It’s still early days, but gene-therapy modifications of bone marrow stem cells may be the solution to many haematological malignancies
Peter Doherty, An insider’s plague year
something like…
Canto: So we’re going to try and educate ourselves with the help of all these videos out there on the immune system, with hopefully occasional references to the SARS-Cov2 coronavirus. And we’re not going to reference all these videos and websites because it’s just too time consuming and nobody else is going to read this stuff, it’s just for ourselves, mostly much.
Jacinta So in a vid about T-cell development (and they’re a product of the adaptive immune system) we hear that T-cells are produced in the red bone marrow. Why red?
Canto: Bone marrow comes in 2 types:
Red bone marrow contains blood stem cells that can become red blood cells, white blood cells, or platelets. Yellow bone marrow is made mostly of fat and contains stem cells that can become cartilage, fat, or bone cells.
Jacinta: So it’s not about red bones. So stem cells are like stems, green shoots that can develop into all sorts of different plants?
Canto: Yes and so you can imagine the potential, if we can induce them to specialise in ways that we want. Homo deus and all that. My brief research tells me that they’re found all around the body, not just the marrow. But it doesn’t tell me how they came into being. And there are apparently different types, as in ‘blood stem cells’. So these particular cells are pushed out into the world via sinusoidal capillaries…
Jacinta: Capillaries are the narrowest of blood vessels, I know that much…
Sinusoid capillaries allow for the exchange of large molecules, even cells. They’re able to do this because they have many larger gaps in their capillary wall, in addition to pores and small gaps. The surrounding basement membrane is also incomplete with openings in many places.
Canto: I must say that the number of high-quality, comprehensive videos on immunology, e.g. on YouTube, is such a boon. The comments say it all, ‘if only I had this info available when I was doing my PhD’ etc etc. So back to T cells. They move, I think as precursor T cells, to the thymus, via those capillaries. The thymus is a small gland near the top of the lungs (in the thoracic cavity) which is an essential component of the lymphatic system, itself a part of our general immune system.
Jacinta: It’s described as a primary lymphoid organ – at last I’m going to find out more about lymph! I hope. So the thymus is where T cells develop, and the red bone marrow, another primary lymphoid organ, is where B cells develop.
Canto: And B cells are a ‘type of white blood cell that makes infection-fighting proteins called antibodies’. Whereas T cells fight infections more directly as well as doing a lot of signalling…
Jacinta: Interesting thing about the thymus – it functions mostly through early childhood and adolescence, after which it atrophies, its tissues becoming fibrous and non-functional. So its role in T cell maturation occurs in our early years.
Canto: The thymus secretes different types of chemokines, or chemotactic agents (thymosin, thymotaxin, thymopoetin and thymic factors) which are somehow able to pull these undeveloped T cells in the right direction. This process is called chemotaxis.
Jacinta: A chemical taxi system, how cute. So we mentioned the two primary lymphoid organs, and there are secondary lymphoid organs – the lymph nodes (found in a number of bodily locations) and the spleen (on your left side, just around the bottom of your rib-cage). Just on chemokines – we’ve heard of cytokines, and the worrisome ‘cytokine storm’ that was oft-mentioned during the Covid period. Chemokines are a subset of these cytokines, which are –
‘an exceptionally large and diverse group of pro- or anti-inflammatory factors that are grouped into families based upon their structural homology or that of their receptors. Chemokines are a group of secreted proteins within the cytokine family whose generic function is to induce cell migration’.
Canto: So now we’re looking at these precursor T cells arriving at the thymus. So the thymus has a heap of thymic, epithelial cells which secrete the above-mentioned chemokines, which stimulate certain genes within the T cells to produce two enzymes (proteins), RAG1 and RAG2 (RAG stands for recombination activating gene – the genes encode the proteins). These are types of recombinase…
Jacinta: Think of genetic recombination, or mixing:
Recombinases are a family of enzymes having functional roles in homologous and site-specific recombination. It’s an event in organisms that involves DNA breakage, strand exchange between homologous segments, and ligation of DNA segments using DNA ligase.
Canto: So in this T cell context the gene ‘shuffling’, as it might be called, produces different protein types to deal with different antigen types. For example they produce T cell receptors (TCRs) designed to recognise and ‘receive’ differently-shaped antigens.
Jacinta: So getting back to those chemokines, they’re inducing other genetic activity to produce CD (cluster differentiation) proteins, of which there are various conformations, such as CD4 and CD8. These proteins form on the outside of the T cells, where they, hopefully, bind to MHC (major histocompatibility complex) proteins on the thymic cells. And of course there’s always more complexity – ‘a human typically expresses six different MHC class I molecules and eight different MHC class II molecules on his or her cells’. For now just think MHC-1 and MHC-2. Recognition of the appropriate MHC molecules by the CD4 and 8 proteins is called ‘positive selection’. If positive selection doesn’t happen the T cells will die (apoptosis).
Canto: The next step, assuming T cell survival, has to do with the previously-mentioned TCRs. The MHC molecules on the thymic cells carry a ‘self peptide’, and just to show how complex and relatively recent our immunological knowledge is, here’s a quote from a Pub-Med abstract from late 2001:
Twenty years ago, antigenic and self peptides presented by MHC molecules were absent from the immunological scene. While foreign peptides could be assayed by immune reactions, self peptides, as elusive and invisible as they were at the time, were bound to have an immunological role. How self peptides are selected and presented by MHC molecules, and how self MHC-peptide complexes are seen or not seen by T cells raised multiple questions particularly related to MHC restriction, alloreactivity, positive and negative selection, the nature of tumor antigens and tolerance.
So, if we could imagine ourselves as upper-class kids who entered university in the late 70s, (instead of working in factories or bludging off the dole as we were doing), none of this would’ve been known to anyone and we could’ve helped make the breakthrough…
Jacinta: Woulda-coulda-shoulda. Back again to those T cell receptors (TCRs), which apparently are not supposed to recognise or connect with the thymic cells’ self or antigenic peptides, as that would lead to auto-immune complications. So they’re ‘designed’ for that purpose, so that they don’t recognise those peptides, and don’t connect with them. This is called negative selection. If for some reason recognition does occur, apoptosis will result. That process occurs by the release of FAS (aka APO-1 or CD95 – don’t ask) from the thymic cell to a receptor in the T cell.
Canto: So, up to this point, if the T cell has come through alive, it’s TCR-positive, CD4 positive and CD8 positive. Its CD4 molecule may interact fortuitously with the thymic cell’s MHC2 (but the CD8 doesn’t interact with MHC1). In that case, there will be gene up-regulation of the cell’s CD4 molecules and down-regulation of CD8. That’s to say, CD4s will increase and CD8s will reduce, and it will present other TCRs. This turns it into a ‘T helper cell’. On the other hand, if the cell’s CD8s connect with the MHC1, there will be up-regulation of CD8, down-regulation of CD4, converting it into a cytotoxic T cell. Some of these helper and cytotoxic T cells can further develop into T regulatory cells, aka T suppressor cells, important for auto-immune disease suppression. This is promoted by molecules such as CD25 and interleukin 2.
Jacinta: Ok that’s enough head-spinning for one post, except perhaps just to say that interleukin 2 is ‘a protein that regulates the activities of white blood cells (leukocytes, often lymphocytes) that are responsible for immunity’. And we might find out more about what ‘cluster differentiation’ actually means….
Canto: So we haven’t focussed on bonobos for a while – I’d love to be able to answer the question, How did bonobos become female dominant?
Jacinta: Yes, were they always that way? That would mean, presumably, that they were female dominant at the time of their split from chimpanzees, somewhere between one and two million years ago (a rather vague time-frame, for me), which would then raise the question – how did chimps become male-dominant?
Canto: Haha, a question we don’t ask ourselves, we’re so used to being male-dominant. I seem to recall that one reason, or theory, is that bonobos have evolved in a region that’s densely vegetated, plenty of fruit and nuts, not so much hunting as gathering, which doesn’t require so much physical strength and aggression.
Jacinta: Which is interesting – we humans are evolving, at least in the WEIRD world into a post-industrial species, where manual labour is being replaced by mechanisation, robotics and such, requiring less of the physical strength of old-fashioned factory work. Australia, for example has become, internally, a service economy, exporting raw materials such as iron ore and coal, and importing finished products. There are few labour-intensive jobs these days, and testosterone levels are dropping, happily.
Canto: Yes, if we can take the long view – a very difficult thing for humans – we can see that only a couple of centuries ago women couldn’t get a decent education, couldn’t participate in government or be workplace bosses – though there were always the rare exceptions – but now the gates are opened and the trickle to the top is happening. In a thousand years or so – not so long in evolutionary time – we might have achieved a bonobo-style humanity.
Jacinta: Well on that sort of happy note, let’s see if research has told us anything about bonobo femdom. The quickest click-research brings up this, from the Max Planck Institute:
Some researchers suggest that bonobo female dominance is facilitated by females forming coalitions which suppress male aggression. Others think of an evolutionary scenario in which females prefer non-aggressive males which renders male aggressiveness to a non-adaptive trait.
That’s from ten years ago, and I doubt if we’ve gone much beyond those very reasonable speculations, with both of those developments, female coalitions and less aggressive males, creating a synergistic effect.
Canto: Well, looking more closely at that fairly short article, they suggest that female attractiveness – by which they don’t mean looking like Taylor Swift or FKA Twigs, but displaying sexual receptivity through behaviour or sexual swellings, seems to soften up the males somehow:
If females display sexually attractive attributes, including sexual swellings, they win conflicts with males more easily, with the males behaving in a less aggressive way.
