Allan, Allan, Allan,

The infection by viruses of hosts is not the sex, it is the exchange of genetic material between two viral strains which is the sex part. I was not talking about retroviral infection of the host [although that sometimes occurs]. Nor is bacterial conjugation the same as eusexual process either. And we don't know that bacterial sex is not homologous-it could be.

The main part of this is HGT -the mixing of genes within populations to provide favourable combinations, not the specific process itself. Bdelloids rotifers do not need sex, because they have massive HGT. Thus, although they are "asexual" they avoid most of the costs of asexuality.

Sure, the complex metazoans or plants that have nice sophisticated sexual systems with deiocy, specialised sex chromsomes and all the rest of it is fine. But the sex we see today must have evolved from simpler systems. And for that, bacteria and viruses are good models to show aspects of these processes evolving.

Darwinsbulldog wrote:Allan, Allan, Allan,

The infection by viruses of hosts is not the sex, it is the exchange of genetic material between two viral strains which is the sex part. I was not talking about retroviral infection of the host [although that sometimes occurs].

Soz - misunderstood!

Darwinsbulldog wrote:Nor is bacterial conjugation the same as eusexual process either. And we don't know that bacterial sex is not homologous-it could be.

It really ain't! Correction - parts of the overall process have obvious homologues, eg in the DSB repair pathways (eg RecA homologues RAD51 and Dmc1). Homologous repair is ancient. But the overall processes themselves - the means by which two .. umm... homologous sections of DNA get together in the first place, and the active induction of DSB's - these are not homologous with the bacterial setup. If you see the bacterial process of recombination building around itself a complex set of mechanisms to get not-quite-homologues together in order to recombine their variant genes by crossover (a fundamentally different way of recombining from the bacterial), then I'd say you've put the cart before the horse. I'd doubt that bacterial recombination evolved into eukaryotic recombination, although certain elements were co-opted. Mitosis first, then meiosis (as a derivative of mitosis) and then gametogenetic recombination (as a derivative of DNA topological management and homologous repair). But before you get this, you need diploids - ie syngamy.

Darwinsbulldog wrote:The main part of this is HGT -the mixing of genes within populations to provide favourable combinations, not the specific process itself. Bdelloids rotifers do not need sex, because they have massive HGT. Thus, although they are "asexual" they avoid most of the costs of asexuality.

Sure, the complex metazoans or plants that have nice sophisticated sexual systems with deiocy, specialised sex chromsomes and all the rest of it is fine. But the sex we see today must have evolved from simpler systems. And for that, bacteria and viruses are good models to show aspects of these processes evolving.

Nah. I agree that we must start with simpler systems, which is precisely why I suggest the cellular sequence of events I do. Rotifers are secondary asexuals, and multicellular. Multicellularity is a consequence of sex - we are part of one of several clades that discovered asexual amplification of a diploid soma was an excellent way of protecting an asexually amplified diploid germ line - all competing interests kept largely in check by kin selection and the gamete bottleneck. Rotifers indeed buck the trend among modern eukaryotes that seems to cause elimination of secondary asexuals. But this was not the issue when the world was universally asexual and unicellular. I'm not talking metazoans and plants, but single-celled ancient protists. It is the things that bacteria and viruses don't do that, I think, explain the origins of our process.

All eukaryotes either do recombinational meiosis, or have ancestors that did. The DSB-inducing enzymes in every single one, Spo11, are homologous, derived from archaeal topoisomerase. This lies at the heart of eukaryote recombination. No DSB's, no crossover. But further, DSB's can only create a crossover product in a diploid cell. How do you get a diploid cell? Two ways: endomitosis or haploid fusion. If the source is endomitosis, the recombinant products are identical - recombination has no effect. Which, if variation matters, leaves us with haploid fusion - syngamy. But this has an effect beyond creating homologues for recombination - diploidy. And like many commentators, you scoot straight past that to get to the recombinatorial consequences for the wider population. But diploidy is an important state.

