Posts Tagged ‘genetics’
epigenetics at the very beginning of life – my explorations
So let me see if I can understand epigenetics through other sources, and through what I’ve read so far. First, it’s essential for the very first cell divisions in human – or shall we say mammalian – life, at least for placental mammals. Their lives begin with a fertilised egg, a sperm cell and an egg cell (both known as gametes), each with its complement of DNA (but the egg cell contains much more, and there’s a difference between an ovum and an oocyte, which I won’t go into, as if I could). This cell, also known as a zygote, is the ultimate totipotent stem cell, potentially able to form every type of somatic (diploid) cell. So what causes this cell to divide and multiply, and become, in a few days, a blastocyst?
A blastocyst is already quite a complex collection of cells, with an outer layer, the trophectoderm, an inner cell mass, and a blastocoel, which is a fluid-filled cavity. So, already quite a jump from a zygote, so I need to know how that happens. But even before that, I need to know how a zygote comes into being. Wikipedia puts it this way:
The formation of a totipotent zygote with the potential to produce a whole organism depends on epigenetic reprogramming. DNA demethylation of the paternal genome in the zygote appears to be an important part of epigenetic reprogramming.
That doesn’t help too much, but I’m guessing that this ‘epigenetic reprogramming’ thing is what creates cell diversity – but this description tells us that the formation of the zygote is itself an epigenetic product. Here’s another description of the first steps:
The four stages of embryonic development include fertilization (zygote formation), cleavage (rapid cell division), blastocyst formation, and finally, implantation into the uterine lining.
Cleavage? The website I filched this from (ferty9.com, listed below) fails to elaborate, and looking up the word an sich just takes me to female breasts, which is pleasant but distracting. AI (never lies) gives more detail, claiming four cleavage stages, 1. the zygote stage, 2. the 2 to 8 cell stage, 3. the morula stage, and 4. blastocyst formation. And presumably epigenetics plays a role in the move from one stage to the next?
So, I’ve tracked down a most sciencey article, from ScienceDirect, entitled ‘Epigenetic regulation of early human embryo development’, which I hope to make sense of. Its opening paragraph is a bit daunting though:
Epigenomes undergo profound change during the first few days of embryonic development. The resetting and establishment of epigenomes are coordinated within and contribute to the wider processes of embryogenesis. As a consequence, faithful epigenetic regulation is required to safeguard development and to establish long-lived epigenetic states that have effects on genome function throughout the life course.
So now we have epigenomes, and here’s a definition:
Epigenome: The epigenome consists of all the chemical modifications of DNA and histones of a cell/organism that contribute to regulate gene expression independently of DNA sequence.
Histone modification involves the post-translational modification of specific amino acids that influence the overall structure of histone proteins. Changes in histone structure may then influence their function, resulting in incomplete DNA unwinding that may also effect transcription activity. Major histone modifications include acetylation, methylation, phosphorylation, ubiquitylation, and, less frequently, ribosylation, sumoylation, and citrullination
References
https://pmc.ncbi.nlm.nih.gov/articles/PMC4783933/
https://www.sciencedirect.com/science/article/pii/S153458072101042
https://embryology.med.unsw.edu.au/embryology/index.php/Blastocyst_Development#Introduction
https://www.sciencedirect.com/science/article/pii/S1934590923003314
could I ever manage to get my head around epigenetics?
Nessa Carey’s book, The epigenetics revolution, was published in 2011, and discusses, and introduces, to many of us, gene methylation, histones, a number of different types of RNA, the names of specific genes, karyotypes, selective serotonin re-uptake inhibitors (SSRIs), phosphorylation, the Waddington epigenetic landscape and much else besides. Wikipedia’s account of epigenetics is no doubt more up-to-date, and is just about book-length (how long does a book have to be?), with over 200 references to scientific papers and such. Although the term was coined in the 1940s, the study of epigenetics is very much a 21st century thing, Our current knowledge of the area, like our knowledge of neurophysiology, has been one of the great developments in modern science. To read about it is exasperating, because there’s just too much to learn, to explore, to get your head around, and yet it’s vital to an understanding of who and what we are. When I think of SETI, for example, the Search for Extra-Terrestrial Intelligence, I wonder – how could such ineffable super-complexity have developed more than once in the universe, even given its incalculably massive extent?