Which is the opposite of male chimp behaviour, so why, and when, the difference?
Jacinta: Well, the article mentions two changes – subtle differences, no doubt, in female sexuality and in male mating strategies over a million or two years. And, okay, that doesn’t tell us anything much. As to when, obviously these are changes that developed gradually. Emory University, in Atlanta Georgia, which has done a whole-genome comparison of chimps and bonobos, makes a more specific claim for the divergence:
Chimpanzees and bonobos are sister species that diverged around 1.8 million years ago as the Congo River formed a geographic boundary and they evolved in separate environments.
Canto: But is it likely that genomic comparisons will tell us much about these subtle – or, ok, not so subtle, differences in behaviour? I mean, comparing the genes of Taliban Afghans and Aussie radical lesbians isn’t going to tell us much, is it? It seems to me to be largely a cultural shift.
Jacinta: Well, the Emory website, I must say, has the most interesting little article I’ve found for a while, and it relates to diet, which we’ve looked at before, and hormone production, which we haven’t, because it’s a bit sciencey for us dilettantes. Let me quote at length from the site, as I think this will provide us with a sense of direction for our own future research, if you can call it that:
The whole genome comparison showed selection in bonobos for genes related to the production of pancreatic amylase — an enzyme that breaks down starch. Previous research has shown that human populations that began consuming more grains with the rise of agriculture show an increase in copies of a closely related gene that codes for amylase.
“Our results add to the evidence that diet and the available resources had a definite impact on bonobo evolution,” Kovalaskas says. “We can see it in the genome.”
Compared to chimpanzees, bonobos also showed differences in genetic pathways well-known to be related to social behaviors of animals — as well as humans. Bonobos had strong selection for genes in the oxytocin receptor pathway, which plays a role in promoting social bonds; serotonin, involved in modulating aggression; and gonadotropin, known to affect sexual behavior.
“The strong female bonds among bonobos, in part, may be mediated by their same-sex sexual behaviors,” says co-author James Rilling, professor and chair of Emory’s Department of Anthropology. “Our data suggest that something interesting is going on in the bonobo pathways for oxytocin, serotonin and gonadotropin and that future research into the physiological mechanisms underlying behavioral differences between bonobos and chimpanzees may want to target those specific systems.”
Canto: Yes, that’s a most interesting finding, and one to follow up – pathways for serotonin, oxytocin and gonadotrophin, think SOG. And think not testosterone. And of course it’s not about opening up these pathways artificially, with, I don’t know, hormone supplements and such, but engaging in and encouraging behaviour that takes us along those pathways….
Jacinta: Haha I think oxytocin comes first, even if it wrecks the acronym. Looks like we need a crash course in endocrinology.
Canto: Or a crash course in how to raise our levels of, or expression of, those hormones? Over the next million years or so? With lots of orgasm-inducing touchy-feelies?
Jacinta: Well I can’t see that happening for as long as we have anti-sex religions dominating many nations. I seem to remember there were a few ‘free love’ cults back in the hippy days, but things have dulled down since then. You’d think there’d be a return, what with the mechanisation of labour, and the growth of the service economy. What better service can we offer our fellows than body rubs? Mind you, the Japanese seem to be leading the way there – a notably non-religious people. And yet, still far too patriarchal….
Canto: Interesting that Japanese teams have led the way in bonobo studies. Let’s hope they’re spreading the news among their countrywomen.
Jacinta: Well the sex video industry in Japan, and its sex industry generally, is enormous, though doubtless very exploitative. I presume it’s being driven by men rather than women – not exactly the bonobo way. A country that forces its few female politicians to wear high heels is far from being female-dominant. At least that was the case in 2019, when there was a backlash against this grotesque policy. I presume it has changed, but it isn’t clear.
Canto: Well, this has been interesting. We need to look more at endocrinology and happiness, or at least pleasure-inducing practices, in future… meanwhile, Vive les bonobos!
I’m still feeling anger, after all these years, at the free will proponents who, I feel, have benefitted from a cushy upbringing and have no idea what it’s like to have had nothing like the opportunities they’ve had. Of course, it’s always a worry that we can just attribute our relative failure to that lack of opportunity, but facts are facts, and it’s simply a fact that our macro world is determined.
And so to Steven Pinker, who, in his 2002 book The blank slate, ventured a few remarks on free will. I’ve written about Pinker before, and I consider it amusing to compare my life with his. We were both born in the mid 1950s’ – he’s a bit older – but that’s just about where the similarities come to an end (though I, too, have quite a big personal library – just saying). On the free will issue, I’d be inclined to make the small point, and I think Sapolsky makes it too, that successful career people would be more inclined to believe in free will than more or less abject failures – which of course isn’t saying anything about me.
Chapter 10 of The blank slate is titled ‘The fear of determinism’, and in it he starts looking at determinism from what I would call the wrong end – what he calls ‘molecules in motion’. My own thinking on this always starts from ‘thrown-ness into the world’, at an unchosen time and place, and as an unchosen living specimen. From there we get to our own parentage, our genes and our pre-natal and antenatal development, and their epigenetic effects.
Pinker also jumps quickly into the confusion I always find when I speak to people about this topic – that between determinism and predeterminism/fatalism:
‘All our brooding and agonising over the right thing to do is pointless, it would seem, because everything has already been preordained by the state of our brains’.
Pinker highlights the fear of determinism for a reason, claiming that ‘it is the existential fear of determinism that is the real waste of time’, though it seems to me that few people suffer such fear – and this appears to be borne out by experimental evidence. When we’re primed by tricky lab-coated types to reflect on ‘victims of circumstance’, there is an effect, but it appears to be minimal and short-term.
Of course, it isn’t the fear of determinism that concerns me, but the lack of acknowledgment of its factual basis. Pinker goes on a long and rather facile discourse about lawyers, medicos and neurologists seeking to get wrong-doers off the hook on the basis of defective genes and/or brain processes. Note that Sapolsky admits to having offered his services in this way, generally to no avail. I would note, just in passing, that the USA has the highest per capita incarceration rate in the WEIRD world, by a huge margin. It’s the land of free will after all. No excuses.
Some of Pinker’s ‘analyses’ here really miss the mark badly. For example, he references Dennett, who…
points out that the last thing we want in a soul is freedom to do anything it desires. If behaviour were chosen by an utterly free will, then we really couldn’t hold people responsible for their actions. That entity would not be deterred by the threat of punishment, or be ashamed by the prospect of opprobrium, or even feel the twinge of guilt that might inhibit a sinful temptation in the future, because it could always choose to defy those causes of behaviour….
And so on. But this is obvious bullshit – even if you fully believed in free will, the threat of imprisonment would be a massive deterrent, especially given the horrific private prisons of the US. And so would the opprobrium directed at you for your wrong-doing, given that we’re the most socially constructed mammalian species on the planet. Others’ opinions of us massively matter. Free will doesn’t preclude a sense of right and wrong. It should also be obvious that we are determined, by evolution, to survive and thrive as best we can – so in a world of severe punishments, such as exists in the USA, we’ll obviously be determined to avoid such punishments as best we can, even given a deprived background or a shrunken amygdala.
But where Pinker goes wrong in a way that is, to me, more offensive, is in his mockery of what he calls environmental determinism. It’s the typical upper middle class response, I must say:
The most risible pretexts for bad behaviour in recent decades have come not from biological determinism but from environmental determinism: the abuse excuse, the Twinkie defence, black rage, pornography poisoning, societal sickness, media violence, rock lyrics, and different cultural mores….
This little parade of glibness doesn’t, of course, begin to address any real issues. Firstly, there’s little real difference between biological and environmental determinism. Our biology evolves in adaptation to changing environments, as every evolutionary biologist knows, and, to be fair to Pinker, there has been a revolution in our understanding of environmentally-induced gene expression (epigenetics) in the two decades since The blank slate was published. Even so, my experience of growing up in a profoundly working-class environment, in which classroom illiteracy was commonplace, as well as vandalism, neglect and police harassment, makes me flare up when I hear the life-shattering experiences of kids in the street where I lived being dismissed in terms of ‘the abuse excuse’. I also note that in mocking these ‘excuses’ his target is invariably the lawyers (his own class) that bring these claims, rather than the accused themselves, about who’s background he appears to be indifferent. It’s the same clubbish elitism that I found in the dated Berofsky collection I re-read recently, but more focussed on law than philosophy.
Another of the irritations I found in revisiting Pinker’s determinism-free will piece, is that he focusses almost exclusively on crime, ignoring the much larger issues of lives lived in struggle because of determining forces beyond their control – a Palestinian in modern Israel, a woman in Afghanistan, a Dalit in India, an Australian Aboriginal at the time of the British colonisation of that island, a Jew growing up in Germany in the 1930s, the Tainos visited by the Spanish horror in the late 15th and 16th centuries, the Scots massacred in the reign of Edward I, the East Timorese massacred by Indonesian forces, the isolated old women burned as witches… millions of people who found themselves members of the wrong gender or ethnicity at the wrong time – murdered, raped, enslaved, or simply deprived of the means to live a life in which there’s some hope of an upward trajectory. None of us got to choose our ethnicity, our class (yes it does exist), our early upbringing, our parentage, even our level of intelligence, and this is so obvious, and so overwhelming a fact, that it seems to me almost embarrassing to have to point it out. And all of this is profoundly determining. That’s why reading history, as I often do, can be such an affecting experience. It is so full of innocent victims. And of course it continues….
So, finally, it isn’t the fear of determinism that should concern us – it’s the very fact of determinism.
