I think the phenotype of the sperm (including its behaviour) is determined mainly by the genes of the parent (the sperm producer), not the sperm itself. So I'm not sure that Hamilton's rule really comes into it.

Hamilton's rule implies that as relatedness increases, the benefit must be nearer and nearer the cost in order for altruism to evolve. That seems pretty counter-intuitive. I would've expected exactly the opposite, altruism more likely to evolve in more related populations.

That is, if you have something of fixed cost, let's say 1, as the entities become more and more related the benefit to the recipient must approach 1 in order for altruism to evolve. Learn something every day, I guess. Or am I misunderstanding?

Tim, You have it backwards- as relatedness increases, the the likelihood of helping increases as well

P-ter- nitpicking here, but it is an important point- Hamiltons rule is not general to altruism, but instead is specific to one particular hypothesis for it evolution- kin selection.

There are 2 other hypotheses for th eevolution of altruism: 1, Reciprocal altruism by Trivers, and Group Selection.

On an aside- I blogged this story as well, and have more or less the same content as you do. I however propose that studies like this be based not in indirect measures of sperm competition (like testes size) but instead a direct measure like Clutton Brock's extra group copulation, or data from mating systems study.

I think the phenotype of the sperm (including its behaviour) is determined mainly by the genes of the parent (the sperm producer), not the sperm itself.

what do you mean? the phenotype of the sperm is determined mainly by the genes of the parent because the sperm has half of those genes, right? you could make the same argument about any individual- their behavior is determined mainly by the genes of their parents (since they get half from each). this doesn't negate hamilton's rule.

That is, if you have something of fixed cost, let's say 1, as the entities become more and more related the benefit to the recipient must approach 1 in order for altruism to evolve

if there's a fixed cost of one, as relatedness increases, the necessary benefit for altruism to evolve decreases. if both the cost and the benefit are fixed, once relatedness passes a certain point, altruism can evolve.

Hamiltons rule is not general to altruism, but instead is specific to one particular hypothesis for it evolution- kin selection.

true, true. but none of those hypoetheses are mutually exclusive; this seems like a perfect situation for altruism through kin selection to evolve.

If there's a fixed cost of one, as relatedness increases, the necessary benefit for altruism to evolve decreases.

an example: if r=0.5 and C=1, altruism can evolve if B>2C.

now, if r=1, altriusm can evolve if B>C.

So yes, you have it reversed.

p-ter:

If the genes in the sperm aren't the ones building and controlling the sperm's behavior while swimming up to fertilize the egg, then there's no mechanism for kin selection (or any other kind of selection) to operate from those genes. Instead, the father's genes are probably selected for producing sperm that work together to make one of their number a winner.

Now, if the genes in the sperm are the ones controlling some aspect of the sperm's construction or behavior, we'd expect kin selection. In that case, we would expect both trying to gang up with other sperm from the same parent to make sure one of your number wins, and trying to gang up with other sperm which share more of your genes, if there's a mechanism available to make that distinction. Right?

Matt: Thanks, a biologist friend of mine explained on a different forum.

Albatross: “If the genes in the sperm aren't the ones building and controlling the sperm's behavior while swimming up to fertilize the egg, then there's no mechanism for kin selection (or any other kind of selection) to operate from those genes.”

Yes.

Many species have an extended haploid life stage. In the haploid stage there aren’t backup gene copies, so harmful mutations would be fully exposed to selection.

Wouldn’t it be cool if the human sperm life stage filtered harmful mutations in the cellular “housekeeping” genes? However, there seems to be no transcription during the sperm life stage (the DNA is tightly packed) so the genes carried in the sperm don’t affect the sperm competition. No filtering. Sigh.

Could mitochondria be filtered during sperm competition? During the sperm stage the mitochondria are very active. However, in humans little to no male mitochondria are incorporated into the fertilized egg. No filtering. Sigh.

haploid sperm are built from diploid progenitor germ cells. the diploid to haploid transition occurs at a particular stage. you'd have to know when the mechanism is established to know what genome is involved. it could go either way, but i'd bet on the haploid genome being involved.

http://devcell.bio.uci.edu/ image...MATOGENESIS.jpg

here's a good cartoon of spermatogenesis

I don't see the trains?

role of the haploid genome in sperm development:

In addition to gene transcription in diploid cells during meiotic prophase, certain genes are transcribed in the spermatids (reviewed in Palmiter et al. 1984). This evidence for haploid gene expression comes from studies involving heterozygous mice, in which two different populations of sperm are seen to exist—one population expressing the mutant phenotype and one population expressing the wild-type trait.

it is also hypothesized that dwarves (who are heterozygous for the causal mutation) preferentially pass on the causal allele becuase it conferrs some benefit to the sperm:

The observed human sperm mutation frequency cannot explain the achondroplasia paternal age effect...a number of alternatives may explain this discrepancy, including selection for sperm that carry the mutation

I don't see the trains?

the big multi-tailed white blobs are bunches of sperm, and the little ones are single sperm.

PLoS writes: "If there were some mechanism by which more closely-related sperm could preferentially group together, the necessary benefit for Hamilton's rule to apply would be greatly decreased, and the number of sperm willing to act altruistically greatly increased."

