Inherited Learning? It Happens, but How Is Uncertain
quantamagazine.org
quantamagazine.org
Furthermore, most, if not all, transgenerational effects of epigenetic inheritance even in C. elegans is transient. Meaning, the effect attenuates over just a few generations and then vanishes completely.
To be absolutely clear: Learning is not inherited in humans. There are good reasons to make this a categorical statement. What’s called “learning” in C. elegans is completely different from “learning” in humans, and adaptive changes in mouse behaviour are, so far, still not clearly demonstrated to be caused by epigenetics, and there are good reasons to be sceptical, as summarised by Kevin Mitchell: http://www.wiringthebrain.com/2013/01/the-trouble-with-epige..., and by Bernhard Horsthemke: https://www.nature.com/articles/s41467-018-05445-5
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6127768/
""" One the most provocative observations regarding Holocaust offspring was the report that Yom Kippur war veterans were more likely to develop post‐traumatic stress disorder (PTSD) in response to combat if they had a Holocaust survivor parent25. A higher prevalence of PTSD, mood and anxiety disorders was also observed in Holocaust offspring, largely selected from a convenience sample of people seeking treatment for Holocaust‐related problems, compared with controls26. These findings were replicated in a study assessing the relationship between PTSD in offspring and their own parents, assessed directly by clinical interview of the parent (s)27. """
1. "Holocaust offspring" may have been told by their parents about their experiences, and that could sensitize them in various ways (e.g. more inclination to envisage very bad worst cases; vivid examples of terrible things available to their imaginations; some sort of unconscious fear of losing their parents; feelings of guilt at being upset about something less bad than what their parents went through).
2. "Holocaust offspring" are, necessarily, offspring of people who survived the Holocaust. Those people might be different genetically from the population at large, in all sorts of ways. Maybe some of them happen to correlate with greater susceptibility to PTSD.
3. "Holocaust offspring" might have a greater tendency to put themselves into the sort of situations that produce PTSD. (Either for #1-like reasons -- e.g., their parents' example makes them feel a greater obligation to put themselves into danger if they think it may save others -- or for #2-like reasons -- e.g., maybe people who survived the Holocaust tend to be braver or show more initiative or something like that.)
And a couple of other reasons to be cautious about interpreting these findings.
4. "largely selected from a convenience sample of people seeking treatment for Holocaust-related problems". That seems like an extremely fruitful source of selection bias.
5. PTSD is a thing that has to be diagnosed. The people making the diagnosis know their patients' history, or ought to. It's possible that a psychologist may be more inclined to diagnose PTSD if they know that their patient is the child of a Holocaust survivor.
No. That review paper doesn’t discuss an actual mechanism, with good reason: the authors don’t have a mechanism. At the risk of sounding harsh, the underlying research has been throughly rubbished by the community [1, 2]. It uses a tiny sample size, tenuous correlation and, as mentioned, utterly fails at highlighting a plausible mechanism. It’s bunk: there’s absolutely no need to invoke the spectre of epigenetics to explain why children of traumatised parents may likewise be jumpy, just as there’s no need to invoke epigenetics to explain why children of English parents speak English. In fact, even the review you link to acknowledges as much:
> studies in humans have not yet demonstrated that the effects of trauma are heritable through non‐genomic (i.e., epigenetic) mechanisms
[1] http://sciblogs.co.nz/code-for-life/2015/08/28/epigenetics-a...
[2] https://www.theguardian.com/science/blog/2015/sep/11/why-im-...
I'm not sure what you're referring to here? There appears to be quite a significant body of literature on epigenetic inheritance -- just to pick a few: [1,2,3,4]. The term "Transgenerational epigenetic inheritance" even has its own wikipedia page: https://en.wikipedia.org/wiki/Transgenerational_epigenetic_i...
[1] https://www.nature.com/articles/ng1199_314
[2] https://www.nature.com/articles/nrg1834
[1] https://www.theguardian.com/science/sifting-the-evidence/201...
[2] https://twitter.com/ewanbirney/status/1014494822525296640
Why are we significantly less likely to have mutations on our mitochondria than in our fingers? It seems obvious to me that our DNA has error correction mechanisms, and some subsystems are more stringently error corrected than others. This amounts to a control on how much different aspects are allowed to deviate from the last generation. I would be incredibly surprised if a crocodile, who has been in a state of relative homeostasis for millions of years, has the same rate of mutation as a human. Note that I haven't suggested that a directional bias exists, just a set of mechanisms for changing variability of different traits. I wouldn't be particularly surprised by a mechanism for directional bias in some cases, but I don't assume there is one and I certainly don't feel comfortable making the case for it.
