roman catholic by birth; scientific atheist by choice; sinner by merit. blogging on brains, evolution and language. gaidhlig-speaking neuroscience student at oxford. likes to
Question Everything!
Apoptosis is the process of programmed cell death. Unlike necrosis, the premature death of cells, apoptosis is essential to life. For example, in embryogenesis, apoptosis occurs as the developing embryo pares away unneeded or unwanted cells and tissues. It’s part of the process that results in the separation and definition of the fingers. Apoptosis is one way the body fends off invasive cancers.
In the average human adult, an estimated 50 to 70 billion cells die each day due to apoptosis. In children, it’s about half that amount. When cells apoptose, they appear to collapse, forming misshapen bodies marked by blisters (called blebs) and sac (called vesicles). In the above image, by Thomas Deerinck and Mark Ellisman at the National Center for Microscopy and Imaging Research at UC San Diego, an apoptotic HeLa cell is surrounded by healthy counterparts.
If I remember rightly one of the most remarkable things about apoptosis is that it’s not really controlled by the nucleus of the cell. In fact free radical leakage along the respiratory chain in the mitochondria acts as a signal to mitochondrial genes to switch on and release small caspase-like mitochondrial proteins. These travel into the cytosol and inhibit the expression of anti-apoptosis proteins which gives caspase enzymes free reign to kill the cell.
It’s weird to think that the ancient bacteria swimming around inside our cells have the cell’s fate in their hands. Nick Lane wrote a really good book on the subject:
The K.E. clan are the first family of linguistics. A dynasty with over thirty members, their seat is in London, England. But what have they done to merit their title? To put it bluntly, they can’t talk.
Over three generations, around half the family suffers from a disorder whose name changes from verbal dyspraxia to dysphasia depending on who’s writing the paper. The key characteristic of this disorder is that their speech sounds like gobbledegook to the rest of the family – indeed, the impairment is so severe they now rely on simple hand signals to get things done. The family was first discovered by Myrna Gopnik in 1990 and a quick glance at the family tree was enough to confirm that she was dealing with an autosomal dominant disorder caused by a mutation in just one gene. The unmutated gene would presumably code for the ability the sufferers lacked – namely, language! Journalists jumped at the news, and the language (or, even more remarkably, grammar-) gene meme dominated the popular picture of genetics for the rest of the decade.
Early research fuelled the press perception that this was the gene for language. For instance, the affected family members were shown to repeatedly fail Wug Tests. In a Wug Test the subject is given a drawing of a made-up animal and told this is a wug. Then they are given a drawing of two of these wugs and asked to complete the sentence: ‘Now there are two…’ The affected family members simply could not generalize the plural add ‘s’ rule to an unfamiliar noun like wug. Similarly, they could make no sense of sentences whose meaning depended on the rules of syntax – they were unable to answer the question: ‘The lion was killed by the tiger. Which one is dead?’ All this pointed to a specific inability to parse syntax.
Nonetheless, it was clear from just listening to the subjects that effect of the impairment was much wider than a mere grammatical deficiency. The affected family members couldn’t control the muscles in the mouth and tongue properly, making it very difficult to produce the tiny changes in tongue position that produce different phonemes. This manifested itself in the subjects struggling to repeat multisyllabic words that demanded quick sound shifts. Steven Pinker went as far as to conclude in the Language Instinct that the so-called language gene was really a gene affecting mouth and tongue muscle movements. He guessed that fine motor control of these muscles must have been a prerequisite for the evolution of vocal language.