I’ve been lucky, on balance. I was brought, as a five-year-old, to live in one of the richest and most peaceful nations in the world. I can’t praise or blame myself for this. Certain aspects of my treatment both at home and at school resulted in, for me, a fairly extreme anti-authoritarianism, and something of an over-self-reliance, which has its positives and negatives. But I benefitted from a world-full of books in our house, which took me to places of wonder outside myself. And I’ve benefitted from a nation with a strong social safety net, a minimum wage which is the highest of any nation outside of Luxembourg, a justice system that eliminated the death penalty nationwide almost 60 years ago, and a political system that was the first in the world to grant votes, and the right to stand for parliament, to women. It also rates as one of the least religious nations on earth – which for me is a godsend.
More on determinism from me, no doubt, as I plough into the second half of Sapolsky’s Determined.
John Hospers (1918 -2011), US philosopher and first presidential candidate of the Libertarian Party
The philosopher John Hospers lived to the ripe old age of 93 and died in 2011. His essay “What means this freedom?” was published in a 1961 philosophical compendium, Determinism and freedom in the age of modern science, edited by Sidney Hook, and reprinted in Free will and determinism, edited by Berofsky. I haven’t been able to ascertain exactly when the essay was written. The internet tells me Hospers was strongly associated with libertarianism, and was once a good friend of Ayn Rand, which strikes me as bizarre considering that the above-mentioned essay presents an argument against free will. Perhaps a closer study of the essay will clarify the apparent contradiction.
Hospers brings up the concept of unconscious motivation in his first paragraph. He reflects on a ‘criminal act’:
The deed may be planned, it may be carried out in cold calculation, it may spring from the agent’s character and be continuous with the rest of his behaviour, and it may be perfectly true that he could have done differently if he had wanted to; nonetheless his behaviour was brought about by unconscious conflicts developed in infancy, over which he had no control and of which (without training in psychiatry) he does not even have knowledge. He may even think he knows why he acted as he did, he may think he has conscious control over his actions, he may even think he is fully responsible for them; but he is not. Psychiatric casebooks provide hundreds of examples. The law and common sense, though puzzled sometimes by such cases, are gradually becoming aware that they exist; but at this early stage countless blunders still occur because neither the law nor the public in general is aware of the genesis of criminal actions.
The conscious/unconscious division, born of psychoanalysis, seems dated now, but there’s plenty of evidence of retarded neural development in childhood, and of the epigenetic effects of early developmental experiences, both pre- and post-natal. It’s also worth noting that Hospers here confines himself to ‘criminal actions’, without seeming to recognise the much wider implications of the determinist world we live in. Our deterministic world is massively more encompassing, something that perhaps remains hidden to many of us because of the more or less infinite variety of human individuals the chains of cause and effect produce. And, of course, because of the modern WEIRD emphasis on human freedom.
A problem with Hospers’ argument is that, as he claims above, it supposedly relies on ‘training in psychiatry’. In a marginal note to Hospers’ analysis of Hamlet’s inability to act, due to an unconscious ‘Oedipal conflict’, I wrote this, more than 40 years ago:
I can’t accept this – it suggests that someone else knows my motives better than I do. This is the insidious power structure on which psychoanalysis is built.
Of course it’s true that if you want an accurate description of a person’s character, you ask those who know her well rather than the person herself, because for sound evolutionary reasons, we emphasise our ‘best’ qualities and minimise our worst. However the psychiatric view misses a great many other factors in determining character – genetic, epigenetic, cultural, hormonal, traumatic, dietary, and probably countless others still insufficiently researched. All of these factors create a self, which, according to many ‘compatibilists’, including Sidney Hook in Berofsky’s collection, is the agent which ‘freely’ acts. What means this freedom, indeed!
It’s hardly Hospers’ fault that he didn’t widen the determining factors I’ve just mentioned, as so little was known about them, mid-twentieth century. And yet, much further along in his essay, he makes this extraordinary claim:
I want to make it clear that I have not been arguing for determinism.
And much of what follows makes little sense to me. The philosophical language, it seems to me, gets in the way of basic reasoning (not only here but in most of the essays in the Berofsky volume). For example, much is made of the question ‘Are our powers innate or acquired?’ This is a non-issue. We acquire certain ‘powers’ or skills or world-views or whatever because of the family we’re born into, the zeitgeist that surrounds that family, and particular mentors or events that have influenced us, particularly at an early age. We have no control over our early brain development, over whether we’re attractive or ugly by our community’s standards, whether we’re short or tall, ‘black’ or ‘white’ skinned, or introduced as babies into the English or Tagalog language. And these factors and a thousand others heavily influence what we will become. To sort them into innate or acquired characteristics is largely a mug’s game.
Essentially the reason Hospers and others are fearful of the determinist label is the idea that all is ‘fixed’, that nothing could have been otherwise, or can be otherwise in the future. So what’s the use of trying? What I do tomorrow is already set. No need to think about it, to worry about what to wear to work, what to prepare for tomorrow’s lesson – it’s already taken care of. But that’s not how things work. What’s missing is the complexity of interacting determining factors that make us, the most hyper-social mammalian species on the planet, want to survive and thrive within the social web that has created us. Some of us, largely due to the luck of our early years and environment, are very good at doing this, sometimes to the detriment of others, sometimes not. Others are overwhelmed and seek to withdraw into a more ‘safe’ and static environment. In any case, things are not fixed, due to the dynamic, albeit determined, world that we have to negotiate constantly throughout our lives. A determined world is far from being predictable, because we’re constantly encountering unexpected events, conversations, challenges, requests, crises, accidents, insights, and so on. They often come at us thick and fast, and we must deal with them, determined though they be. And our own dealing with them has always been determined, because we dealt with them in this way and not that. How we deal with a situation in the future isn’t yet determined – nor is it entirely predictable, because the elements of that future situation are always unique, and complex.
To return to Hospers, let me analyse some remarks towards the end of his essay:
What of the charge that we could never have acted otherwise than we did? This, I submit, is not true. Here the proponents of … ‘soft determinism’ are quite right. I could have gone to the opera today instead of coming here; that is, if certain conditions had been different, I should have gone. I could have done many other things instead of what I did, if some condition or other had been different, specifically if my desire had been different.
Hospers goes on to examine ‘could’ as a ‘power word’, but in my view that is beside the point. The point, as Sabine Hossenfelder bluntly states in her video on free will, is that, given all the things you could have done in response to situation x (which are virtually infinite), you did y. And this decision was the result of all the impinging circumstances of the moment together with the character you have become due to a virtually infinite combination of historical events, neural connections, hormonal flows, genetic inheritances and so forth. Hospers mentions desire, as if this is something we have control over. I can attest that, when young, I became pathetically sick with desire for certain young women while unmoved by others who seemed equally attractive by general standards. I felt like the plaything of strong emotions which I wasn’t sure whether to feel proud of or ashamed of. I’ve also felt extremely violent emotions towards people who mistreated me, in my view, such as an old headmaster, but also toward long-dead dictators and war-mongers I’ve read about. None of these feelings are under my control. Nor is it really under my control that I haven’t acted on my violent or libidinous passions. My desire not to go to gaol or make a fool of myself, which are pretty commonplace desires, shared by the vast majority of people, have kept me well out of the spotlight. That desire is, of course, the result of experiences that have befallen me, and shaped me. Not of my own free will – whatever that means.
References
Free will and determinism, ed Bernard Berofsky, 1966
I was going to entitle this post ‘How did bonobos become female dominant?’, but that assumes that they weren’t always so. To assume makes an ass out of u and me, and I don’t care about u, but I have my pride. And speaking of pride, lions live in those groups (of up to forty, but usually much smaller) and malely dominate, even though the women bring home most of the bacon, chevaline (well, zebra), venison, rattus and the occasional long pork, if they’re lucky.
The point is, we wouldn’t consider this a product of leonine (okay, lion) culture. It’s just what lions – male and female – are genetically programmed to do, just as marmosets, magpies (Australian) and macaroni penguins are programmed to be monogamous (more or less). But considering that separating genetic and cultural evolution in humans is a tricky business, the same would surely go for our closest living relatives. We’re generally convinced that the male dominance in most human history is cultural. I’ve often read the claim that the transition to an agricultural lifestyle in many parts of the world from about 11,000 years ago resulted in a more patriarchal society, with the concept of property, including women, becoming essential to power and dominance. This seems plausible enough, though I would assume that the first claims to property relied primarily on brute strength. Male muscularity is different from that of females, and, more importantly, they’re not hampered by pregnancies and child-rearing. And whereas hunter-gatherers (and it now seems the distinction between these lifestyles is by no means cut and dried) tend to migrate along with food resources, some concept of land ownership, based on kinship over time, clearly developed with an agricultural lifestyle. Again, such a fixed lifestyle would have essentially created the notion of ‘domesticity’, which became associated with the female world. And it seems also have encouraged a degree of polygyny as a sign of male social status. And as we left all this behind, in the WEIRD world so fulsomely described in Joseph Henrich’s book, we’re starting to leave patriarchy behind, though way too slowly for my liking.
So, let’s get back to bonobos. I was struck by an observation I read a while ago in some otherwise forgotten piece on bonobos. Female bonobos are smaller than male bonobos to much the same degree as in chimps and humans, but slightlyless so. Considering that the split between bonobos and chimps occurred only between one and two million years ago (and I’d love that margin of error to be narrowed somehow), any reduction in this sexual dimorphism seems significant – and surely genetic. But then genes are modified by environment, and by the behaviour that environment encourages or necessitates. Here’s what I found on a Q&A forum called Worldbuilding:
Bonobos have less dimorphism because they all feed close together and females can almost always protect each other. Male A tries to monopolize female A and gets driven off by female B, C, and D.