I’m afraid this is simply not a biologically meaningful statement to begin with. Mitochondria are subcellular organelles. Fingers are complex organs that are formed from spatial arrangements of multiple cell types. Furthermore, mutations happen on the level of DNA, not on the level of either organelles or organs.
Apart from that, mutation rate is (not quite, but more or less) uniform across the whole genome (the exceptions, due to e.g. GC bias, are not relevant here). Viable mutations are not uniformly distributed because of selection; that’s precisely the striking insight that Darwin had (though he was unaware of DNA and genes). Importantly, this does not require a guided error correction mechanism. Simply put, even slight variations in the oxidative phosphorylation pathway of the mitochondrion are likely to kill you during gestation; whereas similarly extreme variations in finger morphogenesis, at worst, make you unable to hold a tool.
> some subsystems are more stringently error corrected than others
This is virtually certainly not the case, because of what I’ve just described. Selection is sufficient to describe the outcome, and there is no evidence whatsoever to point to the mechanism you postulate.
> I would be incredibly surprised if a crocodile, who has been in a state of relative homeostasis for millions of years, has the same rate of mutation as a human.
Evolutionary mutation rate is governed by effective population size and generation time. That’s why fruit flies evolve fast and crocodiles evolve slowly. This, too, doesn’t require variable mutability of different traits, and no biologist has yet seriously suggested such a mechanism.
This is all besides the point. Mitochondria are just an easy example because of the marked difference in mutation rate, and my loosely worded bit about fingers evolving should obviously be taken as "some parts of the genome associated with the development of fingers."
> Apart from that, mutation rate is (not quite, but more or less) uniform across the whole genome (the exceptions, due to e.g. GC bias, are not relevant here).
Not my field, but I'm pretty sure you're incorrect. Here's a citation:
https://www.ncbi.nlm.nih.gov/pubmed/11057667?dopt=Abstract
>> A few patterns have been found: proteins involved in antagonistic co-evolution (for example, immune genes, parasite antigens and reproductive conflict genes) tend to be rapidly evolving, and there is a correlation between the rate of protein evolution and the mutation rate of the gene. Here we report a new highly statistically significant predictor of a protein's rate of evolution, and show that linked genes have similar rates of protein evolution.
>This is virtually certainly not the case, because of what I’ve just described. Selection is sufficient to describe the outcome, and there is no evidence whatsoever to point to the mechanism you postulate.
This is virtually certainly not the case, because of what I've just cited.
> Evolutionary mutation rate is governed by effective population size and generation time.
I'm not arguing that these aren't factors, but we do have good reason to believe that the rate of change for some subsets of the genome can itself change.
Here's another source:
https://www.ncbi.nlm.nih.gov/pubmed/10469563?dopt=Abstract
>> Our results provide the first substantial statistical evidence for the existence of a regional variation in the synonymous substitution rate within the mammalian genome, indicating that different chromosomal regions evolve at different rates. This regional phenomenon which shapes gene evolution could reflect the existence of 'evolutionary rate units' along the chromosome.
As for the second article, I’ve made reference to that in my previous comment, too (that’s GC bias). And, as mentioned, this isn’t relevant here.
That seems entirely possible.
> As for the second article, I’ve made reference to that in my previous comment, too (that’s GC bias). And, as mentioned, this isn’t relevant here.
Can you unpack why you think this isn't relevant? The rate of change varying across regions of the genome seems highly relevant to me, even if our current knowledge of it were hypothetically confined to a specific type of change.
^1 I’ve never seen anybody explicitly quantify this but the relative impact of GC content and negative selection on mutation rate must be several orders of magnitude different … at a guess at least thousandfold, more likely millionfold.
That seems fine. If some genes are more stable than others, and this can vary by normal random mutation, it can be selected for. I'm still failing to see why this isn't relevant to the current discussion.
Selecting is not blind, selecting is sexual or based on survival. The mutation that changes the rate of other mutations is random, but once that mutation occurs it can be selected for via normal means.
Evolutionary selection (regardless of whether natural, sexual, artificial or whatever) happens in aggregate over multiple generations, it canʼt account for guided mutations in the germ line that encode “learned” behaviour (which, as my initial comment explained, simply donʼt exist).
> But this isnʼt what you were talking about here, which is the hypothetical existence of a biological mechanism enacting differential, directional selection.
