Study suggests a single point mutation facilitated increase in human brain size

Has anyone considered that the fossil record doesn’t show a tripling of brain size (or even neocortex size) in a single generation?

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I’m by far the least expert person in this discussion, with perhaps one exception, but it would seem to me producing a new sub-species of super-intelligent marmosets was not the objective of this study, nor relevant to the question it intended to answer. Rather, the question was whether and how a mutation of this sort could produce a larger neo-cortex in a primate. I know how disappointing it must be for you that this does not require any interventions from an intelligent designer. Them’s the breaks.

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A larger neo-cortex that disappears in one generation, because the mutation causing it cannot be transmitted via reproduction – gotta make the babies, no evolution without offspring – has no relevance to evolution.

Design does not enter into this; we’re talking Evolutionary Theory 101.

If I had to place a bet: these big-brain marmosets will have more than a few problems, if allowed to develop past the fetal stage where they were sampled for the experiment.

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Neither does this paper. The increases in length and thickness of cortex are far less than that. The only threefold change I see is in number of a specific type of progenitor. The numbers of some specific cortical neuron types are increased by about a third.

I know you know this and your point is well taken, just thought we’d want clarity given the immediate and unfortunate obfuscation introduced into this discussion.

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That’s my fault for writing a title carelessly.

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It is wholly irrelevant to the paper, this is true. But it’s worse than that. The claim that this effect on cortical size and composition would be detrimental is made with no reference (or, as near as I can tell, consideration) of what we know about cortical development in primates and about variation in cortical size and composition in primates including humans. The confident claim that this phenotype would hinder reproduction is actually a vacuous one without any reflection on the context. Calling this a “dramatic morphological mutation” is potentially very misleading; the only “morphological” change is gyrification and the changes in the tissue involve increases in the numbers of cells that were already represented there.

When this human-specific mutation occurred in our ancestor, would it have amounted to a dramatic change in morphology? A dramatic change in intelligence or behavior? Well that all depends on what you mean by ‘dramatic’ and that means those questions are silly. What isn’t silly is the open question of what the mutation did at the moment it appeared and how its effects interacted with all the other influences on brain development that were occurring (and changing) at the time.

That, and not idle speculation about detrimental effects, is “Evolutionary Theory 101.”

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Of course. OTOH, if it persists in the population because the organisms are not massively disadvantaged by having a bigger brain, then…

Your opinion is duly noted.

So, just for interest’s sake, how does Intelligent Design address this problem? If primates cannot survive and reproduce if they have bigger brains, which is what you are betting, then how did primates end up getting bigger brains?

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Another hypothesis to consider is that marmoset’s would survive to adulthood and reproduce just fine in a laboratory context, perhaps even with enhanced cognition, but in the wild they would have negative fitness and this mutation would be selected against.

Why would this cause negative fitness in the wild? It is not clear that enhanced cognition would help marmosets in the wild more than the extra energy costs of a larger brain (which is 20% of human metabolism).

If this hypothesis is correct, we would not expect this mutation to fix in wild marmoset populations, but it would not in any way undermine the hypothesis that this mutation arose and was fixed by natural processes in humans.

In fact, improved cognition on these marmosets (even though their mutation would not fix in the wild) provide strong evidence that this mutation was in fact an important step in human brain evolution.

To connect with other discussions, we know this mutation took place after the split from chimpanzees, and it could have had a very large effect. Such a large effect, it is possible, might have been behaviorally observable in different populations of our ancestors.

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You have it, that means it was a viable mutation when it occurred in one of your ancestors.

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This is a good time to remind us (the biologists) to consider that while the mutation arose first in a single individual, it was then introduced into a population that we must assume already exhibited variation in cortical size and cell number. It is all too easy to think of “cortical size” as a single fixed parameter, which is then increased by some specific fixed amount by the mutation. Both of which are wildly wrong. Instead, cortical size/thickness/cell number/whatever is today and was then a varying trait, with a median and with extremes that we may assume were associated with significant fitness effects. The mutation, which we see from several papers on the topic, exerts a quantitative (NOT qualitative as near as I can tell) effect on those traits. This means that the mutation moves an individual “up” the scale, either closer to or away from the median depending on everything else in the milieu at the time. The mutation affects a metabolic process in a particular cell type, so we assume (I would say we know) that its effect will vary depending on individual variation in related processes.

All of which is to say this, which among professional biologists should be obvious but is easy to forget when answering questions from confused laypeople: this is a quantitative effect on a quantitative trait. It is mistaken to ask whether “it” will have a “large” or “beneficial” effect. It is much better to think along the lines that evolution is known to work: on phenotypes expressed in varying populations.

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There is such confusion here. Of course this point mutation can transmit by reproduction. The question about whether or not there would be negative selection against it in marmosets, which is a category error to think this has much at all to do with human evolution.

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Certainly true, but if I read the paper right, this tripled the number of Cortex neurons. That is an extremely large effect, well outside the range of usual variation, right?

No, that’s wrong. See Figure 3 below. It shows an increase of about a third in two specific types of upper-layer cortical neurons. The tripling was in a specific kind of progenitor cell.

No. The effect on neuron number is most definitely not extremely large. I don’t know whether the effect on progenitors would be judged “extremely large” but that’s why the authors looked at neurons and their types, and again, it’s a pretty specific population that tripled. It is flat wrong to conclude that there was a global tripling of cortical neurons or even of cortical precursors.

The authors note that cortical neuron generation is in progress at the stage at which they did their analysis, so this is in some sense a snapshot. At some point the progenitors switch to making glial cells, though.

My read at this point is that we should step back from the overstatement in the title of this thread, from the typical overselling of the press release, and from the red herrings in this very discussion, and see the phenotype as a very interesting quantitative change induced by a single mutation. That change is of course big enough to make an evolutionary difference, in principle, but it’s a quantitative, cell biological, specific change.

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I see. That’s helpful. I missed that, and in fact have not had a chance to read the paper yet. Thanks for the correction.

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This thread continues to be an extremely informative discussion—and one that is very accessible to those of us who are not academically trained in these specializations. I thank you all for so many helpful, well-written posts.

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Hear, hear.

So, bad title on the thread and press release, then.

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Yeah I’ve asked if we can change the title of the thread. The press release doesn’t say anything about tripling and it’s not THAT bad but I wish we saw fewer of them here on PS. Oh and one more thing. Wait I have to go I think there are some kids on my lawn.

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Just to clarify, by evolutionary change, are you referring to a change that will be selected for or against? I.e this kind of mutation wouldn’t be "neutral mutation?

I guess the main point here is that a single point mutation led to this change. Would the following questions be pertinent?

  1. Is this change irreversible? I.e can another single point mutation in the same area destroy the change?

The way I see it, the higher the chances of it being reversed by another mutation, the stronger the effect of selection needs to be to ensure the mutation is fixed in a population? Would this be a correct assumption.

One example of a strong selective effect I can think of would be that most mutation in this gene would lead to non viable fetuses and this particular mutation is one of the few that lead to viable fetuses.

When one is talking about an ancestor with a particular set of phenotypes changing over several generations into modern humans and of a particular single point mutation as a step in that direction… then this mutation needs to be irreversible, either because of strong selection of other reasons.
Does th paper suggest anything with regard to this?

He never said “evolutionary change”. What he said was “an evolutionary difference”; presumably that refers to something that’s subject to positive selection. Neutral fixations are evolutionary changes just like selected ones.

Of course it isn’t irreversible. Any point mutation can be reversed. The rate of back mutation is indeed a factor in the probability of fixation, but not a large one. The rate of forward mutation is a factor too.

No, it doesn’t.