I wish I was young and gifted with the opportunity to work in such a field, one which explains us, or tries to. How we manage to replenish all the cells in our bodies throughout our lives – not perfectly, for then we could live forever – but for a period extended enough for us to learn our own history, to fall in love, to learn from our many mistakes, to experience, delight in and suffer through all the stages of life, to observe all its amazing variety – the birds and the bees as they say, and the flowers and the trees, all of which have their genetic blueprints.
To think we had virtually no idea of this only a century ago, and we are 300,000 years old as a species, and DNA-driven creatures have existed for millions, maybe billions of years on this planet. We only worked out the structure of this molecule in the 1950s, and now we know for example that a spruce tree contains about six times more DNA than a human, and that it’s likely that our world was preceded by an RNA world, which still enlivens the viruses that plague us with influenza, hepatitis, polio, COVID-19 and so much else.
And all this epigenetic stuff – which is mainly about DNA methylation and histone modification – has been going on beneath our awareness, and certainly without our permission, since our life began as an embryo. That’s how our cells differentiate into some 200 different types. It has much to do with whether we’re tall or short, sickly or healthy, extroverted or introverted – even before we’ve ever met another soul. All of these goings-on in our growing bodies, as well as the inter-connections, disconnections and reconnections in our growing brains, in the time spent connected to a placenta and the subsequent years being buffeted by parents, relatives, strangers and frenemies, are what shape us for a lifetime.
So where am I going with all this? Those who know me might guess, and be much annoyed, or much heartened.
To return to Carey’s book, which explores, inter alia, how laboratory creatures like rats and mice show specific patterns of behaviour for a lifetime after early deprivation, stress and other conditions, I was struck by this passage:
The human brain possesses sufficient flexibility to generate adult outcomes in response to similar childhood experiences. Our brains contain one hundred billion nerve cells (neurons). Each neuron makes links with ten thousand others to form an incredible three dimensional grid. This grid therefore contains a thousand trillion connections – that’s 1,000,000,000,000,000 (a quadrillion). It’s hard to imagine this, so let’s visualise each connection as a disk that’s 1mm thick. Stack up the quadrillion disks on top of each other and they will reach to the sun (which is 93 million miles from the earth) and back, three times over.
That’s a lot of connections, so it’s perfectly possible to imagine that our brains have a lot of flexibility. But the connections are not random. There are networks of cells within the giant grid which are more likely to link to each other than to anywhere else. It’s this combination of huge flexibility, but constrained within certain groupings, that is compatible with a system that is mechanistic but not entirely deterministic.
Nessa Carey, The epigenetics revolution, pp 235-6
This is, I believe, the only passage in Carey’s 300-page book that refers to determinism, and of course it struck me enough to write one word in the margin.
‘Really?’
I don’t often write in the margins of my books these days. Decades ago I had a girlfriend who expressed shock and great disapproval at finding margin notes in some of my books. She apparently found this behaviour to be sacrilegious in some way. Texts were sacred even if they were reproduced in their thousands. So, though I respectfully disagreed, I’ve reduced my sacrilegious behaviour, maybe to honour her memory. But this time I couldn’t resist.
– ‘mechanistic but not entirely deterministic’? What is the difference between these two terms? Aren’t these mechanisms determined by other mechanistic processes? Isn’t this what the book is all about? Isn’t this how we know about epigenetic processes, because they produce certain changes under certain specific conditions? Aren’t the determining factors precisely what we’re looking for, and what knowledge is all about. And yet there is, I find, a kind of fear or distrust of the word, even amongst those researchers who rely on mapping out the causal chain, often a complex and elusive one, to make good their discoveries. Whether we’re looking at the causes of cancer, or how one or two bees become queens while thousands more become workers, to mention just two topics explored in Carey’s book, we’re always trying to uncover and explain the determining conditions. It’s the sine qua non of all science.
Maybe I’m mis-representing Carey here. Maybe she meant, when she described the ‘huge flexibility’ of our neuronal system, the impossibility of trying to pin things down, cause-and-effect-wise, with absolute certainty. But then, that’s not what she wrote. She wrote ‘not entirely deterministic’, and that was a red flag to me. So what was the part that escaped determinism? It doesn’t actually make sense.
The idea, it seems to me, and the argument that most people try to use against determinism, is that complexity trumps it (sorry to use the word ‘trump’ here). If complexity was infinite, that might be so, but complexity isn’t infinite, it’s just complex.
