Multiregional

In humans and some other organisms the gamete contributed by the father determines the sex of the child. If the gamete has a Y chromosome the child is a male. If the gamete has an X chromosome the child is a female.

It would be in the selfish interest of the Y chromosome to get itself transmitted to much more than 50 per cent of the next generation. It is possible that more than once in the course of evolution of humans (and their non-human ancestors) mutations in the Y chromosome have resulted in genes that discriminate against the survival of X-bearing gametes. (I am not referring to meiotic drive, which is a separate mechanism.)

If X-bearing sperm could be detected by the male organism while the sperm is stored, the organism might be driven by its Y chromosome to kill the X sperm. Equally, of course, the X chromosome in the male organism might drive the organism to kill the Y-bearing sperm if the sex of that sperm could be detected, because the X has the same selfish interest as the Y.

It would be a bit like submarine warfare, in which the first rule of the submariner is to escape detection -- hence the quiet-running propellors, and the prejudice against mechanics who drop heavy wrenches in the engine-room.

Saccone and her colleagues mentioned in a 1995 paper that 'In mammals, too, mtDNA contributes to the synthesis of a structural product (ND1) in the maternally transmitted component of the minor histocompatibility antigen'. Histocompatibility antigens are exposed on the surface of a cell, and could therefore be detected. The mtDNA contribution will of course appear in both X sperm and Y sperm, but I assume that the rest of the maternally transmitted component of this antigen is coded for by genes on the X chromosome.

If there is no paternally transmitted analogue of this antigen component, coded for by genes on the Y chromosome, the Y gametes might be undetectable during maturation. Perhaps the battleground between the Y and the X was tilted in favour of the Y when the Y lost genes that had coded for a paternally transmitted component of a histocompatibility antigen. In that case the Y sperm could not be detected and killed, but the X sperm could be detected and killed. (I do not imply an immunological attack.)

In any evolutionary competition between the X and the Y to be the sex chromosome in most of the gametes formed in a male organism, the Y has two advantages in speed of adaptation. Firstly, if we look at many generations of transmission, the X spends a third of its time in a male organism and two-thirds in a female one. The Y spends all of its time in a male organism, so mutations that allow it to reduce the number of X-bearing sperm cells can always be naturally selected for.

Secondly, a recent scientific article concluded that the average mutation rate in male organisms was about four times greater than that in female ones. Since a Y spends all of its generations in a male organism and an X spends only a third of its generations in a male organism, the Y will be mutated more quickly. (These two advantages will also help the Y in acquiring meiotic drive against the X.)

Selected mutations of the Y chromosome that caused the male organism to kill gametes bearing the X chromosome would give the Y chromosome a tremendous evolutionary advantage. It might ensure that (for example) an average of four out of six of the offspring of male organisms were males.

In the case of humans this mutated Y chromosome could spread quickly through a widespread established population, generation by generation (assuming that a short-displacement wavelike movement of people, lasting a long time, was always possible).

However, no other chromosomes would accompany it far on its journey. It would be a bit like the gene for 'hornlessness', which can be introduced into a herd of horned black Angus cattle by a cross with a hornless red Shorthorn bull and, under the artificial selection of the cattle-breeder, be spread throughout the herd. After about 20 years the herd consists of hornless black Angus cattle. It would be incorrect for a stranger to assume that the black cattle he or she sees in the field were of a breed that had been hornless for hundreds of years.

Under natural selection a human population in which the males had the 'anti-X gamete' Y chromosome would suffer the disadvantages of a surplus of males and a scarcity of females. In the long run natural selection would favour subsequent mutants of the 'anti-X gamete' Y chromosome in which those mutant genes that discriminated against the production of X-bearing gametes in spermatogenesis or sperm maturation were deleted or rendered inactive.

The result after many millenia of evolution of humans (and their evolutionary precursors) would be a human Y chromosome from which many genes had been deleted and in which many of the remaining DNA sequences were permanently inactivated.

The most recent series of mutations to the Y chromosome enabling the human male organism to detect and kill sperm cells bearing X chromosomes might (hypothetically) have occurred in Africa 70,000 or 60,000 years ago. This Y chromosome might then have been spread throughout a previously established population in all of the Old World in only a few thousand years.

The above hypothesis has not yet been tested, but it is worth noting that genetic studies of such a Y chromosome could give a misleading picture of the chronology and routes of human migration from Africa.