It should be noted that I never said directional -- I actually made it explicitly clear in my first post that I was not arguing for a direction, only for modified rates of change: "Note that I haven't suggested that a directional bias exists, just a set of mechanisms for changing variability of different traits." So, I think this is what I've been talking about from the beginning. Perhaps it's due to my lack of familiarity with domain specific language, but I'm not sure that you're understanding what I've been arguing for. Please don't get bogged down in the specifics of this example (it's the pointing finger, not the moon), but I'm not suggesting that cheetahs evolved a tendency to evolve faster running, I'm suggesting that they might have had a period of evolution where a variety of genes related to running were more likely to change in both beneficial and non-beneficial ways, but because faster running was such a beneficial trait it actually made sense for some portion of the population to have offspring who were more likely to have both beneficial and harmful changes happen over the relevant sections of genetic code. In times of less rapid environmental/adversarial change, where stagnation is good enough and the reward for beneficial deviation is more outweighed by the risk of harmful deviation, the rate of change can be toggled back down (again through normal evolution).
1) Do we agree that random mutations of the germline can result in differing rates of change across subsets of the genome?
2) Do we agree that this can affect the viability of offspring?
3) If yes to both of the above, is any component missing for evolution to select for different rates of variability in different subsets of the genome?
That’s correct, but we’re not discussing the cutting edge here but relative basics. I’m clearly not articulating myself well but I can assure you that this discussion wouldn’t take place between two biologists because there’s nothing here.
> It should be noted that I never said directional -- I actually made it explicitly clear in my first post that I was not arguing for a direction
You did say that, but, respectfully, you implied directionality — otherwise it would be completely unclear what your initial comment wanted to say, because it seems to specifically have objected to my assertion that no directed changes of the germ line exist.
> Do we agree that random mutations of the germline can result in differing rates of change across subsets of the genome?
Not within a single generation, no. Across evolutionary time, by virtue of selection, yes (that’s in fact the very basis of evolution). But this is irrelevant in the context of this comment thread, started by my initial comment: I asserted that there is no mechanism to encode learned behaviour in the germ line. This would require a direct mediator of mutations on the molecular level, not across evolutionary time but in the here and now. A molecule in the gametes (or their precursor cells). Such a molecule does not exist. Stochastic variation that shapes patterns of mutation across multiple generations is fundamentally a red herring here.
No, I did not mean directionality. I meant what I said, and was very explicit about it. In my first post I quoted the exact bit of your comment I was replying to, which went like this: "So far there’s no known mechanism for systematic, guided DNA changes, and no good reason to assume that such mechanisms exist (on the contrary)." I wasn't even sure if there would be disagreement between us when I originally replied to that, because I'm not sure how broad the definitions you're using for "systematic" and "guided" are. I could see arguing that evolution changing the variability of a subset of the genome is "guided" in some sense, as it can "guide" the process towards more changes in a particular subsystem, but I could also see not arguing that since it lacks direction. Language is mushy. I was trying to qualify your statement, and I posed questions and made statements of my own to that end, but I wasn't sure if my positions were in conflict with yours until you replied. Now I think our positions probably weren't in conflict, but you made assumptions about what I meant to convey based on the larger context of your own post rather than the actual content of mine.
It's like how infants inherit the instinct to cry and suckle. Inheritance of learning would be if the mother (since childhood ) was taught to wink and she'd get more attention and food/milk and her infant winked at her instead of crying when the infant wanted attention.
Building a little (but speculatively... I don't know much about wasps and their nest-building instincts): I often wonder what (if any) fractions of behavior that gets chalked up to "instinct" are actually the result of some biological/mechanical affordance, normal learning, and reasoning.
(I don't mean to deny instinct as such, but I guess I feel like the razor should exclude it until it's the only option left?)
To use the hexagonal example, the term "instinct" implies that the creature could do this thing in a variety of ways, but doesn't. But it wouldn't quite be "instinct" in the sense we mean it if the hexagonal structure is just a coincidental emergent byproduct of some detail of the species' visual system, physiology, etc.
Many other animals have much more complicated instincts, but even then you can often see the instinct starts as something very simple. A fawn "knows how to walk" at birth, but, look at video of a fawn at birth. I say it's a lot more like "a fawn knows to recognize it is falling and trigger an only-modestly complicated reaction to stab the closest leg out in that direction", a neural circuit so simple with a bit of effort you could almost assemble it by hand in some sense. A little bit of control circuitry on top gives it a small amount of mobility.
I think one of the reasons "nervous systems" are so evolutionarily successful is that they do give that mechanism to go from simple instinct to a much richer learned behavior, and it's obviously a combination of many things to get to that point. It's amazing how some of these things work on not necessarily all that many "instincts".