach in general). Here is a 2011 survey where white Americans claimed that white people face more discrimination than black people. I don’t think this gives us any valuable information about how much discrimination white people actually face.
(I do see the value of lived experience for hypothesis generation, of course.)
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.