tag:blogger.com,1999:blog-3563811638411839784.post7528376923509654961..comments2023-05-15T07:11:30.874+02:00Comments on Leherensuge: African R1b is distinct single haplogroupMajuhttp://www.blogger.com/profile/12369840391933337204noreply@blogger.comBlogger119125tag:blogger.com,1999:blog-3563811638411839784.post-5389221035800008232010-02-11T09:42:06.309+01:002010-02-11T09:42:06.309+01:00Ok, glad that we finally come to some sort of agre...Ok, glad that we finally come to some sort of agreement. FYI, I have just posted <a href="http://leherensuge.blogspot.com/2010/02/eurasian-y-dna-note.html" rel="nofollow">a map on what might have been the spread of Y-DNA in Eurasia early on</a>.Majuhttps://www.blogger.com/profile/12369840391933337204noreply@blogger.comtag:blogger.com,1999:blog-3563811638411839784.post-183045019216563752010-02-11T09:31:31.759+01:002010-02-11T09:31:31.759+01:00"If correct, it would mean that a K sublineag..."If correct, it would mean that a K sublineage, MNOPS (or pre-MNOPS) migrated eastward from South Asia, scattered around Oceania and backmigrated as the important P and NO haplogroups, that dominate nowadays the Eurasian Y-DNA landscape". <br /><br />Thanks. I've been trying to convince you of that for ages (and everyone else). I was able to deduce the basic outline from J. D. McDonald's 2005 haplogroup map, but with the increase in data since that time we can now see the picture even more clearly. You may well be correct in placing K1 tentatively with T and L in India. <br /><br />"Somehow all these K forths and backs would seem associated with mtDNA N (and R), right?" <br /><br />Again I find myself in total agreement. And I had deduced exactly that from the same haplogroup maps.terrythttps://www.blogger.com/profile/17327062321100035888noreply@blogger.comtag:blogger.com,1999:blog-3563811638411839784.post-87302711454174857762010-02-11T06:23:33.347+01:002010-02-11T06:23:33.347+01:00"OK. Back to the topic of Y-hap R1b in Africa..."OK. Back to the topic of Y-hap R1b in Africa". <br /><br />Good. :)<br /><br />"The African Y-hap is related only distantly to European R1b, and presumably they separated before R1b had even entered Europe".<br /><br />This is something I have not totally clear. I see highest R1b basal diversity in Italy, though admittedly only slightly higher than in West Asia. I also see great basal diversity in Italy for R1b1a and for R1b1b2(xR1b1b2a1). <br /><br />"Therefore R1b most probably entered Africa via the Levant, the traditional route both into and out of Africa".<br /><br />It's possible but it's found at greater numbers (and diversity probably too) levels the further south you go (more in Upper Egypt than Lower Egypt, more in Sudan than in Egypt, so if you propose a crossing of the Red Sea in the anti-biblical direction, I'd take it as valid too. And if someone proposes a crossing from Italy into NW Africa, I'd consider it as well - though at this moment I think it's very much unlikely. <br /><br />There is nothing to suggest that the Sinai desert is any "traditional route". Semitics backmigrated to Africa first by the Bab-el-Mandeb and other Red Sea crossings (Eastern Egypt was Arab already in Roman times) and we have no further clear evidence on what may have happened before. Between Africa and Asia there is the Red Sea primarily... and loads of more or less desertic lands. The Red Sea looks like an oasis in comparison often. <br /><br />"So, what is Y-hap R's deeper history? It forms a single branch of P*. And P is just one of eight related clades, the product of an apparently star-like expansion".<br /><br />This is very difficult to determine at this stage. The various phylogenetic levels of K are only being clarified right now and, as you surely know, it will take months or probably years till they are satisfactorily resolved.<br /><br /><i>The original paper that separated T and L from K specifically states, 'Also of great interest is the updated Y-chromosome phylogeny, with two new branches (star: M522 that join IJ and KT, and diamond: M525 that unifies KMNOPS)'. Couldn't be more straightforward</i>.<br /><br />Yes, it could be more "straightforward" because the terminology is not ISOGG: KT is not any haplogroup: K is, and it includes T, etc.<br /><br />Also not being open access, I (and probably you too) can only speculate on the details of this new proposed phylogeny. Even ISOGG seems confused and has not yet incorporated this super-lineage to its "official" phylogeny, and certainly it does not mention anywhere that K1-4 or other K* could be within the proposed MNOPS. It seems that the author believes that some K(xL,M,NO,P,S,T) also belongs to the new MNOPS macro-haplogroup but is not clear which clades exactly, neither to me nor to ISOGG nor to Wikipedia, so quick to adopt the new proposed phylogeny. <br /><br />In my humble opinion, K is likely to end up with 4 basal lineages: K1, L, MNOPS and T, which suggests a centroid in South Asia, probably towards Pakistan. The derived haplogroup MNOPS would hence have 7 sublineages: K2, K3, K4 (assuming these are not rearranged somehow: a problem is that we know too little about these minor lineages), M, NO, P (or NOP) and S. <br /><br />So, if the MNOPS proposal stands, it's likely it represents a SE Asian/Oceanian specific lineage that expanded in Asia as NOP or NO and P separately, most likely the latter. <br /><br />This is the most parsimonious interpretation of the current confuse data. If correct, it would mean that a K sublineage, MNOPS (or pre-MNOPS) migrated eastward from South Asia, scattered around Oceania and backmigrated as the important P and NO haplogroups, that dominate nowadays the Eurasian Y-DNA landscape. <br /><br />Somehow all these K forths and backs would seem associated with mtDNA N (and R), right? Though not to fine detail maybe, they are almost the only Eurasian haplogroups that have been going forth and back through tropical Asia after the initial M explosion.Majuhttps://www.blogger.com/profile/12369840391933337204noreply@blogger.comtag:blogger.com,1999:blog-3563811638411839784.post-106098804119823352010-02-11T01:16:04.153+01:002010-02-11T01:16:04.153+01:00"Anyhow it's all off topic".