Hmmm. There’s something in this, but not quite enough. Why wouldn’t the males bond together to monopolise a particular female? In non-euphemistic human terms this is called pack rape, and it does seem to be confined to humans, though coercive sex, on an individual level, is quite common in other species, and for obvious anatomical reasons it’s always the male who coerces.
This leads to the reasonable conclusion, it seems to me, that for females to have control in the sexual arena – at least in the mammalian world – requires co-operation. And that requires bonding, arguably over and above the bonding associated with ‘girl power’ in WEIRD humans. So here’s how the Max Planck Society explains it:
To clarify why same-sex sexual behavior is so important specifically for female bonobos, we collected behavioral and hormonal data for over a year from all adult members of a habituated bonobo community at the long-term LuiKotale field site in the Democratic Republic of Congo. In addition to our focus on sexual interactions, we identified preferred partners for other social activities such as giving support in conflicts. We also collected urine to measure the hormone oxytocin, which is released in the body in other species after friendly social interactions, including sex, and helps to promote cooperation.
We found that in competitive situations, females preferred to have sex with other females rather than with males. After sex, females often remained closer to each other than did mixed sex pairs, and females had measurable increases in urinary oxytocin following sex with females, but not following sex with males. Among same-sex and opposite-sex pairs, individuals who had more sex also supported each other more often in conflicts, but the majority of these coalitions were formed among females. “It may be that a greater motivation for cooperation among females, mediated physiologically by oxytocin, is the key to understanding how females attain high dominance ranks in bonobo society,” explained co-lead author Martin Surbeck, a researcher at the Max Planck Institute for Evolutionary Anthropology and Harvard University.
Now, I know I’ve written about the peptide hormone oxytocin before, somewhere, and suffice to say its role in behaviour and its relation to the general endocrine and neurotransmission systems are extremely complex. Having said that, there will doubtless be strong similarities for its role in humans and in bonobos. And, reflecting on the above quote, what came first, the oxytocin release, or the bonding? Should we encourage more oxytocin doses, or more female-female sex? Doing both sounds like a fine idea.
To tell the truth, I find the willingness to see bonobos as any kind of female model somewhat lacking. They’re ‘jokingly’ referred to as the scandalous primate, and their revolutionary nature is underplayed. Yet their relatively comfortable, largely frugivorous lifestyle in the southern Congo region, where their only real threat is humanity, reflects in miniature the comforts of the WEIRD world, with its hazards of overspending at the supermarket, lazing too long at the beach, or pokies, cocktail bars and ‘Lust-Skin Lounges’ for the true thrill-seekers.
Of course, we got to our ascendant position today through the explorations, calculations and inventions produced by our brains, and the super-brains of our cities, corporations and universities. What can we learn from a bunch of gangly, hairy mutual masturbators dangling about in the Congolese rainforest? Well, we brains and super-brains can still learn a bit more about sharing and caring – as any study of our own history can tell us – and we can certainly learn to stop being so dumb and fucked-up about sexuality, gender and power. Learning lessons from bonobos doesn’t mean getting hairier and improving our brachiation skills, but, well, eating less meat would be a start, given what we know about the environmental damage our current diet is causing. And that’s just one of many lessons we can learn. For me, of course, the most important lesson is the role played by females. How ridiculously long did it take for us – I mean we male humans who have been in control of almost all human societies since those societies came into being – to recognise and admit that females are our equal in every intellectual sphere? This is still unacknowledged in some parts. And although we call this the WEIRD world, the Industrial part of that acronym has lost its machismo essence, a loss Susan Faludi has sensitively analysed in her book Stiffed: the betrayal of the modern man – though I think ‘betrayal’ is the wrong word. After all, men were never promised or guaranteed to be breadwinners and heads of households, they took or were given the role through social evolution, and it’s being taken from them, gradually, through the same process.
Finally, getting back to the question in the title, the answer, for Pan paniscus as surely as for Homo sapiens, is culture, which can affect gene expression (epigenetics), which can ultimately affect genetics. I suspect that the slight diminution in the sexual dimorphism between male and female bonobos, over a relatively short period of time, evolutionarily speaking, might, if they’re left to their own devices (which is unlikely, frankly), lead to a size reversal and a world of male sexual servitude. Vive les bonobos, I’d like to be one, for the next few million years!
Canto: So SNPs are pretty essential to modern genomics I believe, so why, and what are they? I know that they’re ‘single nucleotide polymorphisms’ and that nucleotides are A, C, G, T and U, each of which have a slightly different structure. They’re all based on sugar structures – ribose in the case of RNA and deoxyribose in the case of DNA – attached to a phosphate group and a nitrogenous base. Here’s a diagram of thymine (T) filched from the USA’s National Human Genome Research Institute:
So that’s a nucleotide, one of the building blocks of DNA and RNA, but the real problem, for me anyway, is the connection between single and polymorphic, if there is one. I know that poly means many and that morphology is about shape and size and such….
Jacinta: You can only get so far with interrogating the words themselves. An SNP is a genetic variation in a single nucleotide between one person’s genome and another (I think). But there are many of these variations, which is where the ‘poly’ comes in. I’ll quote this from a NIH website, and then try to make sense of it:
SNPs occur normally throughout a person’s DNA. They occur almost once in every 1,000 nucleotides on average, which means there are roughly 4 to 5 million SNPs in a person’s genome. These variations occur in many individuals; to be classified as a SNP, a variant is found in at least 1 percent of the population. Scientists have found more than 600 million SNPs in populations around the world.
Canto: So they’re called ‘variants’ because they vary from the ‘normal’ pattern in 1% or more of those whose genomes are mapped? So there’s such a thing as a ‘normal’ human genome, but perhaps everyone differs from that normal pattern due to different SNPs? And why is 1% the cut-off? Isn’t that a bit arbitrary? Also, it says that these variations occur in many individuals, which sounds a bit vague. Does this mean that there are many individuals where they don’t occur at all? I mean, what is a normal human genome, if there are so many variants? Is it just some kind of aggregated value?
Jacinta: Uhh, maybe. And note – but I’m not sure if this is relevant to your question – that these SNPs mostly occur in non-coding DNA, where they won’t be affecting the phenotype and its general functioning, though it seems to depend on how close they are to coding regions. Anyway, we’re just scratching the surface here. Look at this diagram, from Wikipedia.
As you can see, there are synonymous and non-synonymous SNPs. Synonymous with what, you might ask?
Canto: As a language teacher I know what a synonym is, obviously. My guess is that a synonymous SNP is associated with, ‘synonymous’ with, some kind of malfunction or defect, or maybe different function or effect. A ‘missence’, as the diagram suggests.
Jacinta: No, it’s the non-synonymous SNPs that cause the problems, because coding DNA generally leads to effective function, that’s what it’s all about. If the SNP is synonymous then it works toward proper functioning, perhaps by a different pathway, or it just doesn’t affect the pathway.
Canto: What I’m learning about genetics/genomics is that the more I delve into the subject, the more there is to learn, and yet I don’t really want to specialise, I want to know a bit of everything. I’ve just learned, for example, that it’s not just a divide between coding and non-coding DNA, because a mutation near a coding region can have effects, deleterious or otherwise, I think.
Jacinta: I don’t know about that, but I’m learning some interesting random facts, for example that there appears to be more C-G base pairings in coding DNA than T-A. Just to get it in our heads, cytosine (a pyrimidine) always pairs with guanine (a purine), and the other pyrimidine, thymine, always pairs with adenine. Always purines with pyrimidines, and purines are the larger molecules, with a two-ring structure, rather than one for pyrimidines. Note the structure of thymine, above. Anyway, back to SNPs, which we’re interested in mainly for what they might tell us about earlier populations. I’ve just glanced through a 2020 research article – generally way to technical for lay persons or dilettantes like us, titled ‘Genome-wide SNP typing of ancient DNA: Determination of hair and eye color of Bronze Age humans from their skeletal remains’. I did get some useful info from it though. The researchers compared the SNP method with ‘single base extension (SBE) typing’, and what they found was interesting enough:
The DNA samples were extracted from the skeletal remains of 59 human individuals dating back to the Late Bronze Age. The 3,000 years old bones had been discovered in the Lichtenstein Cave in Lower Saxony, Germany.
It seems that this was a kind of proof-of-concept piece of research, and they were able to obtain good to excellent results from two thirds of the skeletal samples:
With the applied technique, it was for the first time possible to get information about major phenotypic traits—eye and hair color—of an entire prehistoric population. The range of traits, varying from blonde to brown hair and blue to green-hazel eye colors for the majority of individuals is a plausible result for a Central European population.
Canto: Yes, that’s the exciting stuff – true it’s only going back 3000 years, and you could say that there were no surprises in the findings – but it brings the past back to life in such a vivid way… what can I say?
Jacinta: So you don’t want to know about haplotypes, and homozygous and heterozygous alleles? What’s wrong with you?
Canto: Okay, a haplotype – haven’t we gone through this? – a haplotype is a set of variants, or polymorphisms, along a single chromosome, involving one or more genes, that tend to stick together, inheritance-wise. We know that homozygous inheritance means inheritance from both parents whereas heterozygous means that you have a different genetic marker from each parent. A genetic marker is any ‘DNA sequence with a known location on a chromosome’. They may offer clues to inherited traits, such as diseases. All of this comes from the USA’s National Human Genome Research Institute, and I think I mostly understand it.