Because the IQ Range of the sufferers overlapped with that of the unaffected family members (with one sufferer even having as high an IQ as 111!), commentators were able to claim that the disorder was independent of general intelligence – therefore it just had to be language specific and thus, as night follows day, the gene must also be language specific. Yet, when we look at the stats, the mean IQ of the unaffected group was 104, while that of the sufferers was 85 – with many of them classed as ‘mentally retarded.’ There is clearly a significant difference in IQ between the two groups! Nonetheless, perhaps the sufferers’ low scores can be blamed on poor performance in verbal reasoning caused by their language defect. Unfortunately in 1995 this explanation was proved wrong – the sufferers’ really were stupider, with low IQs in both verbal and non-verbal domains. Moreover, it was shown that the gene affected muscle control in generating facial expressions too. This gene it seemed was about far more than just language…
Oh yeah, this family. FOXP2 is a curious gene. I’m interested in the way other facets of this family’s cognitive capabilities have apparently been affected by the error in their FOXP2 or else a correlated malfunction in other genes linked to the processes herein. I also want to know for sure whether the popular idea is that FOXP2 is a speech gene or more specifically a language gene, and I am strongly suspicious that the two are not the same thing (rather that the former is a vehicle for the latter but that it is not the only such vehicle for linguistic intelligence).
I did a crude test to see if I’m right that the popular idea (misconception is probably a better word) is of FOXP2 = language gene rather than speech gene. Language gene returns 173 million results, the ten of the first ten pages all related to FOXP2. Speech gene returns to 33 million, seven of the first ten pages related to FOXP2. I think FOXP2 will probably end up being known as the language gene forever.
I suppose in the nineties it was very convenient to portray this gene as language-specific because it seemed like the perfect evidence for nativism. This was also in the runup to the Human Genome Project so ‘gene for’ stories would have dominated science reporting.
Here’s a paper (behind a paywall) but whose abstract states categorically that from a sample of 270 (presumably vocal) language impaired children, not one had the G.E. family FOXP2 mutation - so other genes or environmental effects must have caused their impairment. They had low general language scores which I imagine means they struggled with inflection, mangled word order etc. The only FOXP2 mutation induced cases of language impairment I’ve ever read about are K.E and the boy they found the gene in. All this tells us is that language (unsurprisingly) is controlled by many many genes.
Also, if FOXP2 facilitates vocal language by acting in fine motor control of the tongue etc (and from those mouse findings, I guess assisting in synpase formation to store the procedural memories embodying the different motor actions for different phonemes) then FOXP2 appears to have no role to play in sign language as I don’t think its been implicated in fine motor control of the fingers. This in itself disproves the daft idea that FOXP2 is somehow the gene for grammar.
Here’s a 2012 paper I found about how FOXp2 impairs auditory-motor learning in mice.
The K.E. clan are the first family of linguistics. A dynasty with over thirty members, their seat is in London, England. But what have they done to merit their title? To put it bluntly, they can’t talk.
Over three generations, around half the family suffers from a disorder whose name changes from verbal dyspraxia to dysphasia depending on who’s writing the paper. The key characteristic of this disorder is that their speech sounds like gobbledegook to the rest of the family – indeed, the impairment is so severe they now rely on simple hand signals to get things done. The family was first discovered by Myrna Gopnik in 1990 and a quick glance at the family tree was enough to confirm that she was dealing with an autosomal dominant disorder caused by a mutation in just one gene. The unmutated gene would presumably code for the ability the sufferers lacked – namely, language! Journalists jumped at the news, and the language (or, even more remarkably, grammar-) gene meme dominated the popular picture of genetics for the rest of the decade.
Early research fuelled the press perception that this was the gene for language. For instance, the affected family members were shown to repeatedly fail Wug Tests. In a Wug Test the subject is given a drawing of a made-up animal and told this is a wug. Then they are given a drawing of two of these wugs and asked to complete the sentence: ‘Now there are two…’ The affected family members simply could not generalize the plural add ‘s’ rule to an unfamiliar noun like wug. Similarly, they could make no sense of sentences whose meaning depended on the rules of syntax – they were unable to answer the question: ‘The lion was killed by the tiger. Which one is dead?’ All this pointed to a specific inability to parse syntax.