(I sent this article under the title 'The human Y chromosome, evolution and migration' to the internet discussion group 'sci.bio.evolution' on 5 November 2000, where it was subsequently published. I made a slight correction before publishing the article on the present site.)

Published on this site 5 November 2000. © Andrew Gyles

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My hypothesis of a low mitochondrial mutation rate in humans

There is a theoretical possibility that a mitochondrion could eliminate those mutations that cause a distortion of the double-stranded mtDNA, because such mutations are physically detectable by a set of enzymes.

The enzymes could then destroy the entire double-stranded copy of the circular mtDNA genome containing the distorted mtDNA, or alternatively tag it for 'export' and cause it to be ejected from the mitochondrion. (The ejecting of genetic material through a conjugation tube is a known bacterial behaviour. Mitochondria are thought to have a bacterial ancestor.)

The destroyed or ejected copy of the mtDNA genome could be replaced, sooner or later, by the replication of an unmutated copy in the same mitochondrion.

It is interesting to note that enzymes in the nucleus try to do the same thing. But of course, having detected a chromosome distorted by a mutation they cannot destroy the chromosome. If they did that they would not have an unmutated copy to replicate and so make good the loss. The homologous chromosome is not an identical copy. So the best they can do is to 're-pair' the distorted part of the double-stranded nuclear DNA. This is a chancey business because they cannot 'know' which base or bases to leave in and which to cut out. But it is better than doing nothing.

Oxygen free radicals produced by the respiratory chain in mitochondria can damage mtDNA and thus increase the mutation rate. It is conceivable that an abnormally high mtDNA mutation rate in somatic cells is an indication that this hypothetical system for eliminating mutations that cause distortions in double-stranded mtDNA has failed in those cells.

It is worth noting that if such a system is at work in the mitochondria of female germline cells it might have evolved to different degrees in different species of animal.

For example, the development of higher intelligence and memory and the acquisition of language in humans might have depended on a simultaneous evolution of a lower mtDNA mutation rate in human brain cells in particular. However, the lower rate might have been achieved generally, in all cells. In that case it is possible that the mtDNA mutation rate in human female germline cells is much lower than has been assumed in studies of human evolution based on the 'mtDNA sequence divergence rate'. As far as I know this rate has never been objectively measured.

Some indication of whether mitochondria do use the hypothetical system outlined above could perhaps be gained on cell cultures in vitro, using X-irradiation as a mutagenic agent to accelerate the mutation rate.

(I published this summary on the 'message board' of the discussion group 'talk.origins' on 10 September 2000.)

Published on this site 10 September 2000. © Andrew Gyles

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The stout defence of the multiregional theory by Thorne and Wolpoff

The two rival explanations of the evolution of modern humans were set out in plain language and defended in a single issue of 'Scientific American' in 1992. The defenders of the Multiregional Evolution hypothesis were Alan G. Thorne and Milford H. Wolpoff (1). The defenders of the Recent African Genesis of Humans were Allan C. Wilson and Rebecca L. Cann (2). This conflict in print was evolution theory's equivalent of boxing's famous 'rumble in the jungle', which was won by Mohammed Ali.

Anyone perusing the scientific literature in the succeeding eight years would be likely to have concluded that evolution theory's rumble was won by Wilson and Cann. Even the school biology textbooks have given their double-page spreads to Wilson and Cann's (and Stoneking's) hypothesis (the so-called Out of Africa, or African Eve, or Modern Mitochondrial Eve, theory). They relegate Thorne and Wolpoff's hypothesis to a box in a side column, dutifully pointing out that this is an alternative explanation but usually managing to give the impression that these two authors are a couple of diehards who have been run over by the steamroller of modern laboratory technology.

I do not think that Thorne and Wolpoff have been run over. Their defence is worth reading carefully. For example, they wrote:

'The first inhabitants of Australia arrived more than 60,000 years ago, and their behavior and anatomy were clearly those of modern human beings. Their skeletons show the Javan complex of features...

'If the earliest Australians were descendants of Africans, as the Eve theory requires, the continuity of fossil features would have to be no more than apparent. All the features of the early Javans would need to have evolved a second time in the population of invaders. The repeated evolution of an individual feature would be conceivable but rare; the duplication of an entire set of unrelated features would be unprecedentedly improbable'.

