IUBio Biosequences .. Software .. Molbio soft .. Network News .. FTP

The 'bushy' hominid tree and human linkage disequilibrium (hypothesis)

Andrew Gyles syzygium at alphalink.com.au
Mon Aug 20 00:38:20 EST 2001

The 'bushy' hominid tree, hominid extinction and human linkage
disequilibrium (hypothesis)

Fossil evidence indicates that there were many lines of hominid living in
different parts of Africa millions of years ago, one of which led to the
human species. The hominid tree was 'bushy'. A separate line (not a 'bushy'
tree, as far as is known) led from the common ancestor of the hominids and
the chimpanzees to the chimpanzees. (No fossils of chimpanzee ancestors have
been found.)

I propose that the common ancestor of the hominids adapted to a changing
climate and environment by rapid genetic change. This change was not the
gaining of alleles through random mutation (which could hardly be rapid
without being fatal to the survival of the species). It was the rapid loss
of alleles in the germ line through unusually vigorous repairing of
mispaired bases in heteroduplex segments during crossing over in meiosis. In
each of these repairing events an allele is lost. Alternatively the length
of heteroduplex segments might have increased in the hominids; this combined
with the repairing of some of the mispaired bases would have increased the
rate of loss of alleles.

As the hominids spread over a broader area of Africa and became isolated
into several groups or 'gene pools' the vigorous repairing in heteroduplexes
continued and the loss of alleles continued, but because the losses were
random the resulting frequencies of particular alleles in each of the gene
pools began to differ from pool to pool.  This would cause the average
phenotype in each gene pool to differ from that in each of the other gene
pools. Thus the hominid tree developed many branches and became 'bushy', as
the hominid fossils found in different parts of Africa attest.

I propose that in the ape lines of descent the repairing of mispaired bases
in heteroduplexes was not as vigorous as it was in the hominids.

The rapid loss of alleles from the gene pool of a species well stocked with
them would not necessarily be fatal to the survival of the species. (This
cannot be said of the rapid gain of alleles through random mutation.) There
are, however, two important classes of allele that must not be lost from the
gene pool of the species (or from an isolated group of interbreeding
individuals within the species) if it is to survive.

The first class comprises the many alleles of the histocompatibility genes,
which must be present in the gene pool of a species to ensure its survival
in spite of the presence in its environment of any of various parasites.

The second class comprises beneficial dominant alleles that help an
individual to survive and reproduce even if it bears a deleterious recessive
allele at the same locus in the homologous chromosome. If the gene pool of a
species lost too many beneficial dominant alleles and was left with too many
deleterious recessive alleles the species might lose the struggle for

Alleles in the first and second classes would be preserved in the gene pool
by natural selection unless the overall rate of loss of alleles through
repairing of mispaired bases in heteroduplex segments during meiosis left
too few of them for natural selection to preserve. This might explain why
all but one of the hominid lines became extinct: perhaps the line of
hominids leading to humans was the only one lucky enough to retain all of
the alleles needed for survival and to lose many deleterious alleles.

I suggest that the great linkage disequilibrium that has recently been
measured in the chromosomes of some human groups is a reflection of the
(hypothetical) increased rate of repairing of mispaired bases in
heteroduplexes, or of increased length of heteroduplexes (or a combination
of both of these) in hominids, including humans. In particular, an increase
in length of the heteroduplex segments formed during meiotic crossing over
in hominids and humans, combined with a greater rate of repairing of
mispaired bases in these segments, would cause great linkage disequilibrium.
This would be so because the different 'markers' by which linkage
equilibrium is measured - variations in base sequence from one individual to
another in a population - would become fewer at each marker position, and in
some positions might be reduced to no variation.

The end result in the human species would have been remarkably little
sequence variation between individuals as compared with other species.

The (hypothetical) increase in the rate of loss of alleles during meiosis
might have been the product originally of a few random genetic mutations in
the ancestor of the hominids. However, it is worth considering the
alternative possibility that this mechanism might be common to many species
of organism, might have been used many times before in the course of
evolution and might be hundreds of millions of years old. It might be lying
latent in these species waiting to be called into action whenever rapid
environmental change threatened the survival of a species.

Andrew Gyles


More information about the Mol-evol mailing list

Send comments to us at biosci-help [At] net.bio.net