OK. ..."Anyhow it's all off topic". <br /><br />OK. Back to the topic of Y-hap R1b in Africa. The African Y-hap is related only distantly to European R1b, and presumably they separated before R1b had even entered Europe. The fact the African R1b is found in Sardinia is hardly proof of a route to Africa via Europe. R1b had probably become established somewhere in Western Asia before it entered either Africa or Europe, because its relation R1a is spread thickly through Western Asia, as well as along the Indo-Gangetic Plain. Therefore R1b most probably entered Africa via the Levant, the traditional route both into and out of Africa. <br /><br />So, what is Y-hap R's deeper history? It forms a single branch of P*. And P is just one of eight related clades, the product of an apparently star-like expansion. As for the inclusion of the various Ks within this clade: The original paper that separated T and L from K specifically states, 'Also of great interest is the updated Y-chromosome phylogeny, with two new branches (star: M522 that join IJ and KT, and diamond: M525 that unifies KMNOPS)'. Couldn't be more straightforward. <br /><br />Back to the star-like expansion. A second Y-hap (NO), in the form of O and N, is found through India, East Asia and Southeast Asia (O) and across Northern Eurasia from the Saami to the Inuit (N). The Y-hap is too widely spread for us to be able to claim anything definite about its place of origin. <br /><br />The third haplogroup, K1, is found in India. It doesn't matter in what part, but I understand through India, Sri Lanka and Pakistan. <br /><br />That's three of the eight members of the star: K1, NO and P. The fourth one, Y-hap K3, is found in Indonesia and Melanesia, and presumably originated somewhere within that region. The fifth, K2, is found in Australia and New Guinea. Again it probably originated somewhere within that region. Next, K4 has much the same distribution as K2 but extends out into Melanesia, and even out into Oceania. <br /><br />That's six of the eight. We're left the remaining two: S (New Guinea, Melanesia and Australia, and probably originating within that region) and M (spread from eastern Indonesia out into the Pacific, as far as Fiji). <br /><br />So where is the centre of that star-like expansion? Five of the eight clades obviously originate somewhere between Melanesia and Indonesia. And it's by no means impossible that the other three originated there too.terrythttps://www.blogger.com/profile/17327062321100035888noreply@blogger.comtag:blogger.com,1999:blog-3563811638411839784.post-89417358227985113932010-02-10T09:38:18.906+01:002010-02-10T09:38:18.906+01:00Man: T is not so widespread through the Mediterran...Man: T is not so widespread through the Mediterranean, specially not the West Med, where it's almost something exotic. Instead T seems frequent in the steppes, just like J2 again. <br /><br />You dare say: "And in Italy, Crete, Cyprus, Corsica and Sardinia".<br /><br />In Italy it is in the North, that was colonized overland and not from the sea, not in the South. <br /><br />In Crete, Corsica and Sardinia it seems to have very limited distribution. I have not seen any reliable data, except for Crete in all this discussion. And the data for Crete shows it's limited to certain areas and not widespread as would be expected from an ancient clade. The more I look at the Med the less "ancient T" I see anywhere. And that's true for Europe as for North Africa. <br /><br /><i>But why is there such a huge time gap between oceanic crossings in Wallacea and oceanic crossings in the Mediterranean?</i>.<br /><br />There is not that huge leap. West Eurasians were making, not counting Crete, strait crossings >20,000 years ago (Gibraltar) and c. 30,000 years ago (Sicily) but were (mostly) restricted to narrow straits most of the time. It's just common sense. <br /><br />Wallaceans just were plain crazy... or there was some island that does not exist anymore. That's a serious possibility because it's Wallacean crossings which demand explanation, not the scarcity of them in West Eurasia. Getting into a boat and going into the depths of the ocean without knowing what's on the other side is not something any normal person would do, right?Majuhttps://www.blogger.com/profile/12369840391933337204noreply@blogger.comtag:blogger.com,1999:blog-3563811638411839784.post-38796180293914131822010-02-10T04:22:51.864+01:002010-02-10T04:22:51.864+01:00"if an allele is recessive, then it's lik..."if an allele is recessive, then it's like neutral in that state" <br /><br />Exactly. It has every chance of being drifted out, as you say. But heterozygosity itself aids survival so that may help reccesive genes survive. <br /><br />"Or founder effect. Or drift, why not?" <br /><br />But the ultimate product of such phenomena in bringing out double recessives is still inbreeding. <br /><br />"But when colonists headed into the Far North after the Ice Age, then such allele may have become adaptative and selected for quite naturally". <br /><br />But it can still only be 'selected for' once the double recessive appears. And a double recessive can only appear once two people with it produce offspring. If the mutation has happened only once those two people must be related, although possibly a huge number of generations back. <br /><br />"partial dominance/recessiveness seems to exist as well". <br /><br />And is actually quite common. In fact it offers one explanation for how an advantageous recessive may be prevented from being easily drifted out. <br /><br />"Even it may be the case that several different genes are interacting in complex and subtle manners" <br /><br />Again, probably the normal situation. And that's why it's so difficult to achieve large production increaes with artificial selection. You improve one thing and it has a flow on effect disrupting something else. <br /><br />"Andrew mentioned that as few as 10 reproductive