--- In AAT@yahoogroups.com
, "Rob Dudman" <ausell@...> wrote:
> Hello Bill......
> There are always differing opinions, but H.georg are classified as
> Homo as the null hypothesis. That the H.georg dated to c.1.8 Mya are
> the remnants of a population that previously diverged to become H.e/e
> is the proposition that IMO seems to best fit the evidence....the
> contentious issue is this idea that they 'somehow got lost in the
> Caucasus'. Reminds me of the idea that Abel is an A.afarensis that
> 'somehow got lost in Chad'! These silly animals didn't just get lost
> by wandering away from their familiar areas....they got lost by
> wandering thousands of kms!
> It would take numerous generations to travel these sorts of distances
> and to call either Abel or H.georg 'lost' either stretches the word
> beyond any useful meaning, or it reflects a determination to maintain
> that H.'had' to have 'belonged' in East Africa where they 'had' to have
> diverged from an A'pith.
If those in the Caucasus were `lost', what does it say for those
who possibly left evidence of their tool use at Riwat (Pabbi
hills, Pakistan) some 1.9 Mya.
This `they had to be in a certain place' attitude probably also
has a lot to do with the OoA just so story of how humanity first
expanded out of Africa (apparently it was just "60,000 years ago"),
an adaptationist just so story that was heavily promoted at the
end of the last century.
> That H.georg was the ancestral Homo population
> some of whom went to Africa (where they came into contact with P.reich
> malaria), is far more sensible than the 'lost' proposition.
It certainly makes a lot more sense than the `lost' proposition...
for example following the unfortunate encounter t an ancestor of the
extant chimpanzee and P.reich, a number of them as H.ergaster they
could have headed for Morocco and history, while the H.erectus
headed east into Asia and extinction.
> Those RVs......
> > Yohn C.T et al. searched the chimpanzee genome for ERV traces, they
> > only found evidence for one - PtERV1.
> > [quote]
> > "...Based on analysis of finished BAC chimpanzee genome sequence, we
> > characterize a retroviral element (Pan troglodytes endogenous retrovirus 1
> > [PTERV1]) that has become integrated in the germline of African great ape
> > and Old World monkey species but is absent from humans and Asian
> > ape genomes"
> I could find nothing in Yohn et al. that indicates they only found
> evidence for one ERV. In fact they write.....
> '....we identified several members of a full-length endogenous retrovirus
> family that were present in chimpanzee but absent in corresponding human
> genome sequence.'
> They concentrate on the PTERV1 marker, but I couldn't find where they
> say it's the only ERV marker to be found and Todaro provides unambiguous
> evidence that chimps also carry the marker for the C type baboon RV.
In the first sentence of the following quote they say that they found
one marker in the chimpanzee genome that is not shared with humans...
From the summary of Eichler's paper;
"...In a new study, Evan Eichler and colleagues scanned finished
chimpanzee genome sequence for endogenous retroviral elements,
and found one (called PTERV1) that does not occur in humans.
Searching the genomes of a subset of apes and monkeys revealed
that the retrovirus had integrated into the germline of African
great apes and Old World monkeysbut did not infect humans and
Asian apes (orangutan, siamang, and gibbon). This undermines
the notion that an ancient infection invaded an ancestral
primate lineage, since great apes (including humans) share
a common ancestor with Old World monkeys.
On the other hand we share something like 98,000 other
markers with the extant chimpanzee and other primates.
> > > Todaro OTOH, does present sufficiently compelling evidence to shift the
> > > burden of proof onto the A'pith-descent hypothesis to show that the C type
> > > baboon RV did not reach East Africa.....and so far every attempt at this
> > > that I've come across has been constructed on special pleading.
> > Not so certain. Africa is a somewhat large continent; and the respective
> > numbers of a'piths, gorilla and the extant chimpanzee around three million
> > years ago would likely have numbered in the thousands or tens of thousands
> > at most, and most of the primates if not all that succumbed would have been
> > rainforest species.
> Certainty is not the issue for me, it's about the burden of proof and a
> defensible null-hypothesis. Todaro tested 23 African primate species only
> four of which are strictly rainforest species - mandrill, chimpanzee,
> gorilla and the mangabey....the patas is a savanna/open woodland monkey,
> colobus are widespread and are found in East Africa, galagos are native
> to southern Africa. This and paleoclimatic evidence indicating that a
> viable airborne vector was present during the early and mid-Pliocene
> Warm Periods is enough to shift the burden of proof onto those who would
> claim that East Africa was not reached by the baboon RV.
