nhaliday + crispr   34

Ask HN: What's a promising area to work on? | Hacker News
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23 days ago by nhaliday
Genome Editing
This collection of articles from the Nature Research journals provides an overview of current progress in developing targeted genome editing technologies. A selection of protocols for using and adapting these tools in your own lab is also included.
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october 2017 by nhaliday
Genetically engineered humans will arrive sooner than you think. And we're not ready. - Vox
lol "epigenetics" makes an appearance ofc


For now, that’s prohibitively expensive, but it won’t always be that way. In 2003, it cost 4 dollars to press one of the keys on Endy’s hypothetical synthesizer. This month, it costs just two cents—a 200-fold decrease in price in just 14 years. In the same time frame, the cost of tuition at Stanford has doubled, and is now around $50,000. Given all of that, the first question that Stanford’s budding bioengineers get is this:

At what point will the cost of printing DNA to create a human equal the cost of teaching a student in Stanford?
And the answer is: 19 years from today.

But the follow-up question is a little more complicated:

If you and your future partner are planning to have kids, would you start saving money for college tuition, or for printing the genome of your offspring?
The question tends to split students down the line, says Endy. About 60 percent say that printing a genome is wrong, and flies against what it means to be a parent. They prize the special nature of education and would opt to save for the tuition. But around 40 percent of the class will say that the value of education may change in the future, and if genetic technology becomes mature, and allows them to secure advantages for them and their lineage, they might as well do that.


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may 2017 by nhaliday
Solidarity Forever | West Hunter
If you had a gene with a conspicuous effect (like a green beard) that at the same time caused the carrier to favor other individuals with a green beard, you could get a very powerful kind of genetic altruism, one not limited to close relatives. A very strong effect, one that caused you to act as if other carriers were just as valuable as you are (as if other carriers were your identical twin) could exist, but weaker effects (green fuzz) could also be favored by selection – if you were just somewhat more likely to cooperate with others bearing the mark. That could be enough to drive strong selection for the gene, and might not even be terribly noticeable.

This might be especially powerful in humans: we have so very many ways of cooperating or tripping each other up. Now and then you get partial alignment of interests, and remarkable things happen. If we could all just get along, we could conquer the world and make everyone else our slaves and playthings!


Shortly after the Green Beards became influential, you’d see a lot of people wearing fake green beards, which would cut down on the advantage and possibly turn green beards into easy marks, chumps doomed to failure. It would work best if the identifying mark was hard to copy – difficult today, but in the past some things, eye color for example, would have been hard to copy.

This all gets complicated, since it’s not always easy to know what someone else’s best interest is – let along that of the entire Greenbeard race. For that matter it’s not always that easy to know what your own best interest is.

I’m for it, of course: trying to fighting off such a mutant takeover would make life more interesting.

There no evidence, that I know of, of anything like a strong green-beard effect in humans. If there was one, it would have dramatic consequences, which we haven’t observed, so I doubt if one exists. Although we could always create one, for laughs.

Any gene that selected for extended kin altruism would not flourish – would not increase in frequency – because the expensive altruistic effort would not be focused on people who were more likely than average (in that population!) to carry the relevant allele. Which means that every time that expensive altruism happened, the average allele frequency in that population would go down, not up: this is not the route to success. If you can’t understand, that’s your problem.

Frank Salter is entirely wrong. There is no such thing as “genetic interest”, in the sense he’s talking about, not one that makes people feel the way he’d like them to. Sheesh, if there were, he wouldn’t have to argue about it, anymore than you have to argue parents into caring about their children. Now if he said that having more Swedes in the world would result in something he liked, that could well be true: but there’s no instinct that says everyone, even most Swedes, have to favor that course.

You have to do the math: when you do, this idea doesn’t work. And that’s the end of this conversation.

That lady’s mind ain’t right.

Speaking of which, one has to wonder which is the greater threat – the increasing dumb fraction of this country, or the increasing crazy fraction.
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may 2017 by nhaliday
Typos | West Hunter
In a simple model, a given mutant has an equilibrium frequency μ/s, when μ is the mutation rate from good to bad alleles and s is the size of the selective disadvantage. To estimate the total impact of mutation at that locus, you multiply the frequency by the expected harm, s: which means that the fitness decrease (from effects at that locus) is just μ, the mutation rate. If we assume that these fitness effects are multiplicative, the total fitness decrease (also called ‘mutational load’) is approximately 1 – exp(-U), when U is where U=Σ2μ, the total number of new harmful mutations per diploid individual.


interesting, suggestive comment on Africa:
I have reason to believe that few people understand genetic load very well, probably for self-referential reasons, but better explanations are possible.