Thorne and Wolpoff pointed also to continuity of fossil features in China, and remarked:

'... Moreover, because the similarities involve features different from those significant in Australasia, they compound the improbability of the Eve theory by requiring that a second complete set of features was duplicated in a different population ...

'... Perhaps the most telling indication of morphological continuity concerns a peculiarity of tooth shapes. Prominently "shoveled" maxillary incisors, which curl inward along their internal edges, are found with unusually high frequency in living East Asians and in all the earlier human remains from that area. Studies by Tracey L. Crummett of the University of Michigan show that the form of prehistoric and living Asian incisors is unique.

'... Our examinations of the Chinese specimens found no anatomic evidence that typically African features ever replaced those of the ancient Chinese in these regions. Instead there is a smooth transformation of the ancient populations into the living peoples of east Asia'.

I have set the quotations from Thorne and Wolpoff above in Italics to make sure that they are attributed to their authors.

Some paleontologists have looked at the Chinese, and Javan and Australian, fossils and have formed the view that they do not show the morphological continuities in their separate regions that Thorne and Wolpoff claim. However, I think that much of the fossil records of human evolution in eastern Asia, south-eastern Asia and Australia lies on the vast continental shelves that adjoin those regions. If there are some discontinuities in the fossil records I suggest that they might well be perfectly filled by bones that at present lie beneath the shallow Yellow, East China, South China and Java seas and the seas adjoining Australia and New Guinea (see my article immediately below).

Wilson and Cann wrote:

'Proponents of the multiregional evolution model emphasize they have documented a continuity of anatomic morphologies between the archaic and modern residents of different regions; they insist these morphologies would be unlikely to evolve independently in any invading people. For that argument to hold true, it must also be shown that the cranial features in question are truly independent of one another - that is, that natural selection would not tend to favor certain constellations of functionally related features. Yet we know powerful jaw muscles may impose changes on the mandible, the browridge and other points on the skull; circumstances that promoted the evolution of these features in one population might do so again in a related population.

'Other paleontologists also dispute the evidence for continuity. They argue modern populations are not linked to past ones by morphological characteristics that evolved uniquely in the fossil record. Instead fossils and modern populations are united by their shared retention of still older ancestral characteristics. The continuity seen by believers in multiregional evolution may be an illusion'.

I have set the quotation from Wilson and Cann immediately above in Italics to make sure that it is attributed to its authors.

I do not know what the second paragraph in the Wilson and Cann quotation means.

As for the first paragraph in the Wilson and Cann quotation, I do not think that it explains why the skeletons of the first inhabitants of Australia, though clearly modern, show the Javan complex of features. Do they imply that the foodstuffs these people found in Australia were so tough that their descendants had to quickly evolve powerful jaw muscles, which imposed changes on the mandible, the browridge and other points on the skull? The foodstuffs available in northern Australia 60,000 years ago were probably not very different from those naturally available today. On the coast, shellfish, including oysters. Fish, including the gourmet's delight, barramundi. Turtle flesh and eggs. Dugong flesh. Wildfowl, snake, lizard, wallaby and a wide variety of vegetable foods and fruit. Does one need powerful jaw muscles to eat oysters?

The diets eaten by the inhabitants of Australia about 50,000 years ago are something that old Aborigines, and some anthropologists and archaeologists, would know infinitely more about than I do. But since Wilson and Cann implied that their recent African migrants to Australia about 60,000 years ago quickly evolved what Thorne and Wolpoff called 'the Javan complex of features' I think that they should have said what caused them to acquire it.

Nor do I think that the first paragraph in the Wilson and Cann quotation above explains why living east Asians and all earlier human remains in east Asia have prominently shovelled maxillary incisors even though, according to those authors, the living east Asians are descended from modern invaders from Africa. Did they believe that there was something in the east Asian diet that caused the very early humans of China to evolve shovelled incisors? Did they believe that the same thing in the east Asian diet half a million years later caused their newcomers from Africa to evolve shovelled incisors? If so, what was this thing in the east Asian diet? I agree with Thorne and Wolfpoff's view that the shovelled incisors of east Asians evolved simply by chance, and only once.

The evidence of the prominently shovelled incisors seems to me sufficiently strong to disprove by itself Wilson and Cann's hypothesis of 'the Recent African Genesis of Humans'.