What restrictions can be placed on such a mechanism? Such a mechanism must express on the exterior of the sperm some recognizable trait corresponding in a one-to-one relationship to the genetic contents of the nucleus, or at least to a random sample of those contents, right? And wouldn't it need to include a one-to-one expression-to-recognition relationship also be required between any two sperm? That sounds complex and cumbersome, but I cannot think of a simpler mechanism. Can anyone?

"what do you mean? the phenotype of the sperm is determined mainly by the genes of the parent because the sperm has half of those genes, right? you could make the same argument about any individual- their behavior is determined mainly by the genes of their parents (since they get half from each). this doesn't negate hamilton's rule."



I didn't think that the haploid genome was active inside the sperm, but I may be wrong.

Assuming that the phenotype of the sperm is determined by the parental (diploid) genome, then any gene in the parent has an equal chance of being represented in each sperm, and, from the point of view of a gene in the parent, every sperm is equally valuable. It will be advantageous to a gene in the parent to influence the phenotype of sperms in such a way as to maximise the number of sperms (any of the parent's sperms) which succeed in fertilising eggs. If this can be achieved by making sperms polymorphic, with some of them being 'self-sacrificial', then parental sperm-making genes may be selected for this effect. It has nothing to do with Hamilton's Rule. By analogy, some females produce 'trophic eggs', which do not develop but are eaten by other offspring. I don't think anyone would suggest that the genes in the trophic eggs themselves have been selected for altruism!

Yeah that's not how trains work. Sperm bouquets more like.

Yeah that's not how trains work. Sperm bouquets more like

true. maybe in other species it's more train-like.
http://www.plosone.org/article/ s...ne.0000170.g002

What restrictions can be placed on such a mechanism? Such a mechanism must express on the exterior of the sperm some recognizable trait corresponding in a one-to-one relationship to the genetic contents of the nucleus, or at least to a random sample of those contents, right?

yeah, you could sort of imagine a number of expressed proteins at different places in the genome, where sperm tend to associate with other with more similar protein complexes, thus shifting the distribution of r between those sperm up from 0.5. admitedly, it doesn't sound that likely.. What restrictions can be placed on such a mechanism? Such a mechanism must express on the exterior of the sperm some recognizable trait corresponding in a one-to-one relationship to the genetic contents of the nucleus, or at least to a random sample of those contents, right?

I didn't think that the haploid genome was active inside the sperm, but I may be wrong.

it eventually becomes in active, but is definitely active at some points in development.

whoa, must have re-pasted kohler's comment on the end of mine. oops.

...supposing on the other hand that the sperm's phenotype *is* influenced by the haploid genotype, then I agree that Hamilton's Rule would apply. The question then is: would the aggregate benefit to related sperms (with r = 1/2) be greater than twice the cost to the 'altruist'? I don't know, but we should remember that only a very small percentage of sperms are likely to fertilise an egg, so the cost to a self-sacrificial sperm may actually be very small, e.g. it may only be sacrificing a 1 in a million chance of fertilising an egg.

P-ter: “it eventually becomes in active, but is definitely active at some points in development.”

How long does the haploid spermatid cell stage last? How much of the genome is expressed during the haploid stage? My impression from reading your earlier links is that there is some haploid gene expression but probably not much.

I’d like to believe that many of the housekeeping genes are active in the spermatid stage. Those genes are highly conserved and mutations are very unlikely to be beneficial. Filtering harmful mutations at the spermatid stage would be efficient.

Also is there significant gene expression during the haploid ootid stage? Could significant filtering be occurring during egg production?

How long does the haploid spermatid cell stage last? How much of the genome is expressed during the haploid stage? My impression from reading your earlier links is that there is some haploid gene expression but probably not much.

yeah, good questions. I did a quick cursory search, and it doesn't look like there have been any microarray experiements on sperm or developing haploid spermatids. so, well, buy some arrays and figure it out :)

Could mitochondria be filtered during sperm competition? During the sperm stage the mitochondria are very active. However, in humans little to no male mitochondria are incorporated into the fertilized egg. No filtering. Sigh.

The question of why none of the male mitochondria are transferred to the fertilized egg came up in a chemical biology class I'm taking this semester. The professor asked the GSI to look up the answer on the internet, and it turns out the sperm's mitochondria are ubiquitinated so that they are destroyed upon fertilization. Nobody could find an answer as to WHY (in a sense of evolutionary benefit) this happens, though.

arosko: "it turns out the sperm's mitochondria are ubiquitinated so that they are destroyed upon fertilization."

The last time I looked at this topic the result was complex. Purely from a size perspective there should be a thousand times more female mitochondria than male mitochondria in the fertilized egg. And in some mammals about 1 in a thousand mitochondria sppear to derive from the male. But as you note in some mammals none of the mitochondria come from the male. When last I looked, the question of male mitochondria contributing to the human fertilized egg was an open question. In any case the amount contributed would be small and sperm could not act as a filter that maintained mitochrondial quality.

Arosko, do you have a link for "the sperm's mitochondria are ubiquitinated"? I know that ubiquitinated proteins are those that are targeted for recycling. What does that mean for mitochondria? Are the mitochondrial proteins embedded in the mitochondrial membrane tagged?

Fly:

Do you have any idea how that would affect the mapping of human populations done from mtDNA? Once a couple of my mitchondria make it into my daughters, they're all carrying those mitochondria, too, and should be able to pass them normally.