So, that’s enough for now. Again, I wish I was fifty years younger, and a more disciplined person than I was in my youth, because I’d love to be working in the field of organic chemistry, or molecular biology, or neurophysiology, rather than peering at it over a vast stretch of ignorance, as I am today. But never mind…
References
Nessa Carey, The epigenetics revolution, 2011
on epigenetics and the free will debate, and such…
The free will thing has come to the fore of my head again recently because of an offhand ‘no free will’ remark I made, which of course caused some friendly argy-bargy. When the topic comes up I like to throw ‘the lot’ at it, our early neurological wiring, unwiring and rewiring, our hormonal activity, our genetics, our epigenetics, our position in the womb, our early interactions with parents, siblings and others, our culture, our gender, our first language, the time and place of our birth and so on.
Of all these variables, epigenetics is one that’s likely to catch people off guard. If they ask, I’ll say it’s all about gene expression, hoping that will silence them, and even impress them. But if they inquire further, I’d only be able to say something like ‘environmental factors affect how genes are expressed’ – and that would be the limit of my knowledge, even though, some years ago, I read Nessa Carey’s The epigenetics revolution, published in 2011.
So now I’m reading it again, and it seems for the first time. I’m finding it really hard to understand, and I’m sure it isn’t Carey’s fault. I suspect it’s the kind of topic in which you need to be active in the field to fully understand it, and even then….
But, I’ll have a go. Rett syndrome is a rare but devastating neurological disease which occurs almost exclusively in girls. Apparently, if a male child contracts it, it’s more or less immediately fatal. As AI (never lies) puts it:
Infants typically develop normally for 6 to 18 months before experiencing a severe regression in motor skills, speech, and hand use. While there is no cure, symptoms can be managed with targeted therapies and specific medications.
The development of this syndrome happened to coincide with infants receiving the MMR vaccine, which, as we know, caused much controversy some time ago, but the mechanism was worked out in 1999. It mostly has to do with mutations in a gene called MECP2, which severely affects the production of a functional MECP2 protein. Dysfunction/mutation in other genes have caused the syndrome, or something like it, in a minority of cases. The cells are able to methylate their DNA correctly, which is what much of what epigenetics is all about, but they’re unable to read that section of the epigenetic code properly. So Rett syndrome isn’t a mental/psychological disorder at all, it’s purely genetic, and because the dysfunction is on the X chromosome, and because females have two X chromosomes while males have XY, the male karyotype is more vulnerable to the condition.
I choose this extreme condition (suffered by one in 8500 females) as one among many examples of how our genetics can fail us, and there are many others, much more subtle and hard to pin down, both in terms of our genes themselves and how they are expressed. We – I mean the scientists and researchers among us, and those going along for the ride – have learned especially in recent decades just how complex and beyond our control our brains and bodies are, not just in terms of physical make-up, but genetic and cultural inheritance. A regular awareness of this – a mindfulness, if you like – helps me to cope with the people who damage our world – the war-mongers, the bullies, the intolerant and over-confident – as well as to sympathise with the overwhelmed (like myself).
So, again to epigenetics – I’ll keep trying to comprehend at least some of it, as it’s intrinsically interesting when it’s not completely baffling. Meanwhile, I’ve had a book recommended to me, by two humanists and no-free-will proponents, called Being: why it’s harder to be human than a hamster or a herring, by a daughter and father duo, Rachel and Ross Menzies. Sounds like an antidote to all that epiphenomena…
References
Nessa Carey, The Epigenetics Revolution: How modern biology is rewriting our understanding of genetics, disease and inheritance, 2011.
genetics for the faint-hearted
get it got it good
What’s a haplotype? It’s a bunch of alleles, so I have to be clear first about alleles. A haplotype, also known as a haploid genotype, is a set of alleles inherited (as a set) from a single parent.
Alleles are pretty complex, at least to me. I think of Mendel and his peas, but it’s vague. Looking up a definition hasn’t helped much. It might, or might not, be better to start with DNA and/or RNA, and of course I know something about these macromolecules and their structure. They’re made up of nucleotides, and an allele is described as ‘a variant of the sequence of nucleotides at a particular location, or locus, on a DNA molecule’. This doesn’t help much. Do I repeat myself?