However, I still think that the odds of a successful airborne
spread of a RV three to four million years ago are at best
on the low side, when you take into account that the African
continent straddles the equator and amounts to about
11 million sq. miles in surface area (or about 20 per cent
of the total land surface of the planet)
when you combine
that with the likely number of infected individuals at the
height of an RV outbreak three to four million years ago,
the odds would likely worsen.
(gorilla, chimpanzee an hominin numbers at three to four
million years ago, would be in the tens of thousands
sparse populations concentrated in a few locations)
Extrapolating backwards so to speak from the present (in terms
of habitat, behaviour and more) also has a few difficulties,
for example hominins have certainly changed somewhat over the
last four million years, and the sole surviving example -
ourselves - has changed considerably)...in all likelihood the
behaviour and niche preferences' of the ancestors of extant
monkey, baboon and ape species you mention has also changed
somewhat over the last few million years.
> > There are also questions about timing and location, for example the
> > origins of the baboon as such are thought to have been in southern Africa
> > and South Africa with the northern clade of the baboon estimated to have
> > diverged from there southern kin at around two million years ago, so it
> > could be argued that the baboon has only been present in northeast Africa
> > in the last two million years (even today, they are not present in a large
> > part of north Africa).
> > Then there are divergence dates themselves, the Papio-Theropithecus divergence
> > was about 1.4/1.5 Mya after the ancestor of the extant chimpanzee and that
> > of Man went their separate ways, then there are the divergence dates among
> > the baboons.
> > [quote]
> > "...Our divergence age estimates indicate an initial separation into
> > southern and northern baboon clades 2.09 (1.54-2.71) million years ago
> > (mya). We found deep divergences between haplogroups within several
> > species (~2 mya, northern and southern yellow baboons, western and
> > eastern olive baboons and northern and southern chacma baboons), but
> > also recent divergence ages among species (< 0.7 mya, yellow, olive
> > and hamadryas baboons in eastern Africa)."
> > http://www.biomedcentral.com/1471-2148/9/83
> A southern African origin of the baboon seems most likely with an
> original divergence from Theropithecus between 3 & 4 Mya (the period
> of the RVs and a tropical climate in most of Africa). The conclusion
> here is that the C type RV infected the original baboon species and
> then crossed to the other primate species with the marker then being
> inherited by all subsequent subspecies. For the first inter-species
> spread of the RV it was not at all necessary that the baboon had to
> have spread from southern Africa that early....along with the wind,
> the other primate species would have done the job.
Possible, but a horizontal (contact) spread between species
would have same result... though it may have not spread
as far north.
> The CMAH mutation....
> > > And the genetic evidence indicates that it was significantly prior to
> > > c.2 Mya...despite the previously mentioned verbal obfuscation by Chou
> > > et al. that would make c.2.8 Mya 'just before' c.2 Mya.
> > That discrepancy in timing would seem to break any potential link between
> > the inactivation of CMAH at 2.8 Mya and an expansion human brain.
> > at around 2 Mya
> > Energetics and the evolution of human brain size
> > http://www.nature.com/nature/journal/v480/n7375/full/nature10629.html
> > Human brain expansion
> > http://www.nature.com/nature/journal/v480/n7375/fig_tab/480043a_F1.html
> > Intriguingly over 50% of the `expansion' in the human brain occurred
> > between 800,000 and 200,000 years ago which would coincide with the
> > exaptations for language (the use of spoken sounds) in the human lineage.
> > on the other hand there appears to have been no expansion of the human
> > brain over the last 200,000 years( its relative size has reduced), so
> > those AMH who some think ate shellfish by the bucket load on the shore
> > were clearly wasting their time, they would have been better off tucking
> > into a juicy steak (on taste grounds).
> AFAICS, the CMAH mutation was only incidentally connected with an
> increase in brain-size and then only after some considerable time.
> Neu5Ac is a neural nutrient and this would lead to an increase in
> neural density, not to an increase in the overall size of the brain....
> for this I assume an abundant and readily available dietary DHA
> would have been required. It seems most likely to me that the H.e/e
> brain was the result of both the CMAH mutation and a subsequent
> period of high DHA intake (along with a cascade of related genetic
> changes - see below re the SRGAP2 duplication).
As you say the CMAH mutation could simple have been a precursor to
what followed somewhat later, as a surplus of Neu5Ac in itself would
not have led to an increased neuron density, as it is better seen
as an available resource rather than a nutrient (IMO the same
applies to DHA).
The likely difference in humans following the CMAH mutation was
that there would have been a sufficient Neu5Ac available if
there was a need for it...