individuals (5 of each gender) could well be enough to guarantee the viability of a population". <br /><br />That's his view, and not generally accepted. The population of several threatened species are being slowly increased but it takes careful control of who breeds with who, otherwise fertility drops off rapidly. <br /><br />"A real case is Pitcairn island, where 15 men and 12 women created a perfectly viable population". <br /><br />I pointed out at the time that that population was extremely varied. And it only lasted a couple of hundred years. Hardly long term. <br /><br />"Forager bands typically consist of 20-30 individuals, even if they relate in somewhat larger groups of 100-150 people and belong maybe to larger ethnicities". <br /><br />Such groups invariably have times when they get together with much larger groups, or in contact with other groups who do so. To claim they have existed in such small, isolated, inbreeding groups for any meaningful number of generations is completely wrong. <br /><br />"T is just one of the various lineages they carried" <br /><br />I agree that T was not alone. But it's the only really widespread one through most of the Mediterranean, and we have to explain that. 'Phoenician' is not adequate. They were not noted colonisers and probably were a minority even in Carthage and Cadiz. <br /><br />"T instead is pretty much localized in the Phoenician colonies and, very thinly, in SW Iberia". <br /><br />And in Italy, Crete, Cyprus, Corsica and Sardinia. <br /><br />"Boats do not mean oceanic navigation automatically". <br /><br />True. But why is there such a huge time gap between oceanic crossings in Wallacea and oceanic crossings in the Mediterranean? <br /><br />"I quit this discussion, really. Anyhow it's all off topic". <br /><br />Yes. You've got really stupid about it.terrythttps://www.blogger.com/profile/17327062321100035888noreply@blogger.comtag:blogger.com,1999:blog-3563811638411839784.post-42178568161297421852010-02-09T03:21:36.712+01:002010-02-09T03:21:36.712+01:00Because he's studied the problem for years and...<i>Because he's studied the problem for years and is an expert?</i><br /><br />This acritical attitude of submission to authority is religious, not scientific.<br /><br />He doesn't sound convincing anyhow and his reliance on the MC hypothesis does not make his ideas sound more credible but less so. <br /><br />And, yes, they are speculating on MCH grounds, they have not gone to fossil mice and tested their aDNA.Majuhttps://www.blogger.com/profile/12369840391933337204noreply@blogger.comtag:blogger.com,1999:blog-3563811638411839784.post-20326351633411587872010-02-09T03:17:13.160+01:002010-02-09T03:17:13.160+01:00Just a last note:
On what grounds do you assume ...Just a last note: <br /><br /><i>On what grounds do you assume T is Phoenician there?</i><br /><br />On the grounds that in all the area the only other spot where it's found at such levels is Cadiz which is a totally new Phoenician foundation, the first Phoenician colony ever (by their own accounts) and the most important Phoenician city ever west of Carthage.Majuhttps://www.blogger.com/profile/12369840391933337204noreply@blogger.comtag:blogger.com,1999:blog-3563811638411839784.post-15555166977591626232010-02-09T03:14:37.349+01:002010-02-09T03:14:37.349+01:00You used to claim that humans had boats in the Med...<i>You used to claim that humans had boats in the Mediterranean 'since always'</i>.<br /><br />Having a boat is not the same as being a sailor. You can tempt fate by going deep into the sea with kayak or canoe but most sane people would just not do such a temerity. <br /><br />Boats do not mean oceanic navigation automatically. You know that and you know that I say that, so why do you insist in being a confusionist?<br /><br /><i>The islands you mention (Majorca, Minorca and Ibiza) are the most isolated islands so it's hardly surprising that T is basically not found there</i>.<br /><br />Actually Ibiza alone has more Y-DNA T than any other island in whole Mare Nostrum. What the heck are you talking about? <br /><br /><i>I'd presume the original boats into the Mediterranean were fairly primitive</i>.<br /><br />Cardium Pottery culture ships? Are you kidding? We don't know exactly how they were because there are no remains but they were almost for sure pretty good for their age, because they not only reached all islands and remote coasts but it's also attested that the fished deep water fish. Those were not anymore just boats but true sailing ships. I even speculate if they might have invented the pulley in order to raise and fold the large sails they surely used- but maybe this was not strictly necessary yet. Whatever the case, they were the initiators of navigation in West Eurasia, maybe together with Epipaleolithic Danes, who also had longboats (this one left remains in of those peat bogs of the north). <br /><br />By this time we are not anymore talking of mere boats but of something clearly bigger and more seagoing, and surely of sails too (otherwise how could they go into the deep seas forth and back all the time?)<br /><br />You make up a theory on something you read to some guy on Wallacea and you aren't able to read about Epipaleolithic and Neolithic Europe before going into wild speculations about what kind of navigation might have existed at the very beginnings of West Eurasian sailing age? What's wrong with you? Are there not public libraries in New Zealand or what? <br /><br /><i>Expansion of something through the Med is pre-Neolithic. Crete, Cyprus, Sardinia, Corsica. And T is certainly more widespread than is J</i>.