I’ll keep trying. There are haploid cells and diploid cells. In humans they’re called gametes – the sperm and the eggs, and they each have 23 chromosomes. Fertilisation of eggs by sperm creates zygotes which are paired – 23 chromosomes from each gamete type. Twenty-three pairs of haplotype make a genotype.
Why am I bothering with this? I can’t remember now, but I think it was about alleles. There is a problem in my mind about a haplotype, say inherited from Mum, and this ‘bunch of alleles’ thing. I mean, what’s the difference between an allele and a gene?
So I plug this into the machine. It seems that genes are things that code for things. In the phenotype. Your phenotype is the expression of your genes. Hair colour, penis size, intelligence maybe. Also I suppose your species. Bonobos have 24 pairs, but so do chimps. So…
Whales, since I’ve been focussing on them a bit lately, have mostly 44 chromosomes (22 pairs), but some species have 42.
Anyway this all began with talk on social media about XY and XX chromosomes, male and female humans and longevity. XY is male (for humans and some other mammals, and some fish, snakes and even plants). These are the ‘sex chromosomes’, at least in these species. That’s to say, the sex-determining chromosomes.
So a karyotype is, for my information, ‘the general appearance of the complete set of chromosomes in the cells of a species or in an individual, mainly including their sizes, numbers and shapes’. The sex chromosomes, obviously, are part of that karyotype, and they’re not always named XY or XX. Bird sex chromosomes, very interestingly, are ZW for females and ZZ for males. And what researchers are finding, in this doubling up (ZZ for male birds, XX for female humans) has some effect on their longevity – male birds, on average, and somewhat dependent on species – live longer than females, while female humans, and other mammals with XX chromosomes, live longer, on average, than males. Correlation or causation?
But all of this stuff on haplotypes, and full genotypes, is intrinsically interesting, and I could do a complete free online course on it, maybe…?
So if you know the genotypes of both your parents, could you work out their particular contribution to your phenotype? ‘I got my braininess from mum and my good looks from dad’ type thing? I should listen to the Sapolsky videos online maybe…?
If only I was 40 years younger. Still my genotype, and some luck, has kept me alive thus far…
more on the complexities of breeding behaviour – how do we know?
The Hapsburg, and sickly, Charles II of Spain (1665-1700). All in the family.
Here’s a simple thought experiment, if perhaps an unlikely scenario. Imagine two children born to the same parents, a male and a female. For some reason they’re both separated from those parents at a very early age, before they know each other as siblings. For the next twenty years or so they’re brought up in separate households, unaware of each others’ existence.
Guess what happens next – they meet, they ‘fall in love’, because after all they’re each as good-looking as the other, and they share interests, politics and ambitions, and they each want to start a family. What could go wrong?
Or more to the point of these explorations, how would these two individuals have any sense that they might be entering into dodgy territory? Of course they might start comparing backgrounds and entertaining suspicions, but what if they both share a tendency to bullshit about their past? Obviously this is a ridiculously rare scenario, but hopefully it makes a point.
So, when I try to learn about inbreeding I’m quickly taken into the inherent dangers, and the complexities of autosomal inheritance, whether dominant or recessive – all of which is fascinating in itself, but of little interest to bonobos, bats or budgerigars – or bodgies and widgies – when mating season arrives. Inbreeding avoidance is all very well if you know who to avoid. But a lot of the info I’m gathering tells me that we do know who to avoid, and I don’t just mean we humans. According to Wikipedia’s article on inbreeding avoidance, ‘there have been numerous documented examples of instances in which individuals are shown to find closely related conspecifics unattractive’. But this bald statement strikes me as totally unconvincing. I’m sure we could find plenty of ‘documented examples’ of the exact opposite too.
However there does seem to be something, beyond choice or preference or awareness, that promotes inbreeding avoidance, whether it’s pheromones, MHC (major histocompatibility complex) genes, or other evolved mechanisms. We generally manage it – and by ‘we’ I mean just about all breeding entities – but not in a foolproof way, it seems. What interests me is the kind of set process for inbreeding avoidance that we find in chimps, bonobos, Tiwi Islanders and other human societies, which rises to the point of incest taboos in humans. With humans there is knowledge. We know that breeding with siblings and other close kin is problematic, yet we probably didn’t always know that, and our taboos are more about it being ‘icky’ and ‘creepy’ than about giving birth to unhealthy children. What gave rise to those feelings, which seem to be shared by other apes, and perhaps further down the evolutionary bush?