IMO, something else was driving the demand for more processing power
in the brain of humans just under a million years ago. (the acquisition
of a spoken language could have been one possibility)
> > `Cooking' the uniquely human innovation of cooking what they hunted or
> > gathered as food, was probably one of the major factors in the expansion
> > of the human (in increasing its neuron count that is.) as `cooking' their
> > food enabled humans to pre-digest a wide range of foods, and in doing
> > ensured they received the nutrients they needed to develop and sustain a
> > uniquely `large' brain (however among AMH it has become an all too
> > efficient way of getting the nutrition, modern man needs. to extant
> > some food "experts" now advocate returning to what our distant
> > ancestors ate a couple of million years ago. namely raw food).
> In their defense....salads do combine healthy food with good taste
> and a pleasing range of colours (not sure that the latter is apropos
> of much, but y'never know). Trouble is for those who live in colder
> climates salads don't warm you up as much as a good stew. :-)
Probably human ancestors would not have moved into cold climes, if
they had to rely on a diet of raw food
I would guess 30,000 years
ago north of the Arctic Circle a bellyful of hot stew would have
been a lot more satisfying (an appetising), than several
bucketfuls of cold shellfish.
A short paper on the early hominin diet...
Stable isotope-based diet reconstructions of Turkana Basin hominins
Hominin fossil evidence in the Turkana Basin in Kenya from
ca. 4.1 to 1.4 Ma samples two archaic early hominin genera and
records some of the early evolutionary history of Paranthropus
and Homo. Stable carbon isotopes in fossil tooth enamel are
used to estimate the fraction of diet derived from C3 or C4
resources in these hominin taxa. The earliest hominin species
in the Turkana Basin"
Seems to fit well with what Cerling and colleagues (2011)
said a couple of years ago.
> > Sort of related.
> > Extra gene drove instant leap in human brain evolution
> > http://www.pasthorizonspr.com/index.php/archives/05/2012/extra-gene-drove-instant-leap-in-human-brain-evolution
> Thanks for the link.
> As usual when reading papers about genetic research brain-fog was
> almost instantaneous, but I was able to see how important this
> particular research could be for understanding human brain evolution.
> Dennis et al. (http://tinyurl.com/mc3x2h8) estimate the dates of the
> three duplications at 2.8-3.9 Mya, 2-2.8 Mya and 0.4-1.3 Mya and
> isn't that an interesting trio of dates.....with the CMAH mutation
> right between the first and second duplications and heidelbergensis
> at the later end of the estimate for the third duplication.
The heidelbergensis link(the duplication around a million years ago)
was the first thing that stood out for me, as the third duplication
occurred around the time when encephalization in humans underwent a
remarkable change in matter of a few hundred thousand years,
ceasing sometime between 400,000 and 200,000 years ago,
They identify the second as occurring during the `transition' from
a'pith to Homo 2.4 Mya
However they don't appear to given a
reason for the first at around 3.4 Mya.
The latter two duplications are unique to humans.
> It's one thing to identify the nutritional role of Neu5Ac and its
> abundance after the CMAH mutation, but these SRGAP2 duplications
> seem show the nuts and bolts of the way that neural nutrition works
> to feed the growth of dendrites (and I presume, axons)......
Can only but agree...
> 'We used in vitro and in vivo approaches to determine the function
> of SRGAP2 and its human paralogs in the neocortex region of the
> brain, the evolution of which is thought to underlie the emergence
> of human cognitive abilities. Our results uncover a new function
> for ancestral SRGAP2 in promoting dendritic spine maturation and
> indicate that expression of a human-specific paralog of SRGAP2 in
> mouse pyramidal neurons extends the phase of spine development and
> leads to an increased density of longer spines in vivo, a feature
> characterizing pyramidal neurons in the human neocortex.'
> Inhibition of SRGAP2 Function by Its Human-Specific Paralogs Induces
> Neoteny during Spine Maturation.
> By Charrier C. et al.
Taken together, our results suggest that the expression
of SRGAP2C in the human brain inhibits the function of
ancestral SRGAP2 and thereby reduces the rate of spine
maturation, leading to changes in spine morphology and
density that could have important implications for
cognition, learning, and memory"
We may have been looking at the wrong types of mutations
to explain human and great ape differences," Eichler says.
"These episodic and large duplication events could have
allowed for radical potentially earth-shattering changes
in brain development and brain function."
> > > If the inactivation of Neu5Gc conversion resulted from a catastrophic
> > > epidemic of P.reich malaria, then that contact with chimps (and/or
> > > gorillas) would be fairly accurately dated by the CMAH mutation. After
> > > all, how long would it take for the vulnerable to die or become seriously
> > > debilitated as a result of malaria and thus be removed from the reproductive
> > > equation?