Reference

1) Thorne, Alan G. and Wolpoff, Milford H., Scientific American, April 1992, pages 28-33.

2) Wilson, Allan C. and Cann, Rebecca L., Scientific American, April 1992, pages 22-27.

Further reading

'Mitochondrial DNA and human evolution', by Rebecca L. Cann, Mark Stoneking and Allan C. Wilson, Nature, volume 325, 1 January 1987, pages 31-36.

Many other articles on the same subject have been published in the scientific literature (Science, Nature and other journals) by these and other authors since 1987.

Published 24 August 2000. © Andrew Gyles

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Human fossils supporting the multiregional theory might lie on the floor of the China and Java Seas

The so-called 'Out of Africa' theory got its main drive from the paper, 'Mitochondrial DNA and human evolution', which was published in 1987 (1). Its abstract said, in part: 'All these mitochondrial DNAs stem from one woman who is postulated to have lived about 200,000 years ago, probably in Africa'.

At about the same time as this paper was published some paleontologists began to reassess the human fossil evidence. They concluded that it supported the Out of Africa theory. (It is worth noting that the 'Multiregional evolution' hypothesis is an 'out of Africa' theory too: the argument between supporters of the rival theories of human evolution is about when the ancestors of non-African humans left Africa.)

I see an important fault in the conclusion of these paleontologists. The human fossil bones they assessed were all discovered on land that is presently dry. But much human evolution in eastern and south-eastern Asia must have happened on the vast continental shelves of those regions, during the great ice ages that have occupied most of the past 500,000 years. During the ice ages those continental shelves were vast, presumably fertile, plains. Some of the human populations of eastern and south-eastern Asia, perhaps the more adventurous and adaptable ones, must have chosen to live on them. The fossil bones of some of them must still lie where they fell. But they have not been recovered, and perhaps they never will be.

It is as if scientists working in the Western Hemisphere have never looked thoughtfully at a map showing the shallow Yellow Sea, East China Sea, South China Sea and Java Sea. As if it has never occurred to them that human populations must have lived on the floors of those seas for hundreds of thousands of years.

And yet two populations important in the 'Multiregional evolution' hypothesis have lived in China and Java (according to the hypothesis) for about a million years. Part of their fossil record lies beneath the adjacent seas.

Reference

1) Cann, R.L., Stoneking, M. and Wilson, A.C., Nature, 325, 31-36 (1987).

Published 21 August 2000. © Andrew Gyles

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A laboratory experiment to test the central assumption of the 'Out of Africa' theory

I suggest that female chimpanzee germline cells be grown in a glass dish and female human germline cells be grown in another glass dish. (If it is not possible to grow germline cells somatic cells will have to be used instead.)

The cells in both dishes should then be treated with equal doses of mutation-inducing radiation, such as X-rays, for a calculated period of time. This period should be long enough for the radiation to cause mutations in a few of the mitochondrial chromosomes of some of the cells but not long enough for it to cause mutations in the nuclear chromosomes of many of the cells. This should be possible because there are many more mitochondrial chromosomes than nuclear chromosomes in most cells. (For example, some cells contain thousands of mitochondria, and each mitochondrion contains several copies of the mitochondrial chromosome. I do not know typical figures for female chimpanzee and female human germline cells.)

Many experiments have studied the mutagenic effects of irradiation with various doses of X-rays, so the choice of appropriate doses can be guided by a great reserve of experience. Alternatively, specialists in the experimental use of mutagenic agents might be able to suggest more suitable mutagens for this experiment.

After the irradiation has been stopped the cultured cells in each dish should be allowed time to repair or destroy mutated mitochondrial chromosomes. Then their mitochondrial DNA (mtDNA) should be searched for permanently mutated sequences and the net rates of mutation of mtDNA in the chimpanzee cells and the humans cells should be calculated and compared.

The central assumption of the 'Out of Africa' theory is that the sequence divergence rate in human mtDNA (determined by the mtDNA mutation rate) is about the same as that in chimpanzees. But I suggest that humans correct mutations to their mtDNA much more than do chimpanzees (see note below). If this experiment shows that the net sequence divergence rate in humans is about a tenth of that in chimpanzees it will remove the logical support for the 'Out of Africa' theory that this assumption has always provided.

