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If I get my DNA sequenced at 23andMe or DecodeMe, what information do I get? Is my privacy safe?

If my parents do it too, will it tell me where recombination happened in each chromosome? Btw, does anyone know of a visualization of the chromosomes showing some genes (and corresponding phenotypes)?

Kinda like this but more general-purpose and for laypeople.


Apparently, there is uncertainty about exactly which chromosomes contain genes related to eye color. GNXP.

As much as I dislike popsci, being a layman, this looks like the best explanation that I can understand (of the ones I could find through Google) of the fact that two blue-eyed parents can have a brown-eyed child:
Eye color is a complex trait that depends on the state of several interacting genes. The gene that usually decides the issue (blue eyes or brown eyes) is the OCA2 gene on chromosome 15. But it comes in different strengths. A person with a weak form of the OCA2 gene will have blue eyes. Likewise a person with a strong form will have brown eyes.

The plot thickens, though, because an individual also has other eye-color genes that each has a say in the final eye-color outcome. For example, if one of these lesser genes is strong, it can make the weak form (blue) of OCA2 work much more effectively — almost like the strong form (brown). Then the eye color may be a light brown or muddy grey. In fact, the resulting color can be any shade of brown, hazel/green, or blue depending on the strengths of the interactions.
Of course, there's mutation, but I'd expect that to be too rare to explain this phenomenon.


Now, blue-blue couples almost always have blue-eyed kids. This article is about the theory that blue-eyed men are more attracted to blue-eyed women because cheating would be easy to catch... of course, this wouldn't be that useful in populations where >%80 of the men are blue-eyed (and most of the others are heterozygotes).

So should we expect this effect to be stronger in more mixed populations? I imagine so; not because the blue-eyed men in those regions have stronger genes for blue-eye preference (this is bordering on silly), but because sexual attraction has a cognitive component. (The cognitive theory predicts adaptation within 1 generation; the natural selection theory would require many. But my main reason for believing the former is that the idea of such a specific gene sounds silly.)

In any case, this suggests that blue-eyed kids have enjoyed more paternal attention than brown-eyed kids.

The natural selection theory (though I'm not sure if anyone believes it) would be an instance of a common fallacy: "there's a gene for everything, no matter how specific".
gusl: (Default)
cavewomen, talking to each other:

A- Look at his head, he must be at least 30!
B- OMG! To have lived that long, he must have really good genes.
A- I saw him first!
gusl: (Default)
A- Why do peacocks have huge tails?
B- Because peahens find them attractive.
A- and why do they?
B- because it's a handicap: any peacock that survives with such a ridiculously long tail must be pretty fit otherwise. His genes must be good.
A(1)- well, why do we care about "otherwise"? It's not like the peacock can chuck his tail when he's in danger, so any kids coming out of this mate will suffer all the same negative effects of this handicap. Are these females just hoping that future females will find their kids attractive for no good reason too? Are they betting on the Equal Fool Theory?
B(1)- there are probably mathematical principles (as well as empirical evidence) explaining why a peacock with such a handicap is still fitter than one without one.
A(2)- So the purpose of the tail is to impress females, right? Well, this seems to answer all of our questions, doesn't it? The problem is that this is a case of co-evolution: how did the peahens come to find long tails attractive in the first place? It's not like they could reason "well, if he has such a large handicap, then he must be good to mate with!". Attraction doesn't involve logical reasoning*: it is hard-coded genetically! So it would require an enormous coincidence for the long-tail mutation to come at the same time as the long-tails-are-attractive mutation in a large enough number of individuals simultaneously.
B(2) - Larry Gonick to the rescue!

(in case the link breaks, the answer is: learning biases in neural networks. A NN trained to identify "male" will respond more strongly to huge tails.)

(*) it is interesting to think about whether and how logical reasoning affects. In human, such reasoning processes can definitely affect attraction. Maybe this is due to our strong ability to imagine.
gusl: (Default)
from Wikipedia: Liger
It is believed that this is because female lions transmit a growth-inhibiting gene to their descendants to balance the growth-promoting gene transmitted by male lions. (This gene is due to competitive mating strategies in lions.) A male lion needs to be large to successfully defend the pride from other roaming male lions and pass on his genes; also, in prides with multiple male adult lions, a male's cubs need to be bigger than the competing males for the best chance of survival. Thus, his genes favor larger offspring. A lioness, however, will have up to 5 cubs, and a cub is typically one of many being cared for in a pride with many other lions. As such, it has a relatively high survival rate, and need not be huge as it will not need to look after itself very quickly. Smaller cubs are more easily cared for and fed and are less strain on the pride; hence, the inhibiting gene developed.

This is very unsatisfactory! Since it's lacking references, I am including it here as an instance of psychoceramics. It exemplifies a common sort of confusion.