Jacinta: So SNPs can have all sorts of uses, regarding the present and the past, and tracing the present into the past, as with disease gene mapping. Their abundance within the genome has made them the go-to marker in bioinformatics. My guess, though, is we’ll never get to fully understand them without actually working with them. I mean, we can go through ScienceDirect, and jump from underlined term to underlined term (e.g. linkage disequilibrium, QTL mapping, PCR assays, point mutations and the like), but we’ll start to forget it all from the moment we have aha moments, because for us dilettantes, locked out of labs due to dumbness, shyness, laziness, poverty-ness etc, it’s all just book-larnin, sans even books. I suppose we just have to be grateful that we’ve, or they’ve, developed the technology to collect and analyse SNPs, to create libraries of them…
Canto: It seems like, as with so many fields, we’re at what Deutsch called ‘the beginning of infinity’ – but then didn’t they think that at the advent of string theory?
Jacinta: But we know this isn’t theory, this is about results. Tools producing results. Tools within the body, or rather natural phenomena made into tools by human ingenuity, like circles made into wheels, cubes into containers, triangles into struts. And we’re likely to get more and more out of DNA in the future. I recently learned about the petrous bone, though of course researchers have known about it for some years – it’s about the hardest part of the skull, down somewhere near the foramen magnum I think, and its density has, it seems, been a preservative for DNA – generally better than teeth. So that means more analysis of fossil collections. As David Reich puts it, technologies for analysing ancient DNA have created an explosion of information to rival the invention of the microscope/telescope a few hundred years ago.
Canto: Yes, some of the developments he mentions are next-generation sequencing (which has vastly reduced sequencing costs), more efficient DNA extraction methods, improvements in separating human from microbial DNA, and again the use of the petrous bone for extraction – a bone which tends to remain intact longer than others.
Jacinta: Okay, so we might continue to blunder on in trying to make sense of this genomics stuff, or maybe not. Enough for now.
1 in 200 Men are Direct Descendants of Genghis Khan – Answers in Genomics!
Jacinta: So this blog piece is a bit of a change of pace from the science we’re obviously having trouble with – and I should mention that we’ve started watching the 11-part ‘Introduction to genomics’ videos online to help us with the basics – but what we’ve read in Who weare and how we got here and other texts is providing further evidence of a violent past that reflects an ancestry more associated with chimp-like behaviour, much exacerbated by the deadly weapons we developed along the way, than the bonobo togetherness that my endless optimism sees signs of in that part of the world that is increasingly empowering the female sex.
Canto: Yes, that in itself is a long story of gradual release from the masculinist Catholic hegemony of the medieval world, with its witch-hunts and its general suppression of female power and influence…
Jacinta: Going much further back in fact to the ancient Greeks and, for example, Homer’s Odyssey, and the treatment of women therein, as explored on this site years ago (referenced below).
Canto: Yes, this general improvement in the treatment of women, and of each other – the end of witch-hunts (I mean real ones) and public executions and torturings and so on – at least in English-speaking and Western European nations, has been highlighted in Pinker’s The better angels of our nature and other analyses. But we still have the Chinese Testosterone Party, the masculinist horrors of Iran and Afghanistan, and the macho thuggery of little Mr Pudding and his acolytes, to name but a few. The humano-bonobo world is still a long way off.
Jacinta: Yes the Ukrainian horror, getting all the airplay here that Mr Putin’s incursions in Chechnya, Syria and Georgia didn’t, reminds us that the horrors of two major European wars and Japan’s macho offensives in the first half of the 20th century haven’t been enough to reform our world – from a human one to a humano-bonobo one. But I doubt that genetic tinkering would do the trick.
Canto: Vegetarianism perhaps? But then, Hitler…
Jacinta: No easy solutions I’m afraid. But there are some who are interested in using genomics to highlight just how un-bonobo-like our past has been. Or rather, it’s not so much an interest, it’s more like telling the gruesome story that genomic data is revealing to them. In Neil Oliver’s History of Scotland, for example, he recounts how genomic data reveals that the Pictish men of the Orkneys and the northern tip of Scotland were almost completely replaced by men from Northern Europe, the Vikings, in the eighth and ninth centuries CE, while the female line remained largely Pictish. Slaughter, combined with probable rape, being the best explanation. Reading this reminded me of the chimpanzee war of the seventies in Tanzania, which admittedly was more of a civil war, and apparently less one-sided than the Viking invasion of the Orkneys, or the European invasion of the Americas, or the British invasion of Australia, but in some ways it was similar – an attempt, if not entirely conscious, to replace one population with another, and to the victor, the spoils.
Canto: Well, Reich is fairly circumspect in his book, but he does have a small section towards the end, ‘The genomics of inequality’, from which we may draw pretty clear inferences:
Any attempt to paint a vivid picture of what a human culture was like before the period of written texts needs to be viewed with caution. Nevertheless, ancient DNA have provided evidence that the Yamnaya [a relatively advanced steppe culture that emerged about 5000 years ago] were indeed a society in which power was concentrated among a small number of elite males. The Y chromosomes that the Yamnaya carried were nearly all of a few types, which shows that a limited number of males must have been extraordinarily successful in spreading their genes. In contrast, in their mitochondrial DNA, the Yamnaya had more diverse sequences.
and
This Yamnaya expansion also cannot have been entirely friendly, as is clear from the fact that the proportion of Y chromosomes of steppe origin in both western Europe and in India today is much larger than the proportion of steppe ancestry in the rest of the genome.
This is a roundabout or academic way of saying, or ‘suggesting’ (oh dear, I’m becoming an academic) that the Yamnaya forcibly replaced many of the males of earlier populations in those regions and interbred, in one way or another, with the females.
Jacinta: Yes, again very chimp-like, mutatis mutandis. The good thing is that we’re more and more coming to terms with our violent past – and I would love to be able to trace it further back, beyond Homo sapiens, or at least to the earliest H sapiens 100,000 years ago or so.
Canto: Well, I’m thinking that the CHLCA (chimp human last common ancestor) would be a good place to start, but we’ll probably never know what that population was like – was it more chimp-like or bonobo-like in its social (and sexual) behaviour? But there’s a huge difference between that CHLCA and us – just consider brain size.
Jacinta: But that’s a tricky measure – look at H naledi and H floresiensis. Chimps average around 400cc, gorillas 500cc, H naledi has been estimated at anything from 450 to 600cc, and H floresiensis, from the only extant skull, came in at 426cc. And those two hominins are considered relatively modern. Our brain size is about 1300cc. It’s over the place. But forget all these caveats for a moment, I’ve heard that we got our bigger brains courtesy of hunting big game and cooking meat – and the hunting at least strikes me as a macho activity, leading to a hierarchy of the big and strong, and so, alpha males and all the shite that follows…
Canto: Yes, and bonobos have evolved in a more physically restricted but resource-rich environment, and have somehow become less hierarchy-obsessed, though still hierarchical – the sons of the most powerful females apparently have a higher status in the male hierarchy.
Jacinta: Yes all this is important as we strive to establish a humano-bonobo world. In our incredibly diverse human world we have people dying of over-eating in some parts, and of starvation and malnutrition in others. But in the world of relative abundance that you and I live in, mechanisation and other technologies have reduced the need for physical strength, and testosterone levels in males have dropped rapidly in just the last few decades. We’re eating meat more than ever, but in our cities, nobody can hear the victims’ screams. And we don’t have to do the hunting and killing ourselves, so if we want to toughen up we have to do it via gymnasiums and sports, which are no longer gender-exclusive.
Canto: All this has little to do with genomics, but it seems to me that the macho-chimp orientation of early humans since the CHLCA has much to do with increased proliferation, diversity and inter-group competition for resources, especially over the last 20,000 years, or less. The domestication of horses and the invention of the wheel, and sophisticated sea-going vessels would have helped. Different groups advanced at different rates, with some developing better weapons – for hunting and then for warfare, and naturally they hankered for more territory to expand into, to ‘lord over’. Those more advanced groups became more hierarchical, and gaining more territory and ‘winning’ over more people became an end in itself – think of early versions of Genghis Khan and little Mr Pudding.
Jacinta: That’s why, like the female bonobos who gang up on uppity males before they can do too much damage, we need to stick it the Mr Puddings of the world – hit em hard, before they know what hit em.
Canto: So maybe if we got humans to mate with bonobos we’d get a more promising hybrid offspring?
Jacinta: Haha well it’s not that simple, and I don’t mean just physiologically…
Canto: Okay those species wouldn’t be much attracted to each other – though I’ve heard that New Zealanders are very much attracted to sheep, but that just might be fantasy. But seriously, if two species – like bonobos and chimps, can interbreed, why can’t bonobos and humans? And they’d don’t have to canoodle, you can do it like in vitro fertilisation, right?
Jacinto: Well, bonobos and chimps are much more closely related to each other than they are to humans. And if you think bonobo-human hybridisation will somehow create a female-dominant libertarian society, well – it surely ain’t that simple. What we see in bonobo society is a kind of social evolution, not merely a matter of genetics. But having said that, I’m certainly into exploring genetics and genomics more than I’ve done so far.
Canto: Yes, I’ve been trying to educate myself on alleles, haplotypes, autosomal and mitochondrial DNA, homozygotism and heterozygotism (if there are such words), single nucleotide polymorphisms and…. I’m confused.