One key point is that the amount of neutral variation is determined by the long-term mutational rate and population history, while the amount of deleterious variation [genetic load] is set by the selective pressures and the prevailing mutation rate over a much shorter time scale. For example, if you consider the class of mutations that reduce fitness by 1%, what matters is the past few thousand years, not the past few tens or hundreds of of thousands of years.


So, assuming that African populations have more neutral variation than non-African populations (which is well-established), what do we expect to see when we compare the levels of probably-damaging mutations in those two populations? If the Africans and non-Africans had experienced essentially similar mutation rates and selective pressures over the past few thousand years, we would expect to see the same levels of probably-damaging mutations. Bottlenecks that happened at the last glacial maximum or in the expansion out of Africa are irrelevant – too long ago to matter.

But we don’t. The amount of rare synonymous stuff is about 22% higher in Africans. The amount of rare nonsynonymous stuff (usually at least slightly deleterious) is 20.6% higher. The number of rare variants predicted to be more deleterious is ~21.6% higher. The amount of stuff predicted to be even more deleterious is ~27% higher. The number of harmful looking loss-of-function mutations (yet more deleterious) is 25% higher.

It looks as if the excess grows as the severity of the mutations increases. There is a scenario in which this is possible: the mutation rate in Africa has increased recently. Not yesterday, but, say, over the past few thousand years.


What is the most likely cause of such variations in the mutation rate? Right now, I’d say differences in average paternal age. We know that modest differences (~5 years) in average paternal age can easily generate ~20% differences in the mutation rate. Such between-population differences in mutation rates seem quite plausible, particularly since the Neolithic.
more recent: https://westhunt.wordpress.com/2017/06/06/happy-families-are-all-alike-every-unhappy-family-is-unhappy-in-its-own-way/#comment-92491
Probably not, but the question is complex: depends on the shape of the deleterious mutational spectrum [which we don’t know], ancient and recent demography, paternal age, and the extent of truncation selection in the population.
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may 2017 by nhaliday
Interview Greg Cochran by Future Strategist

- IQ enhancement (somewhat apprehensive, wonder why?)
- ~20 years to CRISPR enhancement (very ballpark)
- cloning as an alternative strategy
- environmental effects on IQ, what matters (iodine, getting hit in the head), what doesn't (schools, etc.), and toss-ups (childhood/embryonic near-starvation, disease besides direct CNS-affecting ones [!])
- malnutrition did cause more schizophrenia in Netherlands (WW2) and China (Great Leap Forward) though
- story about New Mexico schools and his children (mostly grad students in physics now)
- clever sillies, weird geniuses, and clueless elites
- life-extension and accidents, half-life ~ a few hundred years for a typical American
- Pinker on Harvard faculty adoptions (always Chinese girls)
- parabiosis, organ harvesting
- Chicago economics talk
- Catholic Church, cousin marriage, and the rise of the West
- Gregory Clark and Farewell to Alms
- retinoblastoma cancer, mutational load, and how to deal w/ it ("something will turn up")
- Tularemia and Stalingrad (ex-Soviet scientist literally mentioned his father doing it)
- germ warfare, nuclear weapons, and testing each
- poison gas, Haber, nerve gas, terrorists, Japan, Syria, and Turkey
- nukes at https://en.wikipedia.org/wiki/Incirlik_Air_Base
- IQ of ancient Greeks
- history of China and the Mongols, cloning Genghis Khan
- Alexander the Great vs. Napoleon, Russian army being late for meetup w/ Austrians
- the reason why to go into Iraq: to find and clone Genghis Khan!
- efficacy of torture
- monogamy, polygamy, and infidelity, the Aboriginal system (reverse aging wives)
- education and twin studies
- errors: passing white, female infanticide, interdisciplinary social science/economic imperialism, the slavery and salt story
- Jewish optimism about environmental interventions, Rabbi didn't want people to know, Israelis don't want people to know about group differences between Ashkenazim and other groups in Israel
- NASA spewing crap on extraterrestrial life (eg, thermodynamic gradient too weak for life in oceans of ice moons)
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march 2017 by nhaliday
Neurodiversity | West Hunter
Having an accurate evaluation of a syndrome as a generally bad thing isn’t equivalent to attacking those with that syndrome. Being a leper is a bad thing, not just another wonderful flavor of humanity [insert hot tub joke] , but that doesn’t mean that we have to spend our spare time playing practical jokes on lepers, tempting though that is.. Leper hockey. We can cure leprosy, and we are right to do so. Preventing deafness through rubella vaccination was the right thing too – deafness sucks. And so on. As we get better at treating and preventing, humans are going to get more uniform – and that’s a good thing. Back to normalcy!