The experiment might be a laborious and difficult one. It is of course an artificial one that speeds up the process of mutation millions of times. There might be questions about the choice of cells to be used, the correct mutagenic treatments and the interpretation of the results. However, until such an experiment is done it remains true that the central assumption of the 'Out of Africa' theory has not been put to the acid test in the laboratory.

(Note: A typical mammalian cell, whether somatic or in the female germline, contains hundreds or thousands of copies of the single mitochondrial chromosome. But no normal mammalian cell contains more than one copy of each nuclear chromosome except during replication: nuclear chromosomes are paired in somatic cells, but the members of the pairs are not identical. The simplest way for a mitochondrion to correct a mutation to its mtDNA would be for it detect any mitochondrial chromosome containing a mispaired region and destroy the entire chromosome. There are several chromosomes in each mitochondrion, and a new chromosome could be produced by the replication of an old one when required. Let me emphasise that this is not possible in the chromosomes of the nucleus.

Another way for a mitochondrion to correct a mutation in its mtDNA would be for it to force its several chromosomes to swap strands, then repair the mispaired region that would be revealed as new pairs of DNA strands formed. There would always be a risk that the mutation might be spread by its being taken as the correct template to which to fit nucleotide bases during enzymatic repairing of the mismatch, but this would be numerically unlikely. It would be rendered virtually impossible if all of the mitochondria in a cell fused for a time and forced their chromosomes to swap DNA strands widely and then form new strand pairs. This would reveal mutated strands because they could not form a perfect pair with a normal strand. The cell could then either destroy the chromosomes containing mispaired bases, or repair the mismatched bases [the latter process being less than perfect because the repairing enzymes can hardly be expected to 'guess' correctly every time which is the correct base or sequence of bases to use as the template in performing the repairing. However, if the cell repeatedly forced the mitochondrial chromosomes to swap strands while the mitochondria were fused, and successively repaired mispaired strands, mutated strands would eventually be corrected].

The mitochondria in a cell do fuse from time to time. I suggest that they do indeed destroy or repair mutated mtDNA strands while fused. Fusing is perhaps a bacterial behaviour inherited from their bacterial ancestors, which swapped or donated sections of DNA through conjugation tubes. Nature is a great opportunist, and might have adapted the conjugating behaviour of the bacterial ancestor, in which one bacterium could donate a mutant gene to another bacterium, to similar behaviour in fused mitochondria, in which mutant mitochondrial DNA was not donated but revealed or exposed and got rid of.

This [hypothetical] process of correcting mutations to mtDNA while the mitochondria of a cell are fused might interfere with the vital energy-converting function of the mitochondria. I suggest that an animal would evolve so that its cells did it only as often as necessary. And I suggest that something in the evolution of humans, perhaps the acquisition of language and abstract thought, and the great need that this created for perfect functioning of the brain cells over a period of many years, caused humans to correct mutations to their mtDNA much more effectively and rigorously than chimpanzees, and that this is done in all human cells, not just brain cells. Alternatively, the mitochondria might be involved in brain function in humans in a more complicated way than in other animals, and this might cause them to behave in the way I have outlined above. I shall write about this possibility in another article.)

Published 19 June 2000. © Andrew Gyles

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Oversights in calculating when mitochondrial Eve lived

On 17 March 2000 I sent a second letter to the Editor of 'Nature', the weekly journal published in London. I introduced it to the editor with a short note, part of which follows:

'I submit a Letter to the Editor headed "Oversights in calculating when mitochondrial Eve lived". The subject has been controversial since Nature published the article by Wilson et al in 1987. Gradually, though, Wilson's model has come to be accepted as the standard one. I have heard that some authors writing up evolutionary studies based on nuclear gene sequences now seek to explain their results in terms of the "standard model" even if they don't obviously support it, because they are afraid that if they contradict the standard model they will not get published. This situation cannot be good for science. I hope you will find room in your Letters page to publish a contrary view that is not based on original research (I am not able to do that) but on an examination of the logic that supports the Modern African Eve model. I believe that that logic is flawed and the conclusions based on it are insecure.

Regards, Andrew Gyles'. My Letter to the Editor of 'Nature' follows:

Oversights in calculating when mitochondrial Eve lived

Cann et al calculated the rate of sequence divergence in human mtDNA by assuming that certain 'region-specific clusters' of these sequences in the aboriginal inhabitants of Australia, New Guinea and the New World had arisen in those countries and therefore could not be older than the first dates of settlement (1). Wilson and Cann later took these dates for Australia and New Guinea to be 50,000 to 60,000 years ago (2). They used the calculated rate to show when the most recent common mitochondrial ancestor of all humans ('Eve') lived.