Jacinta: Well, let’s see if we can make more sense of the science, starting with, or continuing with Whoweare and how we got here, which is mostly about ancient DNA but also tells us much about the past by looking at genetic variation within modern populations. Let me quote at length from Reich’s book, a passage about mitochondrial DNA – the DNA in our mitochondria which is somehow passed down only along female lines. I’ve no idea how that happens, but…
The first startling application of genetics to the study of the past involved mitochondrial DNA. This is a tiny proportion of the genome – only approximately 1/200,000th of it – which is passed down from mother to daughter to granddaughter. In 1987, Allan Wilson and his colleagues sequenced a few hundred letters of mitochondrial DNA from diverse people around the world. By comparing the mutations that were different among these sequences, he and his colleagues were able to construct a family tree of maternal relationships. What they found is that the deepest branch of the tree – the branch that left the main trunk earliest – is found today only in people of sub-Saharan African ancestry, suggesting that the ancestors of modern humans lived in Africa. In contrast, all non-Africans today descend from a later branch of the tree.
Canto: Yes, I can well understand the implications of that analysis, but it skates fairly lightly over the science, understandably for a book aimed at the general public. To be clear, they looked at the same stretches of mitochondrial DNA in diverse people, comparing differences – mutations – among them. And in some there were many mutations, suggesting time differences, due to that molecular clock thing. And I suppose those that differed most – from who? – had sub-Saharan ancestry.
Jacinta: Dating back about 160,000 years, according to best current estimates.
Canto: The science still eludes me. First, how does mitochondrial DNA pass only through the female line? We all have mitochondria, after all.
Jacinta: Okay, I’ve suddenly made made myself an expert. It all has to do with the sperm and the egg. One’s much bigger than the other, as you know, because the egg carries nutrients, including mitochondria, the only organelle in your cytoplasm that has its own DNA. Your own little spermatozoa are basically just packages of nuclear DNA, with a tail. Our mitochondrial DNA appears to have evolved separately from our nuclear DNA because mitochondria, or their ancestors, had a separate existence before being engulfed by the ancestors of our somatic or eukaryotic cells, in a theory that’s generally accepted if difficult to prove. It’s called the endosymbiosis theory.
Canto: So mitochondria probably had a separate, prokaryotic existence?
Jacinta: Most likely, which could take us to the development, the ‘leap’ if you like, of prokaryotic life into the eukaryotic, but we won’t go there. Interestingly, they’ve found that some species have mitochondrion-related organelles with no genome, and our own and other mammalian mitochondria are full of proteins – some 1500 different types – that are coded for by nuclear rather than mitochondrial DNA. Our mitochondrial DNA only codes for 13 different types of protein. It may be that there’s an evolutionary process going on that’s transferring all of our mitochondrial DNA to the nucleus, or there might be an evolutionary reason for why we’re retaining a tiny proportion of coding DNA in the mitochondria.
Canto: So – we’ve explained why mitochondrial DNA follows the female line, next I’d like to know how we trace it back 160,000 years, and can place the soi-disant mitochondrial Eve in sub-Saharan Africa.
Jacinta: Well the term’s a bit Judeo-Christian (there’s also a Y-chromosomal Adam), but she’s the matrilineal most recent common ancestor (mt-MRCA, and ‘Adam’ is designated Y-MRCA).
Canto: But both of these characters had parents and grandparents – who would be somehow just as common in their ancestry but less recent? I want to know more.
Jacinta: To quote Wikipedia…
… she is defined as the most recent woman from whom all living humans descend in an unbroken line purely through their mothers and through the mothers of those mothers, back until all lines converge on one woman.
… but I’m not sure if I understand that convergence. It clearly doesn’t refer to the first female H sapiens, it refers to cell lines, haplogroups and convergence in Africa. One of the cell lines used to pinpoint this convergence was HeLa, the very first and most commonly used cell line for a multiplicity of purposes…
Canto: That’s the Henrietta Lacks cell line! We read The Immortal Life of Henrietta Lacks! What a story!
Jacinta: Indeed. She would be proud, if she only knew… So, after obtaining data from HeLa and another cell line, that of an !Kung woman from Southern Africa, as well as from 145 women from a variety of populations:
The published conclusion was that all current human mtDNA originated from a single population from Africa, at the time dated to between 140,000 and 200,000 years ago.
Canto: So mt-MRCA is really a single population rather than a single person?
Jacinta: Yeah, maybe sorta, but don’t quote me. The Wikipedia article on this gives the impression that it’s been sheeted home to a single person, but it’s vague on the details. Given the way creationists leap on these things, I wish it was made more clear. Anyway the original analysis from the 1980s seems to be still robust as to the time-frame. The key is to work out when all female lineages converge, given varied mutation rates. So, I’m going to quote at length from the Wikipedia article on mt-MRCA, and try to translate it into Jacinta-speak.
Branches are identified by one or more unique markers which give a mitochondrial “DNA signature” or “haplotype” (e.g. the CRS [Cambridge Reference Sequence] is a haplotype). Each marker is a DNA base-pair that has resulted from an SNP [single nucleotide polymorphism] mutation. Scientists sort mitochondrial DNA results into more or less related groups, with more or less recent common ancestors. This leads to the construction of a DNA family tree where the branches are in biological terms clades, and the common ancestors such as Mitochondrial Eve sit at branching points in this tree. Major branches are said to define a haplogroup (e.g. CRS belongs to haplogroup H), and large branches containing several haplogroups are called “macro-haplogroups”.
So let’s explain some terms. A genetic marker is simply a DNA sequence with a known location on a chromosome. A haplotype or haploid genotype is, as the haploid term suggests, inherited from one rather than both parents – in this case a set of alleles inherited together. SNPs or ‘snips’ are differences of a single nucleotide – e.g the exchange of a cytosine (C) with a thymine (T). As to the rest of the above paragraph, I’m not so sure. As to haplogroups, another lengthy quote makes it fairly clear:
A haplogroup is…. a group of similar haplotypes that share a common ancestor with a single-nucleotide polymorphism mutation.More specifically, a haplogroup is a combination of alleles at different chromosomal regions that are closely linked and that tend to be inherited together. As a haplogroup consists of similar haplotypes, it is usually possible to predict a haplogroup from haplotypes. Haplogroups pertain to a single line of descent. As such, membership of a haplogroup, by any individual, relies on a relatively small proportion of the genetic material possessed by that individual.
Canto: Anyway, getting back to mt-MRCA, obviously not as memorable a term as mitochondrial Eve, it seems to be more a concept than a person, if only we could get people to understand that. If you want to go back to the first individual, it would be the first mitochondrion that managed to synthesise with a eukaryotic cell, or vice versa. From the human perspective, mt-MRCA can be best conceptualised as the peak of a pyramid from which all… but then she still had parents, and presumably aunts and uncles…. It just does my head in.
bonobos or chimps? Or both? Or neither? What’s in a name…?
Canto: So we’ve been learning than we did it with Neanderthals, and that Neanderthals did it with Denisovans, and I remember hearing an anthropologist or palaeontologist saying that it’s likely that our split with our last common ancestor with chimps and bonobos – they call it the CHLCA (chimp-human last common ancestor, eliminating bonobos altogether, sigh) – wasn’t necessarily a clean break, which surely makes sense.
Jacinta: Well, yes, as we’ve read, the split was caused by the relatively sudden creation of the Congo River, but the word ‘relatively’, is, well, relative. So this raises the question of speciation in general. Think of those Galapagos finches that so intrigued Darwin. All about differently-shaped beaks, but it didn’t happen overnight.
Canto: Right, so here’s what a website with the rather all-encompassing title “Science” says about our topic:
Tens of thousands of years ago, modern humans slept around with Neandertals and swapped some genes. Now, it turns out one of our closest living relatives, chimpanzees, also dallied with another species. New research reveals that chimps mixed it up with bonobos at least twice during the 2 million years since these great apes started evolving their own identities. Although it’s not yet clear whether the acquired genes were ultimately beneficial or harmful, the finding strengthens the idea that such cross-species mating played an important role in the evolution of the great apes.
Jacinta: Interestingly this Congo River separation which led to a completely different species was repeated by other separations which led to four sub-species of chimps. Which leads me to wonder – what’s the difference between a new species and a sub-species? Why are bonobos ‘deserving’ of being called a different species?
Canto: Well the Science article has some fascinating further information. This was the work of Christina Hvilsom and colleagues, described as ‘conservation geneticists’. They were using any genetic differences they could find to work out where particular chimps were being caught or hunted. But, since the interbreeding of humans and Neanderthals, proven by DNA, had hit the headlines, Hvilsom wondered about the DNA of chimps. So, using the same methods that uncovered Neanderthal in humans –
she and her colleagues determined that 1% of the central chimpanzee’s genome is bonobo DNA. The genetic analysis indicates that this inbreeding happened during two time periods: 1.5 million years ago bonobo ancestors mixed with the ancestor of the eastern and central chimps. Then, just 200,000 years ago, central chimps got another boost of bonobo genes, the team reports today in Science. In contrast, the western chimp subspecies has no bonobo DNA, the researchers note, suggesting that only those chimps living close to the Congo River entertained bonobo consorts.
Jacinta: What this highlights, more than anything to me, is the importance and excitement of genetic and genomic analyses. Not that we’re experts on the topic, but it has clearly revolutionised the science of evolution, complicating it in quite exciting ways. Think again of those Galapogos finches. Separation, some interbreeding, more separation, less interbreeding, but with a few kinks along the way.
Canto: And we’re just beginning our play with genetics and genomics. There’s surely a lot more to come. Ah, to live forever…
Jacinta: So how did they know some inbreeding occurred? Can we understand the science of this without torturing ourselves?