If you start with recombination, you have to explain how and why everything else buit up around it. But to even get to the recombination stage in a sexual organism, you have to get whole chromosomes together. And the assumed 'point' of it all - variation, just like HGT-mediated recombination in other groups - was absent on day 1. You can get a kind of group-selective explanation to work - recombinant populations survived more often than non-recombinant ones - but in order for such populations to arise in the first place, you need to get some organisms recombining, with - for the eukaryotic variety - the necessary complexities of syngamy, meiosis and diploidy all in place. For their causality you need to appeal either to drift or some direct benefit of those processes. And I think there is just too much needing to go on at once for the dubious benefits of recombination to be the driver. Syngamy is complex, diploidy is complex, reduction is complex, recombination is complex. How much unrewarded complexity can we get in place neutrally, before we start to see some return?

I think that elevating recombination to prime cause of the rest is not borne out by the fundamental nature of the process - a haploid-diploid cycle unique to eukaryotes, and near-universal within them. This cycle is something bacteria and viruses do not do. Those eukaryotes that do not do it have 'frozen' at some historic diploid combination that arose through syngamy.

And it is to this fundamental cycle that I would appeal for an explanation of the essence of eukaryotic sex. If you have a population of free-living haploid eukaryotes, replicating through mitosis (with diploidy a transient step), you have a process that can be easily modified to allow periodic mutualism - two haploids come together in the same cell and, when circumstances change, revert to haploidy using the pre-existing machinery of mitosis. The advantages could be nutritional, or there could be a benefit of hybrid vigour, or the masking of deleterious mutations. But, ultimately these organisms are haploid, and that is the state to which they return.

In the diploid state, there is also the opportunity to fine-tune homologous DNA repair. Accidental breaks can be repaired by aligning and splicing in a patch from the homologue in interphase cells, rather than just at mitosis.

Then, the stage is set for homologous recombination during reduction, by the very simple step of inducing DSBs.

This scenario breaks the whole sequence of acquisition of complexity down into bite-size, manageable chunks, mostly co-opting existing processes, and relies more upon local benefit to the organism than distant population-level consequences.

"Recent Acceleration of Human Adaptive Evolution"
(Department of Anthropology, University of Wisconsin)

Genomic surveys in humans identify a large amount of recent positive selection. Using the 3.9M HapMap SNP dataset, we found that selection has accelerated greatly during the last 40,000 years. We tested the null hypothesis that the observed age distribution of recent positively selected linkage blocks is consistent with a constant rate of adaptive substitution during human evolution. We show that a constant rate high enough to explain the number of recently selected variants would predict (1) site heterozygosity at least tenfold lower than is observed in humans, (2) a strong relationship of heterozygosity and local recombination rate , which is not observed in humans, (3) an implausibly high number of adaptive substitutions between humans and chimpanzees, and (4) nearly 100 times the observed number of high-frequency LD blocks. Larger populations generate more new selected mutations, and we show the consistency of the observed data with the historical pattern of human population growth. We consider human demographic growth to be linked with past changes in human cultures and ecologies. Both processes have contributed to the extraordinarily rapid recent genetic evolution of our species.