<br /><br />This sentence is ill-constructed and can't really be understood. How could it be pre-Neolithic if there was only basic boating before CP and there's no clear evidence of any crossing except of the narrow straits of Messina and Gibraltar? You are building a crazy epic out of nothing! <br /><br />T is not more widespread than J either. You can't be serious. Maybe in tropical Africa but that would be about it. <br /><br />I don't deserve this craze! <br /><br />I quit this discussion, really. Anyhow it's all off topic.Majuhttps://www.blogger.com/profile/12369840391933337204noreply@blogger.comtag:blogger.com,1999:blog-3563811638411839784.post-45895952638050862632010-02-09T03:14:31.406+01:002010-02-09T03:14:31.406+01:00Terry: if an allele is recessive, then it's li...Terry: if an allele is recessive, then it's like neutral in that state: it gets no increased chances of either success or defeat because in its recessive state it's dormant. That's how recessive disabling illnesses like hemophilia persist: carriers with both alleles do not show any sign of having them.<br /><br />"In fact a recessive can only become fixed in a population after some level of inbreeding"...<br /><br />Or founder effect. Or drift, why not? <br /><br />Or by being adaptative. A hypothetical recessive gene for paleness might be hidden in its recessive state while the climate does not demand it and even may be essentially neutral in its manifestation in certain climatic conditions like those of most of Europe. But when colonists headed into the Far North after the Ice Age, then such allele may have become adaptative and selected for quite naturally. <br /><br />I'm not saying it's that way, just an illustrative hypothetic scenario. Recessiveness just means that it becomes dormant where an alternative allele is present. <br /><br />Blood group 0 is recessive but is the most common blood group globally and it seems it evolved several times. <br /><br /><i>So once the double recessive appears the gene will expand, possibly rapidly, eventually replacing the original dominant</i>.<br /><br />Well, that's just a possibility. It's not proven in any single case I have ever heard of. It's an interesting possibility in any case and might explain why high melanin seems somewhat dominant over low melanin variants in humans. <br /><br />However Mendelian dominance is not necessarily the case, partial dominance/recessiveness seems to exist as well. Even it may be the case that several different genes are interacting in complex and subtle manners, as happens with human pigmentation. Real genetics is much more complex than the basic Mendelian model. <br /><br /><i>... it's usually accepted a population needs to contain 500 individuals to be sustainable long term</i>.<br /><br />In the discussion on Crete at AVRPI, Andrew mentioned that as few as 10 reproductive individuals (5 of each gender) could well be enough to guarantee the viability of a population. Checking the link, which is a discussion in fact, nobody seems to be really sure and a lot may depend on the individual genetic quality of the founders. A real case is Pitcairn island, where 15 men and 12 women created a perfectly viable population. That's quite less than 49 and I imagine that many founder effects among humans were caused by similarly tiny populations, maybe even smaller. <br /><br />Forager bands typically consist of 20-30 individuals, even if they relate in somewhat larger groups of 100-150 people and belong maybe to larger ethnicities. In the far north actually they work in even smaller groups, almost at nuclear family level.<br /><br /><i>"All have of course more than 50% R1b".<br /><br />Probably indicating a later arrival</i>.<br /><br />Why? It makes no sense to me. The Balearic islands were colonized from SE France, where R1b is high. Sardinia was colonized from central Italy and the R1b1a found in the island, and which looks among the oldest lineages, along with I2a, looks directly derived from Italy.<br /><br />You are assuming maybe that the CP carriers were some sort of specific isolate population. They were not: they were in many cases just the aculturized natives and the culture took more than a thousand years to spread from Albania and Yugoslavia to Southern Portugal, enough time for all kind of admixtures. T is just one of the various lineages they carried, if at all. <br /><br />In fact it's so rare in Iberia outside of certain areas, notably the main Phoenician outposts of Cadiz and Ibiza, that I doubt it's even of Neolithic origin in this part of the world. J2b, I2a, E1b1b or G2 are much more evenly distributed, something we should expect from a Neolithic lineage after so many millennia. T instead is pretty much localized in the Phoenician colonies and, very thinly, in SW Iberia.Majuhttps://www.blogger.com/profile/12369840391933337204noreply@blogger.comtag:blogger.com,1999:blog-3563811638411839784.post-29456412116319988282010-02-09T02:11:28.622+01:002010-02-09T02:11:28.622+01:00"How do they know that the trait did not exis..."How do they know that the trait did not exist some 10,000 years ago". <br /><br />From the article (which may or may not refer to MC), 'genetic analysis performed by Catherine Linnen of Harvard University and colleagues found that back then the deer mouse genome didn't contain the genes for light fur. That means the trait arose from a new mutation which rapidly spread through the local deer mouse population'. <br /><br />"That's what he says. Should I believe him? Why?" <br /><br />Because he's studied the problem for years and is an expert?terrythttps://www.blogger.com/profile/17327062321100035888noreply@blogger.comtag:blogger.com,1999:blog-3563811638411839784.post-86693073419263265602010-02-09T02:05:03.463+01:002010-02-09T02:05:03.463+01:00"Ibiza: c. 20% T (Phoenician probably!)"