Canto: David Reich’s book Who we are and how we got here tells the story of interbreeding between human populations, and how population genetics has revolutionised our understanding of the subject. With dread, I’ll try to explain the science behind it. First, the Science article quoted above mentions a split between bonobos and chimps 2 million years ago. Others I’ve noted go back only about a million years – for example a Cambridge University video referenced below. The inference, to me, is that there was a gradual separation over a fair amount of time, as aforementioned. I mean, how long does it take to create a major river? Now, I can’t get hold of the data on chimp-bonobo interbreeding in particular, so I’ll try to describe how geneticists detect interbreeding in general.
I’ll look at the human genome, and I’ll start at the beginning – a very good place to start. This largely comes from Who we are and how we got here, and the following quotes come from that book. The human genome consists of a double chain of 3 billion nucleobases, adenine, cytosine, guanine and thymine. That’s 6 billion bases (often called letters – A, C, G and T) in all. Genes are small sections of this base chain (called DNA), typically a thousand or so letters long. They’re templates or codes for building proteins of many and varied types for doing many different kinds of work, although there are segments in between made up of non-coding DNA.
Researchers have been able to ‘read’ these letters via machinery that creates chemical reactions to specific DNA sequences:
The reactions emit a different colour for each of the letters A, C, G and T, so that the sequence of letters can be scanned into a computer by a camera.
What anthropologists want to focus on are mutations – random errors in the copying process, which tend to occur at a rate of about one in every thousand letters. So, about 3 million differences, or mutations, per genome (3 billion genes, coding or non-coding). But genomes change over time due to these mutations and each individual’s genome is unique. The number of differences between two individuals’ genomes tells us something about their relatedness. The more differences, the less related. And there’s also a more or less constant rate of mutations:
So the density of differences provides a biological stopwatch, a record of how long it has been since key events occurred in the past.
As Reich recounts, it was the analysis of mitochondrial DNA, the tiny proportion of the genome that descends entirely down the maternal line, that became a corner-stone of the out-of-Africa understanding of human origins, which had been competing with the multi-regional hypothesis for decades. ‘Mitochondrial Eve’ – a rather ‘western’ moniker considering that the Adam and Eve myth is only one of a multitude of origin stories – lived in Botswana in Southern Africa about 160,000 to 200,000 years ago, given the variability of the genomic ‘clock’ – the mutation rate.
So, what does this have to do with chimps and bonobos? Well, The exact detail of how Hvilsom et al proved that their (slightly) more recent interbreeding events occurred is hidden behind a paywall, and you could say I’m a cheapskate but the reality is I’m quite poor, trying to bring up seven kids and a few dozen grandkids in a home not much bigger than a toilet, so… but truthfully I’m just getting by, and I just want to know in general the techniques used.
First, they have to find ancient specimens, I think. But, in a video referenced below, they raised the question – Can we ‘excavate’ ancient DNA from modern specimens? We’ve learned that many modern humans have a certain percentage of Neanderthal DNA, say around 2%, but each person’s 2% may be different. Aggregating those different segments can, if we analyse the genomes of enough humans, create a whole Neanderthal genome, though not one of any Neanderthal who ever lived! At least that’s how I’m reading it, in my dilettantish way. So what exactly does this tell us? I’m not at all sure – it’s a relatively new research area, and completely new to me.
The presenter of this video uses the heading, at least at the beginning of his talk, ‘A little Archaic introgression goes a long way’. So now I need to know what introgression means. A quick look-up tells me it’s:
‘the transfer of genetic information from one species to another as a result of hybridization between them and repeated backcrossing‘.
I’ve bolded two key words here. Hybridisation, in mammals, is ‘breeding between two distinct taxonomic units’. Note that the term species isn’t used, presumably because it has long been a questionable or loaded concept – life just seems too complex for such hard and fast divisions. Backcrossing seems self-explanatory. Without looking it up, I’d guess it’s just what we’ve been learning about. Canoodling after speciation should’ve ruled canoodling out.
But, looking it up – not so! It’s apparently not something happening in the real world, something like backsliding. But then… Here’s how Wikipedia puts it:
Backcrossing may be deliberately employed in animals to transfer a desirable trait in an animal of inferior genetic background to an animal of preferable genetic background.
This is unclear, to say the least. How could an animal, even a human, deliberately do this? We could do it to other animals, or try it, based on phenotypes. We’ve been doing that for centuries. What follows makes it more or less clear that this is about human experimentation with other animals, though.
Anyway, I’m going well off-topic here. What I wanted to do is try to understand the proof of, or evidence for, bonobo-chimp interbreeding. I accept that it happened, well after the split between these two very similar-looking species. What could be less surprising? Along the way I’ve been reminded inter alia, of homozygous and heterozygous alleles, but I’ve been frustrated that straightforward information isn’t being made available to the general public, aka myself. I’ll pursue this further in later posts.
Jacinta: What a mess. Phenotype isn’t everything my friend. To a bonobo, a chimp probably looks like a neanderthal – a real bonehead… They probably only had sex with them out of pity. ‘Boys, we’ll show you a good time – like you’ve never had before.’
Canto: So I’m trying to get my head around meiosis in general, and how the parental chromosomes get assorted in the process. I understand that Mendel arrived at his law or principle of independent assortment by noting the resultant phenotypes from particular crosses, especially dihybrid crosses. He knew nothing about gametes and meiosis, an understanding of which didn’t get underway until a decade or more after his 1865 experiments…
Jacinta: Well, meiosis is a v v amazing process that deserves lots of attention, because if not for, etc….
Canto: But what is meiosis for, I don’t even understand that.
Jacinta: It’s for the production of gametes – the sperm and egg cells in mammals. And that’s interesting, because, according to Medical News Today, ‘Females are born with all the eggs they will ever have in their lifetime. The amount decreases until a person stops ovulating and reaches menopause’. According to a graph they present, the number of egg cells produced is at its peak long before birth, and has reduced about tenfold by the time of birth, to about one or two million. This number continues to reduce through life, though it remains relatively stable during the period of ‘optimum fertility’ from about ages 18 to 31, when the number of eggs is around 200,000, with a lot of individual variation.
Canto: So, meiosis occurs entirely while the infant is in the womb? For females at least. And what exactly is ovulation?
Jacinta: Yes, egg cells don’t regenerate like other cells. Remember, tens of billions of our somatic cells die every day, and are being replaced – mostly. As to ovulation, this occurs as part of the menstrual cycle, which occurs with females at puberty. During menstruation, mature eggs are released from the ovaries, which are on the left and right sides of the uterus and connected to it by the fallopian tubes.
Canto: What do you mean by mature eggs? Aren’t they always mature?
Jacinta: Hmmm. Detour after detour. Four phases are recognised in the menstrual cycle – menstruation, the follicular phase, ovulation and the luteal phase. It’s the follicular phase that produces mature eggs, through the release of follicle stimulating hormone (FSH) by the pituitary gland. Do you want me to go into detail?
Canto: No, let’s get back to meiosis – but I always knew there was something fshy about the menstrual cycle. So meiosis is about haploid cells producing more haploid cells? You mentioned that egg cells, which are haploid cells, are at their peak long before the birth of a female child, a peak of around 10 million. But where does the first haploid cell come from, when a child starts as one fertilised egg – a diploid cell? Haploid cells combining to form diploid cells is one amazing process, but diploid cells separating to form haploid cells?
Jacinta: Okay so here’s what I think is happening. A human being starts as a diploid cell, a fertilised egg. As cells differentiate, which happens quite early, some become germ cells. But they’re diploid cells, like all the others, not haploid cells. So meiosis starts with diploid cells.
Canto: Okay, so what differentiates a germ cell from other somatic diploid cells?
Jacinta: I don’t know, just as I don’t know what makes a pluripotent or totipotent cell become a brain cell or a blood cell or whatever. This presumably has a lot to do with genetics, epigenetics and the production of endless varieties of proteins that make stuff, including germ cells. Which presumably are not egg cells or sperm cells, which are haploid cells, or gametes. And these germ cells can undergo mitosis, to reproduce themselves, or meiosis, to produce gametes. So now, at last, we describe the process, and much of this comes from Khan Academy. There are two ’rounds’ of meiosis – M1 and M2 – each of which has a number of phases. In M1 the diploid cell is split into two haploid cells each with 23 chromosomes, and in M2 the haploid cells reproduce as haploid cells, so that at the end of the cycle you have four haploid cells. And in each of these ’rounds’ there are the four phases, prophase, metaphase, anaphase and telophase. PMAT is how to remember it. And then there’s interphase, where cells just going on being themselves and doing whatever they do – though it’s important to know what happens during interphase for these other stages.
Canto: The complexity of it all is fairly mind blowing. Molecules that have a code for making proteins that perform all these functions that produce a huge variety of cells every one of which – apart from the gametes – has a nucleus containing 23 chromosomes from your mother and 23 from your father. Trillions of them!
Jacinta: Yes, it’s certainly amazing – and billions of those cells die and are replaced every day. And not just in humans but in dogs and bonobos and cetaceans and whatnot.
Canto: But here’s a thing – we’re talking about gametes, also known as germ cells, which may be female or male – sperm cells or egg cells. But sperm are also known as spermatazoa, and they’re much tinier and less complex than egg cells, and also far more numerous. Is a spermatozoon a sperm cell, or do lots of spermatozoa live in one cell, or what? One ejaculation releases – how many of these tiddlers?
Jacinta: Well sperm counts can range from about 15 million or less per millilitre of semen (that’s a low sperm count) to somewhere between 200 and 300 million. An ejaculation can vary in volume of course – generally about a teaspoon, which might be as much as 5mls. And, yes, a single sperm or spermatozoon is a male gamete, much smaller than the female ovum. So, yes, male sperm, like male political leaders, make up in numbers for what they lack in complexity.