focus: https://westhunt.wordpress.com/2017/02/22/neurodiversity/#comment-88691
interesting discussion of mutational load: https://westhunt.wordpress.com/2017/02/22/neurodiversity/#comment-88793

I was thinking again about the consequences of having more small-effect deleterious mutations than average. I don’t think that they would push hard in a particular direction in phenotype space – I don’t believe they would make you look weird, but by definition they would be bad for you, reduce fitness. I remembered a passage in a book by Steve Stirling, in which our heroine felt as if her brain ‘was moving like a mechanism of jewels and steel precisely formed.’ It strikes me that a person with an extra dollop of this kind of genetic load wouldn’t feel like that. And of course that heroine did have low genetic load, being the product of millennia of selective breeding, not to mention an extra boost from the Invisible Crown.

Well, what does the distribution of fitness burden by frequency look like for deleterious mutations of a given fitness penalty?
It’s proportional to the mutation rate for that class. There is reason to believe that there are more ways to moderately or slightly screw up a protein than to really ruin it, which indicates that mild mutations make up most load in protein-coding sequences. More of the genome is made up of conserved regulatory sequences, but mutations there probably have even milder effects, since few mutations in non-coding sequences cause a serious Mendelian disease.

I have wondered if there was some sort of evolutionary tradeoff between muscles and brains over the past hundred thousand years through dystrophin’s dual role. There is some evidence of recent positive selection among proteins that interact with dystrophin, such as DTNBP1 and DTNA.

Any novel environment where higher intelligence can accrue more caloric energy than brute strength alone (see: the invention of the bow) should relax the selection pressure for muscularity. The Neanderthals didn’t fare so well with the brute strength strategy.
Sure: that’s what you might call an inevitable tradeoff, a consequence of the laws of physics. Just as big guys need more food. But because of the way our biochemistry is wired, there can be tradeoffs that exist but are not inevitable consequences of the laws of physics – particularly likely when a gene has two fairly different functions, as they often do.
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february 2017 by nhaliday
Links 2/17: Site Your Sources | Slate Star Codex
The United States not only does poorly on education benchmark PISA, but each decile of wealth also does poorly compared to equivalent deciles in other countries. I find this surprising. Does this torpedo the theory that each US ethnic group does as well as its foreign counterparts, and US underperformance is a Simpson’s Paradox on ethnic distribution?

Twitter: @EveryoneIsDril.

New Study Finds Performance-Enhancing Drugs For Chess. Okay, fine, just modafinil, which we already knew about, but the exact pattern is interesting. Modafinil makes people take longer to make their moves, but the moves are ultimately better. That suggests that its advantage is not increasing IQ per se, but in giving people the increased attention span/concentration to work harder on finding good moves. I think this elegantly ties together a lot of stuff into a good explanation of modafinil’s cognitive-enhancing properties.

New Zealand Wants To Know How Peter Thiel Became A Secret Citizen. Give up, New Zealand; Peter Thiel is a citizen of any country he wants to be a citizen of. Also: Peter Thiel Denies California Governor Run Despite Mysterious Group’s Backing.

I was going to link to the paper Physics Envy May Be Hazardous To Your Wealth, but the part that actually interested me is small enough that I’m just going to include it here as a jpg (h/t Julia Galef).

Nature: Prevalence And Architecture Of De Novo Mutations In Developmental Disorders. There’s been a lot of debate over paternal age effects, and this paper helps clarify that by actually counting people’s de novo mutations and finding that children of older fathers (and to a lesser degree older mothers) have more of them. I am not sure to what degree this answers the objection that fathers with worse genes will tend to get married later; my impression is that it’s circumstantial evidence against (de novo mutations are more specific to paternal age than just bad genes) but not complete disproof.

Psssst, kid, wanna buy a parasitic worm? Key quote: “Those who experience the ‘hookworm bounce’ tend to describe it as ‘feeling as if they are teenagers again'” (h/t pistachi0n).

New paper in Crime And Delinquency: “We find no evidence that the number of fatal police shootings either increased or decreased post-Ferguson. Claims to the contrary are based on weak analyses of short-term trends.” This is especially surprising in light of claims that increased inner-city crime is caused by police withdrawing in order to prevent further fatal shootings; if that’s the police’s plan, it doesn’t seem to be working very well.