..."Ibiza: c. 20% T (Phoenician probably!)" <br /><br />On what grounds do you assume T is Phoenician there? Is T the most common Y-hap along the Levant coastline? Or confined only to regions around the Mediterranean that Phoenicians colonised? And did Phoenicians make up the vast majority of the population in regions where they set up trading depots?terrythttps://www.blogger.com/profile/17327062321100035888noreply@blogger.comtag:blogger.com,1999:blog-3563811638411839784.post-83760319609538819722010-02-09T02:00:53.216+01:002010-02-09T02:00:53.216+01:00"If it's a novel mutation, it's carri..."If it's a novel mutation, it's carried by just one person initially. That means it has all the chances to be drifted out early on in any non-growing population, even if hyper-adaptative". <br /><br />And usually, if not always, recessive. Giving it even more chance of being drifted out before it has any chance at all of producing a phenotype. In fact a recessive can only become fixed in a population after some level of inbreeding, a fact you seem reluctant to accept. <br /><br />"But it's painfully slow anyhow because the estimated advantageous odds are truly insignificant and any other advantage by someone else would neutralize them or even make them negative". <br /><br />No. We're assuming a survival advantage of 1%. So once the double recessive appears the gene will expand, possibly rapidly, eventually replacing the original dominant. <br /><br />"1% of 1 is (rounded to the next entire number) zero. 1% of 49 is still zero by the same method". <br /><br />Aren't you being deliberately obtuse, again? What population consists of just 49 individuals? Especially seeing it's usually accepted a population needs to contain 500 individuals to be sustainable long term. So what's 1% of 500? <br /><br />"All have of course more than 50% R1b". <br /><br />Probably indicating a later arrival. <br /><br />"all those islands were only colonized or at least clearly colonized with the arrival of Neolithic, which West of Crete means CP". <br /><br />You used to claim that humans had boats in the Mediterranean 'since always'. So why are you now claiming a much later arrival? The islands you mention (Majorca, Minorca and Ibiza) are the most isolated islands so it's hardly surprising that T is basically not found there. I'd presume the original boats into the Mediterranean were fairly primitive. <br /><br />"Are you suggesting that the expansion of T through the Med is pre-Neolithic? C'mon!" <br /><br />Expansion of something through the Med is pre-Neolithic. Crete, Cyprus, Sardinia, Corsica. And T is certainly more widespread than is J. <br /><br />"If the median age was 35 and you died at 20..." <br /><br />You could still have several children. <br /><br />"Woodruff says that these 'de novo' mutations – which occur after a species has encountered the situation where they will be useful, rather than before – may be more important for evolution than biologists think". <br /><br />And epigenetics offers an explanation for how they might occur. <br /><br />"If the Agouti mutation occurred in just one mouse, the chances of it spreading rapidly through the whole population would be slim" <br /><br />Not if it offered a survival advantage. The fact that the agouti gene is so widespread in small mammals suggests that it does have survival value. <br /><br />"you can only pinpoint the moment of expansion, not the moment of the original mutation". <br /><br />And that delay is because, as I pointed out above, the recessive gene takes time to even appear in the population. Selection cannot operate until it does so.terrythttps://www.blogger.com/profile/17327062321100035888noreply@blogger.comtag:blogger.com,1999:blog-3563811638411839784.post-86039085285686388772010-02-08T23:47:29.756+01:002010-02-08T23:47:29.756+01:00Maybe. We don't know everything. But Chaos is ...Maybe. We don't know everything. But Chaos is pretty fast, provided there are enough variety of ingredients in the cupboard. Otherwise, the cook (evolution) can only make a very limited array of dishes. <br /><br />It's all up to what can Grandma Nature cook with. Guess that now and then black pepper mutates into cinnamon but her customer, Mr. Evolutionary Pressure is always too much in a hurry to be able to wait for the new ingredient to be produced spontaneously.Majuhttps://www.blogger.com/profile/12369840391933337204noreply@blogger.comtag:blogger.com,1999:blog-3563811638411839784.post-82251694382911156232010-02-08T20:44:50.519+01:002010-02-08T20:44:50.519+01:00Evolution seems to be faster than the simple sprea...Evolution seems to be faster than the simple spread of mutations which makes me think there are a few tricks up evolution's sleeve.Kenhttps://www.blogger.com/profile/01637818790791725275noreply@blogger.comtag:blogger.com,1999:blog-3563811638411839784.post-27317641154241164582010-02-08T17:37:23.549+01:002010-02-08T17:37:23.549+01:00How do they know that the trait did not exist some...How do they know that the trait did not exist some 10,000 years ago. Molecular clock speculation? Ha! <br /><br />Actually, with MC techniques, assuming they'd be correct and perfected, which they are not, you can only pinpoint the moment of expansion, not the moment of the original mutation. <br /><br />Anyhow, mice have generation times that are much shorter than in humans (a year or two for them is like a century for us) and litter sizes that are many times the ones of our species, which seldom has more than one child at a time. So 10,000 years for mice would be like 1-5 million years for us, maybe more than the time of existence of the genus Homo! <br /><br />So not sure which is your point. <br /><br />10,000 years in mice is not "quickly", not at all. <br /><br /><i>He says, "Beneficial mutations occur by both mechanisms: pre-existing variations and de novo mutations. The debate is, what is the proportion of the two?"</i>.<br /><br />That's what he says. Should I believe him? Why?Majuhttps://www.blogger.com/profile/12369840391933337204noreply@blogger.comtag:blogger.com,1999:blog-3563811638411839784.post-40733930696564493832010-02-08T11:13:00.966+01:002010-02-08T11:13:00.966+01:00"If it's a novel mutation, it's carri...<b>"If it's a novel mutation, it's carried by just one person initially. That means it has all the chances to be drifted out early on in any non-growing population, even if hyper-adaptative.