Nonetheless, it was clear from just listening to the subjects that effect of the impairment was much wider than a mere grammatical deficiency. The affected family members couldn’t control the muscles in the mouth and tongue properly, making it very difficult to produce the tiny changes in tongue position that produce different phonemes. This manifested itself in the subjects struggling to repeat multisyllabic words that demanded quick sound shifts. Steven Pinker went as far as to conclude in the Language Instinct that the so-called language gene was really a gene affecting mouth and tongue muscle movements. He guessed that fine motor control of these muscles must have been a prerequisite for the evolution of vocal language.
Because the IQ Range of the sufferers overlapped with that of the unaffected family members (with one sufferer even having as high an IQ as 111!), commentators were able to claim that the disorder was independent of general intelligence – therefore it just had to be language specific and thus, as night follows day, the gene must also be language specific. Yet, when we look at the stats, the mean IQ of the unaffected group was 104, while that of the sufferers was 85 – with many of them classed as ‘mentally retarded.’ There is clearly a significant difference in IQ between the two groups! Nonetheless, perhaps the sufferers’ low scores can be blamed on poor performance in verbal reasoning caused by their language defect. Unfortunately in 1995 this explanation was proved wrong – the sufferers’ really were stupider, with low IQs in both verbal and non-verbal domains. Moreover, it was shown that the gene affected muscle control in generating facial expressions too. This gene it seemed was about far more than just language…
Willing to answer questions on science, philosophy, language, religion, politics, history, gaelic and scotland.
I’m quite knowledgeable (though no expert) on neuroscience, evolutionary biology, evolutionary psychology, linguistics, minority languages, gaelic, catholicism, moral philosophy, the philosophy of biology, british politics, scottish history, polynesian history and general European history.
I always make the effort to provide long interesting answers. Why not ask me? You’ve got nothing to lose!
Also, if you’re that way inclined, I will answer personal questions!!!
Nick Lane on the origin of complex life. He’s my favourite science writer. He researches the origins of life at UCL:
“Evolution provides an explanation for the variety and invention that has arisen in biology but no explanation of life’s seeding. If all the various life forms are traced back along their selective lines, from parent to grandparent until we arrive at the last universal common ancestor (LUCA). This life form must have been the first to be subjected to Darwinian natural selection. It must have a means of producing life forms with heritable characteristics, involving some sort of chemical messenger, a precursor to DNA. This messenger molecule must be “translated” into a heritable characteristic and then replicated so that it is inherited in the daughter units. However, both of these processes require an input of energy, as neither process can take place without something to power them. A generator is as essential as the presence of a messenger, but for many years the exact nature of the process of energy generation remained unknown.
A solution to the energy problem was proposed in the 1980s, taking innovation from a surprising source; volcanic alkaline vents in the Earth’s crust contain iron-sulphur minerals, which have been seen to be present in many enzymes involved in the formation of a multitude of organic molecules. The very specific conditions observed have been seen to give rise to a kind of primordial “cell” involved in energy generation, not dissimilar to the mitochondria.
How much can this system explain about early life? Nick Lane intends to answer some of the questions thrown up by the theory with his own simulation of an alkaline vent. He has built a reactor in the Darwin building, to mimic the conditions seen in the hot oceanic waters, where the vents exist. Progress is slow: the lack of knowledge about the exact structure of the vents lends an element of trial and error to the systems development. I enquired about its progress: “Well it’s not working at the moment… It has taken us ages to get [it] right… We haven’t even started doing experiments yet.”
His aims for the reactor are wide ranging and there are a number of possible inputs and outcomes: “A positive result could be finding metabolic intermediates, amino acids, nucleotides.””
Willing to answer questions on science, philosophy, language, religion, politics, history, gaelic and scotland.
I’m quite knowledgeable (though no expert) on neuroscience, evolutionary biology, evolutionary psychology, linguistics, minority languages, gaelic, catholicism, moral philosophy, the philosophy of biology, british politics, scottish history, polynesian history and general European history.
I always make the effort to provide long interesting answers. Why not ask me? You’ve got nothing to lose!