Intranasal ghrelin vaccine prevents obesity in mice.

Gene drive testing thwarted when organisms quickly develop resistance. There goes that idea.

New poll: Majority of Europeans support banning Muslim immigration. It’s an Internet-based poll, which is always cause for suspicion, but they seem to be a reputable organization and not the sort of group whose results are 100% due to trolling by 4chan, plus it’s consistent with some other results. Still pretty shocking and an existential-terror-level reminder of partisan bubbles. Also: Rasmussen finds most Americans support Trump’s refugee ban order.

Closely related: M.G. Miles makes the case for banning Muslim immigration. Maybe the first person I have seen make this case in a principled way; everyone else just seems to be screaming about stuff and demanding their readers reinterpret it into argument form. Also, he uses the word “terrorism” zero times, which seems like the correct number of times for a case of this sort. This is what people should be debating and responding to. Rebuttals by Americans would probably want to start with the differences between Muslim immigrants to Europe and Muslim immigrants to the US – Miles discusses the European case, but by my understanding these are very different populations with very different outcomes).

Second Enumerations podcast: Grognor reading interesting essays.

SSRN: Extreme Protest Tactics Reduce Popular Support For Social Movements: “We find across three experiments that extreme protest tactics decreased popular support for a given cause because they reduced feelings of identification with the movement. Though this effect obtained in tests of popular responses to extreme tactics used by animal rights, Black Lives Matter, and anti-Trump protests (Studies 1-3), we found that self-identified political activists were willing to use extreme tactics because they believed them to be effective for recruiting popular support.” Cf. The Toxoplasma Of Rage. (h/t Dain)

The Cagots were an underclass of people in medieval France whom everyone hated, with various purity laws around how decent people weren’t allowed to associate with/marry/touch/go near them. In the 1500s, the Pope personally intervened to tell the French to stop persecuting them, but the French ignored him and persecuted them more than ever. As far as anyone can tell, they looked, spoke, and acted just like everyone else, and exactly how they became so despised is one of the minor mysteries of medieval history.
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february 2017 by nhaliday
Embryo editing for intelligence - Gwern.net
My hunch is CRISPR/Cas9 will not play a big role in intelligence enhancement. You'd have to edit so many loci b/c of small effect sizes, increasing errors. Embryo selection is much more promising. Peoples with high avg genetic values, of course, have an in-built advantage there.
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february 2017 by nhaliday
Evolution of Resistance Against CRISPR/Cas9 Gene Drive | Genetics
CRISPR/Cas9 gene drive (CGD) promises to be a highly adaptable approach for spreading genetically engineered alleles throughout a species, even if those alleles impair reproductive success. CGD has been shown to be effective in laboratory crosses of insects, yet it remains unclear to what extent potential resistance mechanisms will affect the dynamics of this process in large natural populations. Here we develop a comprehensive population genetic framework for modeling CGD dynamics, which incorporates potential resistance mechanisms as well as random genetic drift. Using this framework, we calculate the probability that resistance against CGD evolves from standing genetic variation, de novo mutation of wild-type alleles, or cleavage repair by nonhomologous end joining (NHEJ)—a likely by-product of CGD itself. We show that resistance to standard CGD approaches should evolve almost inevitably in most natural populations, unless repair of CGD-induced cleavage via NHEJ can be effectively suppressed, or resistance costs are on par with those of the driver. The key factor determining the probability that resistance evolves is the overall rate at which resistance alleles arise at the population level by mutation or NHEJ. By contrast, the conversion efficiency of the driver, its fitness cost, and its introduction frequency have only minor impact. Our results shed light on strategies that could facilitate the engineering of drivers with lower resistance potential, and motivate the possibility to embrace resistance as a possible mechanism for controlling a CGD approach. This study highlights the need for careful modeling of the population dynamics of CGD prior to the actual release of a driver construct into the wild.
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february 2017 by nhaliday
- quantum supremacy [Scott Aaronson]
- gene drive
- gene editing/CRISPR
- carcinogen may be entropy
- differentiable programming
- quantitative biology
- antisocial punishment of pro-social cooperators
- "strongest prejudice" (politics) [Haidt]
- Europeans' origins [Cochran]
- "Anthropic Capitalism And The New Gimmick Economy" [Eric Weinstein]