His argument basically says that male lions are predisposed to have large children, and female lions to have small children. The problem is that the article tries to explain this difference by talking about 100% Lion prides, in which these children are the same: each cub will be the child of exactly one male lion and one female lion! At each breeding instance (disregarding opportunity costs), the Darwinian score of the father due to this child is exactly the same as the Darwinian score of the mother due to this child. So if anything, natural selection should make them work in unison!

One could read the article as suggesting that the Darwinian score of male cubs would gain from a marginal increase in size, while female cubs would gain from a marginal decrease in size. This seems plausible, but this would be plain sexual dimorphism, and there's no reason why one parent should contribute more to it than the other.

Anyway, a related idea:
If X chromosomes promote smallness and Y promotes largeness,
then a lion's X + a tiger's X should make a female Liger whose size is between that is tiger and lion females.
gusl: (Default)
I've been analyzing more evolution stuff, inspired by [ profile] tdj. Maybe I'm going a bit overboard (I probably misinterpreted the original meaning, but such speculations are fascinating anyway)

In response to Study reveals a way disease bacteria sense antimicrobials and initiate a counter-defense:
Many living things, from fruit flies to people, naturally produce disease-fighting chemicals, called antimicrobial peptides, to kill harmful bacteria. In a counter move, some disease-causing bacteria have evolved microbial detectors. The bacteria sense the presence of antimicrobial peptides as a warning signal. The alarm sets off a reaction inside the bacteria to avoid destruction.

University of Washington (UW) and McGill researchers have revealed a molecular mechanism whereby bacteria can recognize tiny antimicrobial peptide molecules, then respond by becoming more virulent.

I wrote:

Whoa, such a mechanism could evolve even if it kills the host and stops the bacteria from multiplying. How? Co-evolution: the conditional virulence causes hosts to stop producing antimicrobials (since the ones who produce them die more).

Therefore, the bacteria populations that *do* respond by becoming more virulent have a stable strategy. This is game theory! The 2 players are: HOST'S GENES, and BACTERIA'S GENES, and each player has 2 strategies.

Let's assume virulent reactions to peptide kills the host (-10 for the host).
 \   HOST     peptide   no peptide

virulent     (-10, -1)    (-1, +1)

non-virulent (0, 0)       (-1, +1)


as long as there is a credible threat of virulence, hosts may "choose" to not produce peptide. I think the evolutionarily stable solution is "mixed strategies".

Individual bacteria do better by not killing the host, but whole bacterial populations that co-evolve with the host do better by having some individuals who become virulent (sacrificing themselves for the greater good of their family), thus "forcing" the host populations' genes to play "no peptide".

I find it plausible that group selection is a strong enough force in bacterial evolution.
gusl: (Default)
It looks like malaria somehow makes its host more delicious to mosquitoes, via [ profile] tdj
Mosquitoes are more attracted to people already infected with malaria. And this appears to be because the malarial parasite orchestrates its own onward transmission from within the human body, a new study suggests.
“What’s surprising is that this is not to the advantage of anybody but the parasite,”...“This tremendously important interaction for the person and the mosquito – both can die as a result – is being engineered by the parasite.”

This "engineering" is natural selection: parasites who implement the mechanism multiply more.

But it seems really unlikely that you could orchestrate both sides of the deal via random mutations... so one of them must have been accidentally tuned to start with (before this mechanism evolved): either (1) the different human smell became a side-effect of the parasite while the effect on the mosquito's attraction to that smell has always been the same; or (2) the other way around (effect on human smell always been the same, effect on mosquito behavior evolved). The first seems more likely, especially since the evidence says nothing about the parasite influencing mosquito behavior.

I would bet that, if for some reason mosquitos stop being attracted to that smell, there is nothing the parasite can do about it. (the alternative would be that the parasite could quickly adapt to make infected mosquitos attracted to that smell again, but my claim here is there would have to be a big fluke for them to hit upon such a mechanism (since mutation is random), unless a similar thing were already encoded in the parasites' genes)
gusl: (Default)
thread at [ profile] tdj's about carbon-dating individual human cells (it's a very clever idea):

In discussing the required experimental precision / error, I proposed:
Here's a causation network:

A: atmospheric levels of C14 at time of cell's birth
B: initial amount of C14 in cell's DNA (i.e. at birth)
C: time passed since cell's birth
D: amount of C14 in the cell's DNA
E: "measured" amount of C14 in the cell's DNA (this is actually an estimation based on a measurement of radiation emitted by the cell)

  B   C
   \ /

In order to infer C, we need to know B and D (this inference step is pretty much dead-on if you have enough C14 atoms (by the law of large numbers)). We estimate D as E (noisy, experimental measurement), and B from A (also noisy, say due to non-uniform C14 levels + random variation in the cell birth process (?); one estimation for each point in history, although this "estimation" may be analytic, not statistical).

How many carbons atoms are there in DNA?
...discussion continues...

I really love making models like this.

I'm sure I've linked to CMU's Tetrad Project / Causality Lab before. But it never hurts to give them another plug.


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