Let’s look at MHC genes, though I don’t think they’re going to provide an answer that satisfies me. Here are the opening lines from a 2008 PubMed article entitled ‘Major histocompatibility complex alleles, sexual responsivity, and unfaithfulness in romantic couples’:
Preferences for mates that possess genes dissimilar to one’s own at the major histocompatibility complex (MHC), a polymorphic group of loci associated with the immune system, have been found in mice, birds, fish, and humans. These preferences may help individuals choose genetically compatible mates and may adaptively function to prevent inbreeding or to increase heterozygosity and thereby immunocompetence of offspring.
So, yes, I find nothing wrong with this finding, but maybe it’s a bit of a correlation-causation problem for me. I’d like a bit more info on the causal. And obviously all these creatures have no idea whether a potential mate has similar/dissimilar MHC genes, so why mention preference, which is about choice, or intention? But then, doesn’t love, or desire, strike us below the level of awareness? Ain’t love blind? Not to our MHC genes, apparently. And then again, is our preference for sweet rather than sour, or vice versa, really a personal choice or something we find out about ourselves? Do I contradict myself? Very well…
Anyway I’m glad to note the phrases ‘may help individuals choose…’ and ‘may adaptively function to prevent inbreeding…’ here, an acknowledgement, methinks, of the fact that they’ve observed a correlation which hasn’t yet been found as determinative – though probably everyone thinks it is. Meanwhile, we – human and myriad other species – seem pretty good at avoiding inbreeding, mostly, so why worry…
References
https://pubmed.ncbi.nlm.nih.gov/17100780/#:~:text=Abstract,HLA%2DA%20Antigens%20/%20genetics
Why are bonobos female dominant? Culture or genetics?
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 slightly less 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!
References
Joseph Henrich, The WEIRDest people in the world, 2021
Susan Faludi, Stiffed, 1999
exploring meiosis
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 G1 phase. 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.
References
exploring genetics – Mendel, alleles and stuff
Canto: So I’d like to know as much as I can about genetics before I die, which might be quite soon, so let’s get started. What’s the difference between genetics and genomics?
Jacinta: Okay, slow down – but I suppose that’s as good a place to start as anywhere. I recently listened to a talk about the human genome project, which was completed around 2003, and the number I heard the guy mention was 3 billion genes, or something. But according to videos and other sources, each human has between 20,000 and 25,000 genes – though I’ve found another FAQ which estimates 30,000. So I gather from this that our genome is the number of genes we might possibly have – in the whole human population? Which raises the question, how do we know that the human genome project has captured or mapped all of them.
Canto: So there’s an individual genome, peculiar to each of us, and a collective genome?
Jacinta: Errr, maybe. We’re 99.9% genetically identical to each other, supposedly. And if this sounds very paradoxical, we need to zoom in on the detail. And with that, I’ve discovered that the 3 billion refers to base pairs, sometimes called ‘units of DNA’. So what’s a base pair? Well, we need to start with the structure of DNA, the genetic molecule. That’s deoxyribonucleic acid, which is made up of basic components called nucleotides. A nucleotide of DNA consists of a sugar molecule, a phosphate group and a nitrogenous base. The bases come in four types – adenine, guanine, thymine, and cytosine (A, T, G and C). The sugar and phosphate groups provide structure, allowing the bases to form a long string of DNA. Bonds form between the bases to create a double strand of DNA – hence base pairs.
Canto: Here’s how the World Health Organisation defines genomics, obviously from a health perspective:
Genomics is the study of the total or part of the genetic or epigenetic sequence information of organisms, and attempts to understand the structure and function of these sequences and of downstream biological products. Genomics in health examines the molecular mechanisms and the interplay of this molecular information and health interventions and environmental factors in disease.
Now you might think that this definition could cover genetics too, and maybe we shouldn’t be too worried about the distinction. Maybe, in general, genomics is about sequences of genes, especially in detailing whole organisms, while genetics is more about individual genes.
Jacinta: Genomics is the much more recent term, first coined in the 1980s, whereas genetics and genes date back to before we knew about DNA as the genetic molecule. Going back to Mendel and all, though I don’t think he used the term, he talked about ‘factors’ or some such.
Canto: So we know that there’s DNA, and there’s also RNA, another building block of life. How old are they, and which came first? And can species replicate without these molecules?