There's an underdiscussed contradiction between the idea that our society would make almost all knowledge available freely and instantaneously to almost everyone and that almost everyone would find gainful employment as knowledge workers. Value is in scarcity not abundance.
You’d need to turn reputational-based systems into an income stream
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november 2016 by nhaliday
The Third Sex | West Hunter
- eusociality and humans
- chromosome morphs
- green-beards and asabiya
- MHC/HLA and mating
- white-throated sparrows

Strategies: https://westhunt.wordpress.com/2017/12/27/strategies/
There is a qualitative difference between being XY and X0 (Turner’s syndrome). Being XY, a guy, is the physical embodiment of an evolutionary strategy: a certain genetic pattern that has a way of making more copies of itself. It’s a complex strategy, but that’s what it is. X0 people are sterile: they don’t generate more X0 individuals. Not every XY individual succeeds in reproducing, any more than every maple seed starts a new maple tree – but on average, it works. An X0 individual is the result of noise, errors in meiosis: Turner’s syndrome isn’t a strategy. In the same way, someone with Down’s syndrome isn’t Nature’s way of producing more people with Down’s syndrome.

Parenthetically, being a guy that tries to reproduce is a strategy. Actually reproducing is a successful outcome of that strategy. Similarly, being an alpha dude in a polygynous species like elephant seals is not a strategy: trying to be an alpha dude is the strategy. I see people confuse those two things all the time.


Natural selection tends to make physical embodiments of a successful reproductive strategy common. So stuff like Down’s syndrome, Turner’s syndrome, androgen insensitivity, etc, are all rare. Successful evolutionary strategies usually involve actually getting things done: so there is a tendency for natural selection to develop and optimize various useful abilities, like walking and talking and thinking. All part of the strategy. Many non-strategies [like Downs or Fragile X] mess up those abilities


Is there any evidence for alternate evolutionary strategies in humans, other than just male and female? Not really, so far. For example, schizophrenia looks more like noise, sand in the gears. Not much of the schiz genetic variance shows up in GWAS samples: it looks like it’s mostly driven by rare variants – genetic load. There may actually be some truth to the notion that happy families are all alike.

So, is sex a spectrum in humans? No: obviously not. Two basic strategies, plus errors.

Why would a geneticist be unable to make the distinction between an evolutionary strategy and an error of development (i.e. caused by replication errors of pathogens)? Well, the average geneticist doesn’t know much evolutionary biology. And being embedded in a university, the current replacement for old-fashioned booby hatches, he’s subject to pressures that reward him for saying stupid things. and of course some people are pre-adapted to saying stupid things.

My whole point was that you can explain the qualitative difference without being in any way teleological. You’d do better to think about positive igon-values than Aristotle.
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october 2016 by nhaliday
The Future of Genetic Enhancement is Not in the West | Quillette

If it becomes possible to safely genetically increase babies’ IQ, it will become inevitable: https://www.washingtonpost.com/news/volokh-conspiracy/wp/2015/07/14/if-it-becomes-possible-to-safely-genetically-increase-babies-iq-it-will-become-inevitable/

Baby Genome Sequencing for Sale in China: https://www.technologyreview.com/s/608086/baby-genome-sequencing-for-sale-in-china/
Chinese parents can now decode the genomes of their healthy newborns, revealing disease risks as well as the likelihood of physical traits like male-pattern baldness.

China launches massive genome research initiative: https://news.cgtn.com/news/7767544e34637a6333566d54/share_p.html

research ethics:
First results of CRISPR gene editing of normal embryos released: https://www.newscientist.com/article/2123973-first-results-of-crispr-gene-editing-of-normal-embryos-released/
caveats: https://ipscell.com/2017/08/4-reasons-mitalipov-paper-doesnt-herald-safe-crispr-human-genetic-modification/

So this title is a bit misleading; something like, "cells edited with CRISPR injected into a person for the first time" would be better. While CRISPR is promising for topological treatments, that's not what happened here.
China sprints ahead in CRISPR therapy race: http://science.sciencemag.org/content/358/6359/20
China, Unhampered by Rules, Races Ahead in Gene-Editing Trials: https://www.wsj.com/articles/china-unhampered-by-rules-races-ahead-in-gene-editing-trials-1516562360
U.S. scientists helped devise the Crispr biotechnology tool. First to test it in humans are Chinese doctors



lol: http://www.theonion.com/infographic/pros-and-cons-gene-editing-56740

Japan set to allow gene editing in human embryos [ed.: (for research)]: https://www.nature.com/articles/d41586-018-06847-7
Draft guidelines permit gene-editing tools for research into early human development.
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august 2016 by nhaliday

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