Human populations have vastly increased in numbers during the past 50,000 years or more [1]. Under theory, more people means more new adaptive mutations [2]. Hence, population growth should cause an increase in the rate of adaptive substitutions: an acceleration of new positively selected alleles. In humans, this effect may have been augmented by vast changes in cultures and ecology during the Late Pleistocene and Holocene, creating new opportunities for adaptation. Such acceleration does not require any change in the per-genome rate of adaptive mutations; it is a simple effect of changing demography, possibly increased by changing ecology. The best analogy may be the rapid recent evolution of domesticates such as maize [3, 4].
Human genetic variation appears consistent with a recent acceleration of positive selection. A new advantageous mutation that escapes genetic drift will rapidly increase in frequency, more quickly than re-combination can shuffle it with other genetic variants [5]. As a result, selection generates long-range blocks of linkage disequilibrium (LD) across tens or hundreds of kilobases, depending on the age of the selected variant and the local recombination rate. The expected decay of LD with distance surrounding a recently selected allele provides a powerful means of discriminating selection from other demographic causes of extended LD, such as bottlenecks and admixture [3, 6]. Previously, we applied the LD decay (LDD) test to SNP data from Perlegen and the HapMap [7], finding evidence for recent selection on approximately 1800 human genes. We refer to these as ascertained selected variants (ASVs). This number encompasses some 7% of human genes, and is consistent with the proportion found in another survey using a related approach [6]. Because LD decays quickly over time, most ASVs are quite recent [8], in comparison to other approaches that detect selection over longer evolutionary timescales [9, 10]. Many human genes are now known to have strongly selected alleles in recent historical times, such as lactase [11, 12], CCR5[13, 14], and FY [15]. These surveys show that such genes are very common. This observation is surprising: in theory, such strongly selected variants should be rare [2, 16]. The observed distribution seems to reflect an exceptionally rapid rate of adaptive evolution.

What's this mean in english? It all sounds like some kind of religious/evolutionary double-talk to me.

So... basically, More sex --> More highly selective genes --> Faster evolution?? Or what?
I always thought it was the other way around, since rapid depopulation from a meteor or something would lead to more selection pressure.

jamest wrote:The desire to have sex has little to do with wanting to have kids. Indeed, for most of us, the desire to have kids (if we have that desire) has little to do with wanting to reproduce 'something' like ourselves. Further, the sex-drive persists in those that cannot have, or, who do not want kids: gays; lesbians; post-menstrual women; etc.. The sex-drive, then, appears to transcend its physical function.

... The charge then, is that the Darwinian explanation for our sex-drives falls-short. That is, our sex-drive is not primarily grounded in the need/desire to pass on our genes, or to reproduce 'something like ourselves'. Further, as I see it, Darwinism allows for no [prolonged] attributes of a species which do not:

a) Help that species survive amidst its environment.
b) Promote the reproduction of that species.

... Therefore, according to the Theory of Evolution [as I see it], there should not be an abundance of gay/lesbian people, or of any other kind of people who have sex with no hope of reproduction as its yield. An abundance of such individuals, with such desires/attributes, should not exist... since 'evolution' [apparently] selects for the best survivors and the most proficient reproducers. As I see it, gays; lesbians; post-menstrual women; etc., should have been ~phased out~ long ago.

Of course, I'm speaking primarily from a human perspective here. I have no real idea of how my thoughts pan-out with regards to the animal kingdom as a whole. However, I have several memories of dogs trying to shaft my lower leg, which to my mind is an inefficient way of reproducing 'a dog like me'.

Just chewin' the fat, here. Wondering what the experts have to say on the matter. Cheers.

i don't think you understand evolution very well.
what has sex drive got to do with evolution, anyway? how did you put these 2 together, and then as a paradox?
sex drive is the head, it a mental apparition.
as for the animals they have a chemically induced sex drive...mating.
we also actually have pheromones, and such, and also a larger quantity of free time. yep i said it. yes we work and such, but animals are preoccupied with living, getting places, etc. they have little time for creative thinking, although they are intelligent.
see i think we too have chemically induced sexdrives (pheromones, testesarone, etc), but we are just n the process of understanding. These come with evolution, so in this perspective, there you go, sex drive is included in evolution, although I am sure you were referring to sex drive produced by the mind.
as for the extra sex besides this, it is mostly mental, coming from ads, movies and plenty of spare time, plus a false sense of machismo, etc.
I am sure this has already been proven.
hence the extra sex drive is outside evolution.
please also note that we have stepped out from evolution some time ago.
generally humans are have stepped outside evolution. we are shaping our own fate. wether for good or bad, only time will tell.
even know, to phrase it respectfully, the unruling, unlawful, unthinking mob is in charge. people who are creative (i believe our evolutionary advantage) are ridiculed, mocked, and by and large cast away and not able to reproduce, or do it properly.
evolutionarily these would be the kings. however our false world views, etc has created a climate, and view where we reward the idiotic, and make the great average the hero.
i do believe we are all born to be equally creative. nonetheless we end up in other places.
this has nothing to do with color, sex btw.
i know many will crucify me for what i wrote, but someone has to state the obvious.
sexdrive is exactly a good point. sex is important, but the sexdrive is just plain manipulation. in the end all that matters is successful reproduction, not the drive, which is mental, and the rest (see above) accounted for bz evolution, just not fully understood.
what is more interesting is that we (western world) have a higher sex drive and yet are infertile and not reproducing. This is further proof, that it is outside the evolutionary theory.
sex is fun. i love it. however, it is highly overrated. people worry about it too much, attach a false sense of security, etc.
it is just an "act". at best it is a show of emotion.