I argue here that the assumed region-specific clusters of Australia, New Guinea and the New World arose in Asia, might be 500,000 or 600,000 y ears old, and became extinct in Asia after some of the people bearing them had migrated to Sahul and the New World. The people survived in Sahul and the New World because both of these huge regions were benign in climate and rich in food (except for Alaska , the colder parts of Canada and the deserts of Australia). Just as importantly, they were uninhabited until recently in human evolution and remained lightly settled until a few centuries ago, lessening the likelihood of one group of humans exterminating another in order to gain territory.

Most of the New World is more hospitable to human life than Siberia. It is easy to imagine some mtDNA clusters becoming extinct in the human population of Siberia but surviving and flourishing as the first settlers from Siberia and their descendants expanded into the New World.

The settlers of Sahul crossed a sea-channel at least 70 kilometres wide to get there from Asia, when the sea level had been lowered by the last ice age and the great continental shelf east of Asia was a plain. They were presumably a people who took food from the sea as well as the land, and who had sea-faring ability. Some of these sea-using people might have stayed behind on the ice-age coast of Asia, with the plain between them and high ground. That tropical plain was probably productive of food and fairly densely settled.

When the ice age ended and the sea rose it re-invaded the plain rather quickly, at the rate of a kilometre a year in places (3). In this situation the sea-using people on the Asian side of the sea-channel were vulnerable. The inhabitants of the land between them and high ground were not likely to give their territory to refugees driven westward by the invading coast, and the number of refugees would have increased year by year, century by century. The sea-using people might not have drowned, but many of them and their descendants would have been clubbed or speared to death in fights for living area that went on for scores of generations. It is likely that those of them capable of crossing the sea-channel would have made every effort to flee to Sahul.

The sea-using people that had settled in Sahul and their descendants were not vulnerable in the same way. Some of them might have migrated inland long before the sea began to rise, but Sahul was only lightly settled, and refugees from its re-invading coastline could move inland and find new territory without having to fight other human beings for their land. Thus some ancient mtDNA clusters might have been wiped out by the effects of the rising sea in eastern Asia but survived and flourished in Sahul.

If the apparently region-specific clusters of mtDNA sequences used by Cann et al originated as early as I suggest, the divergence rate calculated by those authors is 10 times too high and their 'mitochondrial Eve' must have lived about 1.5 million years ago, not about 150,000 years ago.

This matter will not be settled until laboratory methods are devised of comparing the net mutation rates of the mtDNA sequences of interest in humans and chimpanzees (I can think of two approaches to this problem).

The acquisition of language by humans conferred 'evolutionary leverage' on wise, knowledgeable and communicative old individuals through increased survival rates of their children and grandchildren. But this leverage could last only while the brain was vigorous and free from diseases, including those caused by mitochondrial mutations in brain cells. I suggest that natural selection in this situation greatly reduced the mitochondrial mutation rate in humans, perhaps to about a tenth of that calculated by Cann et al.

The arguments I have advanced above might also apply to some of the apparently region-specific alleles of nuclear genes.

References

1) Cann, R.L., Stoneking, M., & Wilson, A.C. Nature 325, 31-36 (1987).

2) Wilson, A.C. & Cann, R.L. Scientific American 264, 22-27 (1992).

3) Thorne, A. & Raymond, R. Man on the Rim, chapter 2, 28-47 (Angus & Robertson, Sydney, 1989).

Andrew Gyles

This letter was not published in 'Nature'. However, the Editor's guide for authors informs them that 'Nature' has space to publish only one in 10 of the letters to the Editor that it receives each week.

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Crews of hunting, fishing and exploring boats were all-male

Males do not pass their mitochondrial chomosome to their children. Most of the voyages made in historical times on kayaks, umiaks, rafts, canoes and other types of vessel on hunting, fishing and exploring expeditions have been made by all-male crews.