Jacinta: Oh dear – we’ll get there eventually, maybe. Genomics deals with the whole complement of genes in an organism, which we’ve gradually realised is necessary to evaluate, say, how prone that organism is to contracting a disease, or developing some immuno-deficiency, because individual genes often don’t tell us much. And there’s also the matter of dominant and recessive genes. Which takes us to inheritance. All those genes are combined together on chromosomes, of which there are 23 pairs in humans, which we inherit from our parents, 23 chromosomes each.
Canto: Combined together? Can you be more specific?
Jacinta: Okay, a chromosome is a thread-like structure, in which DNA is coiled around structural proteins called histones. Each chromosome has two ‘arms’, flowing from a constriction point called a centromere. These arms are labelled p and q. The p arm is shorter than the q. And these chromosomes contain genes, which may or may not code for proteins. The genes, as mentioned, consist of base pairs, which vary in number from hundreds to millions.
Canto: Okay, so what’s the difference between a gene and an allele?
Jacinta: Well, genes are codes for making proteins – and those proteins affect all sorts of things, to do with taste, smell, hair colour and type, height, and predisposition to various diseases, among many other things. You can call these things ‘traits’, which show up in our phenotype, our physical characteristics. And it should be pointed out that many of these traits are the results of not just one gene but different genes in combination. Now, as mentioned, these genes are in pairs of chromosomes – 23 pairs in humans. Now, say we isolate an area in a chromosome that codes for a particular trait. What about the other chromosome in that pair? Remember, each chromosome comes from a male or female parent, and they are different, genetically – or likely to be. That’s where alleles come in, and it takes us back to Mendel, who found that with pea plants, traits such as colour, or the alleles that carried those traits, could be dominant or recessive. So, for that trait, they could carry two dominant alleles, or two recessive alleles, or one of each. If one or both of those alleles is dominant, the trait will be expressed, but if both are recessive, it won’t be. But as I say, it’s more complicated than that, as traits expressed in phenotypes are generally carried by many genes.
Canto: So alleles are? – how to define them?
Jacinta: Google it mate. Here’s a quickly found definition: “each of two or more alternative forms of a gene that arise by mutation and are found at the same place on a chromosome”. So let’s continue with the work of Mendel. When we find a dominant trait, we use a capital, T. It might be paired with another dominant trait, TT, or with a recessive trait, Tt. On the other hand, both traits might be recessive, tt, and that’s all the combos you have, for single traits. Now, in noting this, and the way that alleles combine, Mendel came up with a ‘law of segregation’. Or rather, he noticed a process, which later became recognised as a law. In fact, he observed three fundamental processes, ‘segregation’, ‘independent assortment’, and ‘dominance’, which we now describe as laws. Now, I’ve used the term ‘trait’ but perhaps I should’ve used the term ‘allele’. So TT combines two dominant alleles. The law of segregation has been stated thus:
During gamete formation, the alleles for each gene segregate from each other such that each gamete formed carries only one allele for each gene.
Canto: Right. Uhhh, what’s a gamete again?
Jacinta: Sex cells, which carry only one copy of each chromosome. They’re created during meiosis, after which we end up with four cells each with only one allele for each gene. So indeed, alleles are segregated during gamete formation.
Canto: Oh dear. I’ll have to brush up on meiosis.
Jacinta: So now we have these segregated alleles, which will be recombined. The law of independent assortment comes next. This also occurs during meiosis. In the fourth or metaphase period of cell division, the chromosomes align themselves on the equatorial plane, also called the metaphase plate. This alignment is random, and that’s the key to the law of independent assortment – ‘genes for different traits assort independently of each other during gamete formation’. But obviously Mendel knew nothing about meiosis, though it was first observed in his lifetime, in sea urchins . Anyway, this law allows for many different combinations of alleles depending on how chromosomes become aligned on the metaphase plate. A dihybrid cross will provide more such combinations.
Canto: A dihybrid cross? Please explain.
Jacinta: Well, a monohybrid cross will be like this – TT x tt. Not much to be assorted there. A dihybrid cross might be like this – TtCc x TtCc, creating four different assortments for each cross. So now to the third law, of dominance. This law simply states that ‘some alleles are dominant while others are recessive. An organism with at least one dominant allele displays the effect irrespective of the presence of the recessive one’. So the phenotype will present the dominant allele regardless of whether it’s double-dominant or single-dominant. Though the terms used are homozygous (TT), or heterozygous (Tt).