Canto: Okay so let’s get started with PMAT and all that.
Jacinta: Well it’s all very miraculous or mind-blowing as Salman Khan rightly emphasises – to think that this complexity comes from mindless molecules and all. But here goes, and it cannot help but be a simplified description. So we start with a germ cell – and I’m not sure how this particular type of diploid cell is distinguished from other diploid cells…
Canto: Or whether, even though it’s called a germ cell, it is essentially different in male bodies as compared to female bodies, since they produce such different gametes…
Jacinta: Yeah well I’ll keep that in mind as we progress. Now we start with the interphase, during which time the chromosomes in the nucleus are synthesised. Interphase is generally subdivided into three phases, Gap 1 (G1), Synthesis (S) and Gap 2 (G2). The cell itself experiences a lot of growth during interphase.
Canto: Too vague.
Jacinta: Well I’m just getting started, but I’m not writing a book here.
Canto: Are you going to explain how the chromosomes are ‘synthesised’?
Jacinta: Probably not, this is just a summary.
Canto: I want to know about chromosome synthesis.
Jacinta: Sigh. You’re right, it sounds pretty important doesn’t it. So let’s focus in detail on interphase, which I think is much the same whether we’re looking at mitosis or meiosis. If you consider a whole cell cycle, from its ‘birth’ – usually through mitosis – to its ‘death’ (through mitosis again? I’m not sure), 95% of its time is spent in interphase, during which it doubles in size. It is, in a sense, preparing itself for chromosomal replication and cell division. Here’s a quote from a text book, Concepts of Biology, which I found online, describing the first stage of interphase:
The first stage of interphase is called the G1 phase, or first gap, because little change is visible. However, during the G1 stage, the cell is quite active at the biochemical level. The cell is accumulating the building blocks of chromosomal DNA and the associated proteins, as well as accumulating enough energy reserves to complete the task of replicating each chromosome in the nucleus.
Canto: So it’s a clever cell, actively accumulating the material to build and replicate its particular and unique DNA – I mean unique to the particular soma that it somatically serves, along with several trillion others.
Jacinta: Actually, another source tells that the G stands for growth, which I think makes more sense. The next stage is the S or synthesis phase. Now at this stage, or the beginning of it, the chromosomes exist largely as chromatin, a kind of mixture of DNA and proteins. Histones, in particular are important proteins for packaging the DNA into a tight enough space to fit in the nucleus. I mean, 23 pairs of chromosomes doesn’t really tell you how much DNA and other molecules it all amounts to. Now, this S phase is really complicated, and summaries don’t do it justice. Here’s a quote from yet another source to kick things off:
The S phase of a cell cycle occurs during interphase, before mitosis or meiosis, and is responsible for the synthesis or replication of DNA. In this way, the genetic material of a cell is doubled before it enters mitosis or meiosis, allowing there to be enough DNA to be split into daughter cells. The S phase only begins when the cell has passed the G1 checkpoint and has grown enough to contain double the DNA. S phase is halted by a protein called p16 until this happens.
So you’re asking how these chromosomes are synthesised. Note how this says ‘synthesis or replication’, so it’s presumably about the same sort of process that occurs when cells and their chromosomes are replicated during mitosis? Here’s another passage from the same source, and I don’t pretend to understand it:
The most important event occurring in S phase is the replication of DNA. The aim of this process is to produce double the amount of DNA, providing the basis for the chromosome sets of the daughter cells. DNA replication begins at a point where regulatory pre-replication complexes are attached to the DNA in the G1phase. These complexes act as a signal for where DNA replication should start. They are removed in the S phase before replication begins so that DNA replication doesn’t occur more than once.
Canto: Wow. That explains not much. Obviously the key to it all is the ‘regulatory pre-replication complexes’ previously attached. How could I not have known that?
Jacinta: Well let’s just say that there are known mechanisms by which DNA replication is regulated, and prevented from occurring more than once in the S phase. I’m sure all those ‘pre-replication complexes’ have been named and studied in detail by scores of geneticists. So that’s enough for now about chromosome synthesis/replication. The S phase also involves continued cell growth and the production of more proteins and enzymes for DNA synthesis. Always looking to the future. And so we move to the next phase.
Canto: Ah yes, reading ahead I see that DNA synthesis is always much the same. The DNA double helix is kind of unzipped by an enzyme called helicase, and the two single strands can be used as templates to form new and identical double strands. I’m over-simplifying of course.
Jacinta: Yes there are different processes going on to ensure that everything goes more or less smoothly, as well as to maintain cell growth outside of the genetic material. A key enzyme, DNA polymerase, binds nucleotides to the template strands using the base pairing code – A binds to T, C to G. This creates an identical new double helix of DNA.
Canto: Apparently there’s a difference between DNA replication and chromosome replication. Please explain?
Jacinta: I’m not sure if I can, but we’re talking about the replication of chromosomes in the S phase, after which each chromosome now consists of two sister chromatids (halves of a chromosome), as you see below.
In the first circle, A and B are homologous pairs. That’s to say, they’re segments of DNA, chromosomes, from each parent, though they might code differently – they might be different alleles. This is a bit complicated. Sal Khan in his video puts it this way:
Homologous pairs means that they’re not identical chromosomes, but they do code for the same genes. They might have different versions, or different alleles for a gene or for a certain trait, but they code essentially for the same kind of stuff.
Make of that what you will. I suppose it means that the homologous pair might have, say, genes for eye colour, but mum’s will code for blue, dad’s for brown. But the same kinds of genes are paired. Anyway, after replication in the S phase, you get, as above, two male and two female chromosomes, joined together in a sort of x shape. They’re joined together at that circular sort of binding site called a centromere (it’s not actually circular). The images above are misleading though, in that there are short arms and long arms leading off the centromere. You could say the centromere is off-centre. So the whole of this new x-shaped thingy is called a chromosome and each half – the right and the left – is called a chromatid. And at the four ends of the x-shaped thingy – I mean the chromosome – is a cap of repetitive DNA called a telomere.
Canto: Ah yes, I’ve heard of those and their relation to ageing…
Jacinta: Let’s not be diverted. So all of this is occurring in the nucleus, and there’s also replication of the centrosomes. Okay they’re a new structure I’m introducing, one that seems to only occur in animal-type or metazoan eukaryotic cells. They serve as microtubule organising centres (MTOCs), according to Wikipedia, which is never wrong, and which goes into great detail on the structure of these centrosomes, but for now the key is that they’re essential to the future separation of the chromatids via microtubules during prophase I. And that’s the next phase to describe. And it’s worth noting that the developments described up to now could be preliminary to meiosis or mitosis.
So, in prophase I the nuclear envelope starts to disintegrate and the pair of centrosomes are somehow pushed apart, to opposite sides of the chromosomal material, and microtubule spindles start extending from them – presumably by the magic of proteins. And another sort of magical thing happens, though I’m sure that some geneticists understand the detail of it all, which is that the homologous pairs line up on opposite sides of a kind of equator line, guided by these spindles, forming a tetrad, and this is where a process called crossing over or recombination occurs, in which the pairs exchange sections of genes. And this recombination somehow manages to avoid duplication and to maintain viability, and indeed to increase diversity. The recombination occurs at points in the chromosomes called chiasmas.
So that’s the end of prophase I. Now to metaphase 1. In this phase the nucleus has disappeared, the centromeres have completed their move to the opposite sides of the cell, and the spindle fibres of microtubules become attached to chromosomes via the kinetochores – protein structures connected to the centromeres. Here’s an interesting and useful illustration of a kinetochore.
All of this is similar to metaphase in mitosis. Then in anaphase I the homologous pairs, which remember had come together and recombined, are separated, or pulled apart, which is different from anaphase I in mitosis, where the chromosomes are split into their separate chromatids. Next comes telophase I, when the separation is complete, the facilitating microtubules break down and cytokinesis, the final separation of the chromosomes and the cytoplasm into two distinct cells, occurs. Telophase I ends with two cells and two nuclei, each containing 23 chromosomes, half of those in the original cells. They’re called daughter cells, for some reason.
Canto: Probably because son cells sounds silly.
Jacinta: Good point. So now these daughter cells start on a whole new PMAT process, which is a lot more like mitosis. Prophase II involves the disintegration of the nucleus once more, the two centrosomes start to move apart as microtubules are formed – and remember this is happening simultaneously in the two daughter cells – and then we’re into metaphase II, where the centrosomes have migrated to opposite ends of the cell, and the chromosomes line up at the ‘equator’, and the spindle fibres attach to the kinetochores of the sister chromatids. Next comes anaphase II, in which the spindle fibres draw the chromatids away from each other, as in anaphase during mitosis. And at the end of this journey they’re now treated as sister chromosomes. And all of this is happening in those two daughter cells, which start to stretch and cleave, which of course means that, in telophase II, you have cytokinesis, and the creation of new nuclear membranes, and the cytoplasm – remember that all the cytoplasm and its organelles have to be replicated too, to make, in the end four, complete haploid cells, or gametes. So that’s the potted version. There’s lots of stuff I’ve excluded, like the difference between centrosomes and centrioles, and lots of details about the cytoplasm, and there’s no doubt much more to learn (by me at least) about the crossing over that’s so essential to provide the variation that Darwin searched for in vain. Anyway, that was sort of fun and thank dog for the internet.
Canto: But I’m still confused about sperm cells and egg cells… If sperm cells are just those little tadpole things – a bunch of DNA with a flagellum, they don’t have any cytoplasm to speak of, do they?
Jacinta: Ah yes, something to look into. There’s spermatogenesis and there’s oogenesis… for a future post. It just never ends.