There is no reason to suppose that the crewing of these vessels was any different in prehistoric times. One of the reasons is that men are stronger than women. A umiak (a stout vessel covered with walrus skins) hunting whales in the Bering Strait needed a strong crew because the chase, the killing and the tow home were hard and dangerous. Whales were still being hunted from umiaks in the 1900s (1). During the ice age the coasts of Siberia and America were closer than they are now. If male Siberian whale hunters crossed the Bering Strait in prehistoric times after America was settled they might have mated with American women, and so added their nuclear genes to the American gene pool, but they could not have added their mitochondrial genes to it.

A north-west monsoon blows from Indonesia to Australia from January to March. For most of the rest of the year a south-east monsoon (sometimes called a south-east trade) blows from Australia to Indonesia. In the 1800s these winds were regularly exploited by trepang fishers from Makasar and Sumbawa Island, who sailed before the north-west wind in large vessels called praus. This constant wind pushed the trepang fleet 1200 miles from Makasar in from 10 to 15 days. The main problem was not to hit Australia too hard. The crews were all-male. They collected trepang, dried and smoked it in camps on Australian beaches, filled the holds of their praus, then sailed home with the south-east wind at their backs.

This 'monsoon-shuttle' was probably blowing throughout the last ice age, because it is powered by the hotness of vast lands in summer. Asia and Australia must have been heated in their alternating summers even during an ice age. There is no reason to believe that Indonesian sailors did not ride this shuttle in prehistoric times, when the north Australian coast (then a coast of the combined land-mass of Australia and New Guinea) was much closer to Timor than it is now (see the maps on page 52 of Man on the Rim). A canoe with the north-west monsoon behind it might have taken only a couple of days to cross from Roti (then a part of Timor) to Hibernia Reef (then a part of Australia), for example.

These prehistoric sailors would not have been searching for trepang (which was sold to China in the 1800s) but they might have sailed for other kinds of fish (which could have been dried), valuable shells, turtles, dugong, wallaby and kangaroo skins, emu feathers and eggs, flint and ochre. (Some of these articles might have had value beyond their utilitarian value, as rarities or possessions conferring prestige.) There is no archaeological evidence of such visits to Australia, but of course the coast on which the evidence might lie is now a hundred metres or so beneath the sea.

And they might have sailed for sheer adventure, an element of human behaviour that some academics seem to overlook.

The crews of the Indonesian canoes sailing to and from Australia on these hypothetical voyages in prehistoric times were probably all-male, just as the trepang-fishing crews were. This might have been because they feared conflict with the Aboriginal inhabitants of Australia, in which men would be better fighters than women. And perhaps they thought the voyage too dangerous, and the work on arrival too hard, for women.

And there would always have been accidental voyages from Australia to Indonesia. 'George Windsor Earl, a visitor to the islands to the east of Timor and only 300 miles from Australia, observed of their seafaring inhabitants around 1840, that nearly every village mourned the loss of praus blown to the south-east' (2). If the vessels sailing in Indonesian waters carried all-male crews then only males could have arrived accidentally in Australia.

However male sailors arrived in Australia from Indonesia, if they had children with Aboriginal women they would have added their nuclear genes to the Australian gene pool, but they could not have added their mitochondrial genes to it.

I think that voyages from Siberia to America, and from Indonesia to Australia, might have been made by all-male crews for tens of thousands of years, and that the sailors might have fathered many children in total on American and Australian mothers. I therefore think that it is not true to say that 'one gene stands for all' in molecular evolution studies if that gene is a mitochondrial one.

References

1) Thorne, Alan and Raymond, Robert. Man on the Rim [:] The Peopling of the Pacific, chapters 4, 5 (Angus & Robertson, Sydney, 1989).

2) Mulvaney, D. J. The Prehistory of Australia, chapter 1 (Penguin, Melbourne, 1975).

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Flaws in the theory of African Eve

There are several of these flaws. I shall describe the smaller ones first, referring mainly to the article that summed up Allan C. Wilson's beliefs about human evolution. This appeared in 'Scientific American' and was published in April, 1992. It was written by him with one of his co-workers, Rebecca L. Cann, and entitled 'The Recent African Origin of Humans'.

I assume that the reader has already read most of the articles on the debate between the 'African Eve' (or 'Out of Africa') supporters and the 'Multi-regional evolution' supporters in 'Science', 'Nature' and other journals. It began in about 1987.