Canto: So are we going to look at punnett squares now? I’ve heard of them…
Jacinta: Well it might help. They were named after a bloke called Punnett back in 1905, the early days of Mendelian genetics. They’re neat little tables, that can start to get quite complicated, for determining the genotypes of offspring, when you breed dominant with recessive, heterozygous with homozygous and so on. It’s useful for simple genotypes, but when genotypes are multifactorial, as they often are, other methods are obviously required.
Canto: Okay, that’s more than enough to absorb for now.
Jacinta: I think, since we’ve started with Mendel, we might do a historical account. Or maybe not….
References
https://www.google.com/search?client=safari&rls=en&q=alleles&ie=UTF-8&oe=UTF-8
https://byjus.com/biology/mendel-laws-of-inheritance/
https://www.yourgenome.org/facts/what-is-meiosis
returning to the race myth
‘My own personal view is that today we over-privilege and fetishise the concept of identity’.
Mark Thomas, Professor of evolutionary genetics, University College, London (quoted in Superior: the return of race science, by Angela Saini, 2019)
A couple of years ago I tackled issues of race and identity politics in a post which focussed on ‘blackface’ among other things. I don’t think there’s much I’d change about it, but my current reading of Angela Saini’s above-mentioned book, in particular the chapter ‘Roots’, which relates what anthropology has found regarding the first indicator of race amongst those who tend to obsess over it, namely skin colour, has updated my knowledge without really changing my outlook.
When we think of ‘white’ people one of the most obvious examples would be the pale, cold-weather Scots, of which I’m one. We’re not called WASPs for nothing. I was amused as an adult to find paperwork indicating that I was baptised as a Presbyterian. WTF is that? Another funny thing about my waspness is the fact that I’ve lived in sunny Australia since the age of five, my skin darkening quite splendidly every summer in the pre-sunblock era. Needless to say my intelligence dipped sharply during those months.
Saini relates a story about a 1903 archaeological discovery in Somerset, of one of the oldest human bodies ever found in Britain. Dating back some 10,000 years, he was given the name Cheddar Man as he was discovered in caves at Cheddar Gorge, and much more recently he was analysed by genetic sequencing. There was naturally a lot of interest in the genetics of this fellow, as English, or British, as cheddar cheese.
… what came as a real shock to many was that his bones… carried genetic signatures of skin pigmentation more commonly found in sub-Saharan Africa. It was probable, then, that Cheddar Man would have had dark skin. So dark, in fact, that by today’s standards he would be considered black.
Superior, Angela Saini, p167
Visual reconstructions based on the genetics also showed him to be far less WASP-looking than genteel society might condone. It was front-page news stuff, but experienced geneticists such as Mark Thomas were unfazed. The fact is that modern genomics has probably done more than anything else to scuttle the notions of fixed identities relating to blackness, whiteness, Europeaness, Asianess, Africaness, Scandinavianess or Irishness. In short the necessity of ness-ness ain’t necessarily so.
This has everything to do with genetic drift. As Thomas explains it, in pre-civilisation times, humans migrated in small groups, and would have varied physically (and of course in other ways) from those they separated from. Later, as groups grew and became more stable, there would have been an opposite effect, a greater homogeneity. Thus we see ‘Asians’, ‘Africans’ and ‘Europeans’, from our limited perspective, as near-eternal categories when in fact they’re relatively recent, and of course disintegrating with globalisation – an extremely recent phenomenon, genomically speaking.
On ‘blackness’ itself, that may have been a more recent phenomenon in our ancestry than ‘whiteness’. My good friends the bonobos, and their not-so-nice chimp cousins, tend to have light skin under their dark hair. As we moved forward in time from our ancestral link with chimps and bonobos, losing our body hair and increasing the number of sweat glands as we became more bipedal and used our speed for hunting, there would have been a selection preference for darker skin – again depending on particular environmental conditions and cultural practices. There is of course a quite large gap in our knowledge about early hominids (and there is controversy about how far back we should date the bonobo-human last common ancestor – identifying Graecopithecus as this ancestor tends to push the date further back) considering that Homo Habilis, which dates back, as far as we know, to 2.3 million years ago is the oldest member of our species identified so far. Beyond H habilis we have the Australopithecines, Ardipithecines, Sahelanthropus Tchadensis and Orrorin tugenensis, among others, which may take us back some 7 million years. DNA analysis can only take us back a few thousand years, so I don’t know how we’re ever going to sort out our deeper ancestry.