<br /><br />Only if it survives for long enough then that process you say begins to make any sense. But it's painfully slow anyhow because the estimated advantageous odds are truly insignificant "</b><br /><br /><a href="http://www.newscientist.com/article/dn17695-newly-evolved-fur-coat-a-quick-hit-in-nebraska.html" rel="nofollow">Newly evolved fur coat a quick hit in Nebraska </a> (New Scientist, 27 August 2009 )<br /><br />'Normally, to achieve such a rapid evolutionary shift a species needs to have an alternative version of a gene already in circulation. A change in conditions – such as trees becoming darker as they get covered in soot, in the case of the peppered moth – can then provide the selection pressure that causes the alternate gene to spread. But in deer mice the new version of Agouti spread rapidly from a standing start.<br /><br />Woodruff says that these "de novo" mutations – which occur after a species has encountered the situation where they will be useful, rather than before – may be more important for evolution than biologists think.<br /><br />If the Agouti mutation occurred in just one mouse, the chances of it spreading rapidly through the whole population would be slim, which is why newly arising mutations like this have been thought to be unimportant.<br /><br />But Woodruff points out that mutations can occur while an animal is in the womb. If this occurs early enough, the mutation may be present in many of its sperm or egg cells. Then the animal could have several offspring with the mutation, making it easier for the mutation to spread.<br /><br />He says, "Beneficial mutations occur by both mechanisms: pre-existing variations and de novo mutations. The debate is, what is the proportion of the two?"'Kenhttps://www.blogger.com/profile/01637818790791725275noreply@blogger.comtag:blogger.com,1999:blog-3563811638411839784.post-61532204886536503912010-02-08T05:11:15.325+01:002010-02-08T05:11:15.325+01:00If it's a novel mutation, it's carried by ...If it's a novel mutation, it's carried by just one person initially. That means it has all the chances to be drifted out early on in any non-growing population, even if hyper-adaptative.<br /><br />Only if it survives for long enough then that process you say begins to make any sense. But it's painfully slow anyhow because the estimated advantageous odds are truly insignificant and any other advantage by someone else would neutralize them or even make them negative. <br /><br />Again you are assuming "all else equal" but in reality all else is wildly unequal. <br /><br /><i>So even at a survival advantage of just 1% the B variant</i>.<br /><br />1% of 1 is (rounded to the next entire number) zero. 1% of 49 is still zero by the same method. You need first to reach a numeric threshold to even consider your chances meaningful at all. <br /><br />Then it would happen what you say if everything else would be equal, but in practice it's not. So it's a mere abstract notion because there are many mutations, epigenetic effects and other unmeasurable randomness competing in that game in reality. It's only theoretical. <br /><br /><i>But as you say, 'Sicily was inhabited before CP'</i>.<br /><br />From Italy, yes. <br /><br /><i>In fact most Mediterranean islands were occupied before Cardium pottery expanded through them</i>.<br /><br />Not really. From Crete westwards, and excepting Sicily, all those islands were only colonized or at least clearly colonized with the arrival of Neolithic, which West of Crete means CP. Sure, there are some indications of earlier visitors in Corsica and Sardinia but nothing that can say that they were continuously inhabited by any sort of thriving population, not at all. <br /><br />See <a href="http://1.bp.blogspot.com/_ro2ijOk8JWc/ST5ONRBvNdI/AAAAAAAAAcE/pbcSablyx50/s1600-h/0.jpg" rel="nofollow">this map</a>: <br /><br />- Majorca: c. 10% J2, c. 15% E1b1b+G, c. 10% I, almost no T (Kx(P))<br />- Minorca: c. 20% E1b1b, almost no T<br />- Ibiza: c. 20% T (Phoenician probably!), c. 25% other East Mediterranean clades. <br /><br />All have of course more than 50% R1b. <br /><br /><i>In fact I'm basically saying that the newer Neolithic haplogroups now outnumber the earlier arrivals</i>. <br /><br />In the Mediterranean islands all or nearly all is Neolithic, Sicily excepted. In some cases much is in fact post-Neolithic, as seems to be the case with Ibiza, a small island where to make a founder effect seems quite easy.<br /><br />Are you suggesting that the expansion of T through the Med is pre-Neolithic? C'mon!<br /><br /><i>It's possible that epigenetic factors associated with adult milk drinking encouraged mutations in that portion of the genome, one of which became succesful</i>.<br /><br />I don't think genetics works that way. Epigenetics may buy some time but making cheese, eating lentils or whatever else, is a simpler solution than waiting for an extremely unlikely random mutation to happen. In fact most Neolithic peoples in West Eurasia did exactly that: they ate cheese.<br /><br />Why exactly is the lactose tolerance allele so common in Western Europe? Probably for some absolutely random founder effect, the same that other genes are (Y-DNA R1b, mtDNA H, Rh-, etc.)<br /><br /><i>"it seems that stress in early life, something that the individual genome is unable to affect, dramatically affects lifespan".<br /><br />But that doesn't affect survivability in an evolutionary sense. A longer lifespan belongs pretty much at the end of reproductive life</i>.<br /><br />Not in Paleolithic times possibly. If the median age was 35 and you died at 20... <br /><br />"I am myself and my circumstances" said Ortega y Gasset. In this case we could well say: "I am my genes and their circumstances".Majuhttps://www.blogger.com/profile/12369840391933337204noreply@blogger.comtag:blogger.com,1999:blog-3563811638411839784.post-20825695449500684452010-02-08T04:19:06.702+01:002010-02-08T04:19:06.702+01:00"But how do you measure advantage?"