Flaw 1

Wilson and Cann said that the model of multi-regional evolution of modern humans was wrong because 'Huge levels of gene flow...would be necessary to maintain human populations as one biological species'. Why? There is hardly any difference between the genes of a modern human and a chimpanzee. Our nuclear DNA is 98% to 99% identical to that of chimpanzees. The physiologist Jared Diamond has called us 'the third chimpanzee' ('Science', 4 September 1998).

Where was the huge level of gene flow that kept the genes of these two species so alike? Chimps and humans are at the ends of lineages that diverged about 5 million years ago. Obviously there has been no gene flow between the two since they diverged.

What was the genetic difference between Homo erectus and Homo sapiens? There was probably hardly any. In other words, if we wished to classify species genetically, we humans alive today should probably call ourselves Homo erectus, or alternatively we should call all earlier human species by our own name, Homo sapiens.

This is what the 'multi-regionalists' have been saying for years. As Ian Tattersall (not a multi-regionalist) wrote, the multi-regional model 'holds that the highly archaic H. erectus (including H. ergaster) is nothing more than an ancient variant of H. sapiens and that for the past two million years the history of our lineage has been one of a braided stream of evolving populations of this species in all areas of the old world, each adapting to local conditions, yet all consistently linked by gene exchange' ('Scientific American', April 1997). My contribution to the debate is to point out that the gene exchange was not essential.

That is not to say that gene exchange did not occur in certain situations. And that brings me to my next point.

Flaw 2

M. Krings and fellow workers sequenced mitochondrial DNA from a fossil bone of a Neanderthal specimen. I read a short review of their work in 'Nature', 17 July 1997, by Ryk Ward and Chris Stringer, who said: 'Clearly, Neanderthal populations represented by the type specimen did not contribute mtDNA to the modern human population. But, as the authors are careful to point out, this does not exclude the possibility of exchange of nuclear genes. In our view... half a million years of independent evolution of two highly specialized forms of human, with all the attendant behavioural implications, make such an exchange unlikely'.

Not so fast. One behaviour that is consistently observed in humans is that males are attracted to gracile women and females are attracted to robust men. My next contribution to the debate is therefore to point out that Neanderthal males might have eagerly sought modern human females as marriage partners because they would have seemed very gracile to the males. And modern human females might have eagerly sought Neanderthal males as marriage partners because they would have seemed very robust to the females.

However, it is less likely that modern human males would have eagerly sought Neanderthal females as marriage partners because the latter would have seemed robust to the former. And modern human males would have seemed gracile to Neanderthal females. Result: no (or, allowing for human idiosyncrasy and the well-known saying that 'a bird in the hand is worth two in the bush', few) marriages between modern human males and Neanderthal females.

Males do not pass their mitochondrial chromosome to their offspring (some exceptions have recently been reported but they seem to be rare). Therefore, in a situation where Neanderthal and modern human beings were living close together, Neanderthal males might have contributed many nuclear genes to the modern human population but no mitochondrial genes. And Neanderthal females would have contributed few or no nuclear and mitochondrial genes to the modern human population.

It would be very helpful if a molecular geneticist were to sequence the part of the Y chromosome that male Neanderthals passed on exclusively to their sons, and compare it with the Y chromosomes of a sample of living modern human males. This part of the Y chromosome is transmitted in a way analagous to the way the mitochondrial chromosome is passed on by females exclusively to their daughters. Do some modern European males have Neanderthal Y chromosomes? Alas, we shall never know. Nuclear chromosomes (in this case Neanderthal ones), unlike fossil bones, decay rather quickly. This leads me to my third point.

Flaw 3

Wilson and Cann implied that molecular geneticists are in a stronger position than paleontologists because they work with the genes of living subjects; 'living genes must have ancestors, whereas dead fossils may not have descendants'. Are we really to believe that molecular geneticists would refuse to sequence the nuclear genes of a really ancient human fossil if they got the chance?

Paleontologists can work with living subjects and the fossilised remains of dead ones. Molecular geneticists will probably never be able to work with nuclear genes extracted from fossils more than a few thousand years old. But they have sequenced mitochondrial DNA from a Neanderthal fossil bone (see under Flaw 2). It seems they were not dissuaded by the fact that 'dead fossils may not have descendants'.

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" . . . and suddenly a puff of wind, a puff faint and tepid and laden with strange odours of blossoms, of aromatic wood, comes out of the still night - the first sigh of the East on my face".

Joseph Conrad, 'Youth'