QuantumKitty wrote:
What's this mean in english? [...]

So... basically, More sex --> More highly selective genes --> Faster evolution?? Or what?

No, it's not saying more sex, just more survival among offspring, hence population growth.

QuantumKitty wrote:I always thought it was the other way around, since rapid depopulation from a meteor or something would lead to more selection pressure.

You don't need something external to destroy the members of a niche in order to adapt towards it. Beneficial mutations increase offspring, which both supplants weaker alleles in the species, and supplants other species competing in the niche. The concept of selection 'pressure' can be misleading. To the metaphorical extent that it is a 'force', it is one of high pressure from the population, not low pressure 'sucking out' change from the genome. Empty niches are easier to occupy, though.

jamest wrote:The desire to have sex has little to do with wanting to have kids. Indeed, for most of us, the desire to have kids (if we have that desire) has little to do with wanting to reproduce 'something' like ourselves. Further, the sex-drive persists in those that cannot have, or, who do not want kids: gays; lesbians; post-menstrual women; etc.. The sex-drive, then, appears to transcend its physical function.

... The charge then, is that the Darwinian explanation for our sex-drives falls-short. That is, our sex-drive is not primarily grounded in the need/desire to pass on our genes, or to reproduce 'something like ourselves'. Further, as I see it, Darwinism allows for no [prolonged] attributes of a species which do not:

a) Help that species survive amidst its environment.
b) Promote the reproduction of that species.

... Therefore, according to the Theory of Evolution [as I see it], there should not be an abundance of gay/lesbian people, or of any other kind of people who have sex with no hope of reproduction as its yield. An abundance of such individuals, with such desires/attributes, should not exist... since 'evolution' [apparently] selects for the best survivors and the most proficient reproducers. As I see it, gays; lesbians; post-menstrual women; etc., should have been ~phased out~ long ago.

Of course, I'm speaking primarily from a human perspective here. I have no real idea of how my thoughts pan-out with regards to the animal kingdom as a whole. However, I have several memories of dogs trying to shaft my lower leg, which to my mind is an inefficient way of reproducing 'a dog like me'.

Just chewin' the fat, here. Wondering what the experts have to say on the matter. Cheers.

I think the experts' line on this is that the extra sexual activity is probably about bonding. It's summed up succintly in Wikipedia on sexual intercourse: bonding and affection:

Wikipedia wrote:Humans, bonobos, dolphins, and chimpanzees are all intelligent social animals, whose cooperative behavior proves far more successful than that of any individual alone. In these animals, the use of sex has evolved beyond reproduction, to apparently serve additional social functions.[13][14][15] Sex reinforces intimate social bonds between individuals to form larger social structures. The resulting cooperation encourages collective tasks that promote the survival of each member of the group.[3]

For humans, cooperation is vitally important. Individuals who can cooperate somewhat better are more likely to have surviving offspring, and if using sexual pleasure reinforces bonding then this provides the selection pressure. Two of the three other species quoted above by Wikipedia as showing the same behaviour are also our closest relatives, and also highly social.