Also, if you’re that way inclined, I will answer personal questions!!!
Today, I’m going to be stepping back into that same political minefield that I did on the topic of race, and discuss a hypothesis regarding the cause of male homosexuality that some people may not like. People will not like this hypothesis for reasons extrinsic to the hypothesis itself, but do your best to contain any moral outrage you may be feeling. My first task in presenting this hypothesis will be to convince you that male homosexuality is not genetically determined - despite what an eccentric young pop-star might tell you - and is also not an adaptation.
Excellent article. I had heard about the kin selection, sexual antagonism and compound heterozygosity hypotheses. I always thought the first was frankly ridiculous. The second and third, though, I found rather elegant. But as you say, the fact more than 50% of the variance can’t be attributed to genetic factors is a knife to the heart of the hypotheses. So something else is probably going on here. I can’t help but think of the fact younger sons are more likely to be gay than elder. Many people immediately assume the mother ‘mollycoddles’ the baby of the family or something, but I would say its far more likely to do with conditions in the womb. Who knows? - maybe the more kids you’ve had, the more likely it is for this pathogen to infect the foetus! I’m gonna quote the virus section of your article for the benefit of my followers. It’s an interesting and plausible idea, and, as you rightly say, you can’t go from ‘is’ to ‘ought.’ Proving homosexuality was a developmental ‘defect’ caused by a virus should have no bearing on the ‘gay debate’
“There is one last hypothesis that may hold some potential, though, as I mentioned, I suspect many people won’t like it:the “gay germ” theory. The general idea is that some outside pathogen - be it a bacteria or a virus - manipulates development in some way, the end result being a homosexual orientation. This hypothesis seems to have potential for a number of reasons: first, it neatly deals with why homosexuality persists in the population, despite the massive reproductive costs. It could also account for why monozyogtic twins are often discordant for homosexual orientation, despite sharing genes and a prenatal environment. As of now, it remains an untested theory, butother lines of researchsuggest some preliminary success using the same basic idea to understand the persistence of disorders like schizophrenia and obsessive compulsive disorder, among many others. Of course, such a theory does come with some political baggage and questions.
The first set of questions concern the data speaking to the hypothesis: what pathogen(s) are responsible? When do they act in development? How do they alter development? Are those alterations an adaptation on the part of the pathogen or merely a byproduct? These are no simple questions to answer, especially because it won’t be clear which children will end up gay until they have matured. This makes narrowing the developmental window in which to be looking something of task. If concordance rates for monozyogtic twins are similar between adopted and reared together twins, that might point to something prenatal, depending on the age at which the twins were separated, but would not definitively rule out other possibilities. Further, this pathogen need not be specific to gay men; it could be a pathogen that much of the population carries, but, for whatever reason, only affects a sub-group of males in such a way that they end up developing a homosexual orientation.
The second set of questions concern potential implications of this theory, were it to be confirmed. I’ll start by noting these concerns have zero, absolutely nothing, to do with whether or not the gay germ theory is true. That said, these concerns are probably where most of the resistance to the hypothesis would come from, as concerns for data (or lack thereof) are often secondary to debates. Yes, the hypothesis cries out for supporting data so it shouldn’t be accepted just yet, but I’m talking to those people who would reject it as a possibility out of hand because it sounds icky. In terms of gay rights and social acceptance, it shouldn’t matter whether homosexuality is 100% genetically determined, caused by a pathogen, or just a choice someone makes one day because they’re bored with all that vanilla heterosexual sex they’ve been having. That something may be, or is, caused by a pathogen should really have no bearing on it’s moral status. If we discovered tomorrow that it was a virus that caused men to have larger-than-average penises, I doubt many people would cheer for the potential to cure the “disease” of large-penis.”
This is the weirdest science music video I’ve ever seen. Some ‘vanilla-face’ is rapping about DNA, and a harem of young women are belly-dancing in a sexual fashion around him…
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