S..."But how do you measure advantage?" <br /><br />Simply by counting the proportion of individuals in the population that have the gene each generation. If the proportion is increasing by as little as 1% the gene is providing a survival advantage. Anyway our discussion is based on the hypothetical case of assumed 1% survival advantage. I agree it's possible in domestic breeding to actually measure production advantage (and so survival in the herd for example) but in nature survival is always more complicated, as you keep reminding us. <br /><br />"It has to be an advantage much larger than just 1% anyhow to make a clear difference". <br /><br />I've explained above why it need be only 1%. The proportion of the advantageous gene in the base population keeps increasing, with genes responsible for any survival advantage whatsoever ultimately increasing exponentially. <br /><br />"in real life a perfectly healthy animal can still die before reproducing" <br /><br />In which case its genes don't count as 'survival'. <br /><br />"In practical terms, SNPs (mutations senso stricto) only happen once each many many million years". <br /><br />I agree with you on that one. <br /><br />"You also have to consider that most individuals are, to begin with, very well adapted" <br /><br />That's true. And it's why we're seriously considering a survival advantage of just 1%. <br /><br />"But what is almost sure is that it did not mutate just because people began having sheep" <br /><br />It might have in a way. It's possible that epigenetic factors associated with adult milk drinking encouraged mutations in that portion of the genome, one of which became succesful. <br /><br />"it seems that stress in early life, something that the individual genome is unable to affect, dramatically affects lifespan". <br /><br />But that doesn't affect survivability in an evolutionary sense. A longer lifespan belongs pretty much at the end of reproductive life.terrythttps://www.blogger.com/profile/17327062321100035888noreply@blogger.comtag:blogger.com,1999:blog-3563811638411839784.post-62193441406142291802010-02-08T04:18:34.746+01:002010-02-08T04:18:34.746+01:00"Ok, the chances for BB are slightly higher b..."Ok, the chances for BB are slightly higher but insignificantly so. It's not really different from drift". <br /><br />But we're dealing with a changing base population each generation. Even 'insignificantly higher' survival will mount up over generations. In each generation the chance of BB increases. So BB actually increases exponentially, even if from just a very small basal proportion to start with. So even at a survival advantage of just 1% the B variant can completely replace the A over generations. Technically I suppose we should refer to the genes as being B and b, with b being the recessive that eventually displaces the B dominant. I agree that 'In reality everything is much more complex', but we're dealing with the hypothetical case of a single gene providing 1% survival advantage. <br /><br />"Individual fitness surely has almost nothing to do with haplogroups (there may be a correlation sometimes but that would be about all)". <br /><br />In most cases I doubt that the survival and expansion of particular haplogroups has anything at all to do with the genes on the mtDNA or Y-chromosome. It has everything to do with whatever particular cultural or technological advantage the particular haplogroup possesses. <br /><br />"Doesn't J2b, as well as other haplogroups, like E1b1b, follow the coastal pattern of Cardium Pottery?" <br /><br />Yes. But as you say, 'Sicily was inhabited before CP'. In fact most Mediterranean islands were occupied before Cardium pottery expanded through them. And neither J2b nor E1b1b are as widespread through the islands as is T. As you say, J2b and E1b1b tend to be associated with 'Cardium Pottery'. <br /><br />"It's not like you find anywhere T above 10% of frequency, often much less, so your argumentation of sweep just doesn't make any sense". <br /><br />I'm certainly not claiming T replaced previous haplogroups, so 'sweep' has nothing to do with the situation. In fact I'm basically saying that the newer Neolithic haplogroups now outnumber the earlier arrivals.terrythttps://www.blogger.com/profile/17327062321100035888noreply@blogger.comtag:blogger.com,1999:blog-3563811638411839784.post-71438195253904013292010-02-08T02:09:14.393+01:002010-02-08T02:09:14.393+01:00Addendum: way too many crucial events in effective...Addendum: way too many crucial events in effective survivability are unrelated to genes or the fitness these may confer. <br /><br />For example, check <a href="http://www.sciencedaily.com/releases/2010/02/100204204315.htm" rel="nofollow">this article at SD today</a>: it seems that stress in early life, something that the individual genome is unable to affect, dramatically affects lifespan. I have dealt elsewhere in this blog on how stress in early life causes epigenetic alterations that affect a whole life, so there's much more in circumstances than in just the genetic base. <br /><br />I am positive that people's intelligence, for example, is highly affected by early life circumstances, such as nutrition, traumas, education, etc. and not just by genes. <br /><br />In practice it's never "everything else equal", in fact it's always "everything else wildly different", so predicting the result even with the best genetic fundamentals is simply impossible.Majuhttps://www.blogger.com/profile/12369840391933337204noreply@blogger.comtag:blogger.com,1999:blog-3563811638411839784.post-40054957425274805862010-02-07T23:53:35.893+01:002010-02-07T23:53:35.893+01:00Siberians and NE Asians in general have fairly lig...Siberians and NE Asians in general have fairly light skin. This trait may have co-evolved in both regions (regressing to darker, but not brown/black, shades in tropical America). The high population densities allowed in the unusually warm climate of North Europe since the end of the Ice Age have no parallel anywhere else and I presume that the extremely pale phenotypes found in that area are only a recent evolution, maybe by exploitation of genes already present in other European populations and/or accumulation of such advantageous traits to create an even more milky skin color. <br /><br />Whatever the case, what these differences evidence is that there is no determinism in how evolution can proceed. East Asians have different pigmentation