In any case, the new racial ‘ideas’, given impetus by various thugocracies in the former Yugoslavia as well as today’s Burma/Myanmar, China, India and the USA (where it may yet lead to civil war) are an indication of the fragility of truth when confronted and assaulted by fixed and fiercely held beliefs. Social media has become one of the new and most effective weapons in this assault, and when thugocracies gain control of these weapons, they become so much more formidable.
Truth of course, is, and should be its own weapon against identity politics. Knowledge should be the antidote to these supposedly indelible identities, of blackness, whiteness, Jewishness, Hindu-ness and so on. Unfortunately, too many of us are interested in confirmation than in truth. In fact, according to the psychologists Hugo Mercier and Dan Sperber, in their book The enigma of reason, we use reason more often to confirm beliefs that we want to be true than for any other purpose. And when enough of the ruling class are concerned to confirm erroneous beliefs that happen to advantage them, as is the case for the current Indian Hindu government, the result is a thugocracy that oppresses women as well as the so-called ‘untouchables’ and other victims of the two-thousand year old caste system.
But having just read the chapter entitled ‘Caste’ of Angela Saini’s book, I should modify those remarks. The current Indian government is only reinforcing a system the disadvantages of which are more clear to ex-pats like Saini (and some Indian students I’ve had the pleasure of teaching) than it is to those that remain and ‘belong’. It involves more than just caste and religion, as it’s practiced by Christians and others, and enforced by families and broader relational and cultural units. My own detachment from family and cultural constraints makes it easy for me to judge this rather harshly. And in faraway Australia we hear of the horrors of in-group fealty without feeling its comforts. And naturally as a working-class lad and anti-authoritarian my sympathies are definitely with the underclass.
So how do we overcome the inwardness of caste and class systems, which are ultimately destructive of genetic diversity, not to mention causing the immiseration of millions? The answer, also provided by Mercier and Sperber’s thesis, is interaction and argument. They argue that reason developed as a social rather than an individual phenomenon. Evidence of course also must play a part. Saini’s book provides an excellent example of this, and the scientific community generally does too. Mercier and Sperber give an interesting example of how the marketplace of ideas can produce effective results over time:
The British abolitionists didn’t invent most of the arguments against slavery. But they refined them, backed them with masses of evidence, increased their credibility by relying on trustworthy witnesses, and made them more accessible by allowing them to see life through a slave’s eyes. Debates, public meetings, and newspapers brought these strengthened arguments to a booming urban population. And it worked. People were convinced not only of the evils of slavery but also of the necessity of doing something about it. They petitioned, gave money, and – with the help of other factors, from economy to international politics – had first the slave trade and then slavery itself banned.
The enigma of reason: a new theory of human understanding, H Mercier & D Sperber, p314
Some would say, of course, that slavery is still flourishing. I’ve even heard the claim that Jeff Bezos is the quintessential modern slave-owner. But nobody is credibly claiming today that slavery is reasonable. It has long ago lost the argument. That’s why evidence-based argument is our best hope for the future.
References
Superior: the return of race science, Angela Saini, 2019
The enigma of reason: a new theory of human understanding, Hugo Mercier & Dan Sperber, 2017.
reading matters 7
She has her mother’s laugh, by Carl Zimmer , science author and journalist, blogger, New York Times columnist, etc etc
content hints – inheritance and heredity, genetics and epigenetics, Darwin and Galton, the Hapsburg jaw, eugenics, Hugo de Vries, Theodor Boveri, Luther Burbank, Pearl and Carol Buck, Henry Goddard, The Kallikak Family, Hitler’s racial hygiene laws, morons, the five races etc, Frederick Douglass, Thomas Hunt Morgan, Emma Wolverton, PKU, chromosomal shuffling, meiosis, cultural inheritance, mitochondrial DNA, Mendel’s Law, August Weismann, germ and soma, twin studies, genetic predispositions, mongrels, Neanderthals, chimeras, exosomes, the Yandruwandha people, IVF, genomic engineering, Jennifer Doudna, CRISPR, ooplasm transfers, rogue experiments, gene drives, pluripotency, ethical battlegrounds.