strategies than West Eurasians and they seem to work well for them. Much about these adaptations is not yet well known, though it seems to protect from skin cancer almost as well as high melanin even with fair skins. <br /><br />It's an interesting case of convergent, yet divergent, evolution. It shows clearly that there is no determinism on how people or other species adapt to their environment. Different strategies may be equally valid. And the existence of such diversity of adaptations is good for the species overall because it allows humankind to have a huge reservoir of genetic potential for whatever may come... or almost.Majuhttps://www.blogger.com/profile/12369840391933337204noreply@blogger.comtag:blogger.com,1999:blog-3563811638411839784.post-67329417543188403072010-02-07T23:43:52.294+01:002010-02-07T23:43:52.294+01:00"Yes; but a mutation can arise more than once..."Yes; but a mutation can arise more than once"...<br /><br />In practical terms, SNPs (mutations senso stricto) only happen once each many many million years. <br /><br />"... you seem to be talking about a mutation's chance on just one of these occasions".<br /><br />Of course, I'm oversimplifying. But for each occasion the chances are those. Randomness can perfectly annihilate adaptative traits, as they only offer better chances not any certainty. If you play any sort of game of odds, like blackjack, you will know it is that way: you can lose with 21 and win with 17.<br /><br />Overall there is a tendency to favor the most adaptative traits and suppress the least adaptative ones. But a tendency is not any automatic certainty for every one of such traits, and very specially not for those traits that are only mildly adaptative or deleterious, who don't play with odds significantly different from a truly neutral trait.<br /><br />You also have to consider that most individuals are, to begin with, very well adapted: their lineages have gone so far, so they are good enough. Meanwhile novel mutations only rarely are advantageous: most are deleterious or just neutral. So for evolution is a lot easier to pick a neutral trait that is already fairly common and put it to a novel use somehow. That "somehow" is where the tricky part is: it may be via epigenetic modifications, cultural exploitation of such trait or fortunate combination of two or more of such neutral genes to form a complex trait that is somehow more adaptative. <br /><br />A gene such as the lactose tolerance allele might have been dormant in West Europeans for millennia before cattle and milk (other than the mothers') arrived. It might have been common at unknown levels, it might even have been fixated by drift (as it's neutral in absence of dairying) or whatever. But what is almost sure is that it did not mutate just because people began having sheep: it was surely favored (somewhat - how much?) by that new factor but must have existed before, behaving as a neutral (trivial) allele.<br /><br />In fact it's just a polymorphism of a gene that all mammals must have to survive early on in our lives. Its absence among babies and toddlers may be deadly but its presence among adults is trivial. It's a paedomorphic trait, just like blondism, certain facial features (short flat nose for instance), etc.Majuhttps://www.blogger.com/profile/12369840391933337204noreply@blogger.comtag:blogger.com,1999:blog-3563811638411839784.post-16612566235417659502010-02-07T22:13:20.114+01:002010-02-07T22:13:20.114+01:00I was a bit careless there, sorry. The correct lin...I was a bit careless there, sorry. The correct link for <a href="http://www.kaluefflab.com/pdfs/publications/2009Touhimma.pdf" rel="nofollow">Vitamin D, nervous system and aging</a>Kenhttps://www.blogger.com/profile/01637818790791725275noreply@blogger.comtag:blogger.com,1999:blog-3563811638411839784.post-19621884381843468722010-02-07T22:07:19.982+01:002010-02-07T22:07:19.982+01:00A 100% advantageous trait in my previous example w...<b>A 100% advantageous trait in my previous example would still only have 66.67% chances of fixation [...]That's a crucial difference between real life and breeding: in real life a perfectly healthy animal can still die before reproducing,</b><br /><br />Yes; but a mutation can arise more than once you seem to be talking about a mutation's chance on just one of these occasions. In a favourable environment a mutation that fails due to 'bad luck' will be likely to be taken up when it recurs . Of course the greater the population size the less time till the mutation pops up again. A small population will maybe need to react faster than the spread of an alelle; that's what I was getting at when I mentioned canalization and evolutionary capacitance. <br /><br />White Australians get enough cancer for UV to be a selection pressure. But UV is a very weak selection pressure. You're assuming the Black Africans' and Europeans' skin colour is the result of UV but in fact there are nativre north Americans and Siberians who live at the same or greater latitudes as Europeans and who don't get a lot of vitamin d in there diet who are not white or anything like it. In the same way there are the !Kung who get by very well in the high UV (due to altitude) Kalahari with ligh brown skins that make a mockery of the idea that black Africans have very dark skin to protect them from UV. In fact black Africans are 'black' even on parts of the body that are never exposed to the sun unlike all other dark skinned ethnic groups native Australians included. <br /><br />Incidently, a photo of two mice of the same age one has been genetically modified to have high vitamin D activity, try and guess which is which. <a href="http://4.bp.blogspot.com/_tMgToYs_oYc/S2X7nnX-wtI/AAAAAAAAAFI/a9vz8P37e8Y/s1600-h/Tuohimaa+_etal_2009_F01.JPG" rel="nofollow">Here</a>.<br /><br />It's from <a href="http://4.bp.blogspot.com/_tMgToYs_oYc/S2X7nnX-wtI/AAAAAAAAAFI/a9vz8P37e8Y/s1600-h/Tuohimaa+_etal_2009_F01.JPG" rel="nofollow">Vitamin D, nervous system and aging</a>Kenhttps://www.blogger.com/profile/01637818790791725275noreply@blogger.com