> > Not long... if hominins some three million years ago, had not previously
> > encountered malaria.
> > Assuming the CMAH mutation happened around 2.8 Mya, then the hominin
> > ancestors of Man would have had to return to mainland Africa prior to
> > that date if they had been absent entirely from Africa between four and
> > three million years ago, as they would have had to returned prior to
> > that date to have that disastrous encounter with the ancestor of the
> > extant chimpanzee that `introduced' them to an infection (malaria) that
> > still plagues mankind today. (2010 - Worldwide death toll from malaria,
> > 1.2 million)
> > Which in itself raises the question, did they remain in Africa after
> > that disastrous encounter with the ancestor of the extant chimpanzee,
> > or did they leave again, only to return again at around 2.4 Mya?
> The first indisputably H. fossils in Africa are less than 2 Mya, so I
> see no reason to think that they had to have returned around 2.4 Mya.
> Given that fossilisation is not a common occurrence I would have
> thought a return around 2 Mya would take taphonomic bias into account.
The habilis (2.33 1.4 Mya) may not be generally accepted, but it
highly unlikely that the H.erectus was the first member of genus
H., in north east Africa
so I would go with the earlier date
(2.3 - 2.4 Mya, based on evidence for tool use and meat eating.
This is sort of related, and intriguing...
"...Recent research indicates that stone points the oldest kind
of spear point are about 500,000 years old," he said. "But people
have been killing animals for at least 2 million years, and eating
animals for about 2.6 million years."
"...That means that for about 1.5 million years, when people
hunted, they basically had nothing more lethal to throw than a
pointed wooden stick," he continued. "If you want to kill something
with that, you have to be able to throw that pretty hard, and you
have to be accurate. Imagine how important it must have been to our
ancestors to throw hard and fast."
Researchers say ability to throw played a key role in human evolution
Some primates, including chimpanzees, throw objects occasionally,
but only humans regularly throw projectiles with high speed and
accuracy. Darwin noted that the unique throwing abilities of humans,
which were made possible when bipedalism emancipated the arms,
enabled foragers to hunt effectively using projectiles."
Elastic energy storage in the shoulder and the evolution
of high-speed throwing in Homo
Neil T. Roach, Madhusudhan Venkadesan, Michael J. Rainbow
& Daniel E. Lieberman
Found this brilliant piece of research intriguing for two reasons,
firstly for the insight into how the human ability to throw developed,
and secondly because it firms up the date at which hunting became the
way human ancestors procured their food.
> > Either way it does not seem very parsimonious that early hominins would
> > have migrated en masse once out of Africa far less migrate en masse in
> > an out of Africa several times.
> They moved en masse from somewhere to either Central or West Africa
> c.3 Mya (to catch P.reich malaria and leave no Neu5Gc producing
> survivors), they then moved away again en masse to evolve into H.e/e
> either in eastern or southern Africa or somewhere out of Africa.
> The question is not how many times they moved, but how far. In terms
> of parsimony the c.3 Mya move to either Central or West Africa is
> required by the A'pith-descent hypothesis, as is the move away again
> after the infection as there's no evidence or reason to think that
> H.e/e emerged in either of these places.
The difficulty for any other hominin decent theory is that other
than a'piths in north and eastern Africa from four and two million
years ago there is no fossil evidence for any other hominins in
or out of Africa at that time
yet the a'piths left plenty.
(That the A'piths could
> make this sort of journey is undeniable; but Abel, poor lost thing,
> was in Central Africa c.3.5 Mya when the RVs were active so it's
> unlikely that it was them who later caught P.reich malaria and then
> adapted into H.e/e sans Neu5Gc.)
The long lived a.afarensis (3.9 Mya to 2.9 Mya) a long lived a'pith
species, as its name suggests it hailed from the Afar like the earliest
members of AMH
they would have been in north east Africa when the
ancestor of the extant chimpanzee succumbed to PtERV1. ("Lucy" an her
kin were a.afarensis, as probably was "abel "who went walkabout
in Chad some 3.6 Mya)
Also the disastrous encounter some hominin unfortunately had in the
jungle around 3.0 Mya with an ancestor of the extant chimpanzee, seems
to have occurred at around the time the a.afarensis gave way to the
a.africanus in Africa.
> The A'pith-descent hypothesis then has to propose a move out of East
> Africa by the newly emerged H.e/e as their fossils are found in East
> Asia dating to shortly after the first African fossils. OTOH, the
> proposal that our ancestors left Africa immediately after the P.reich
> epidemic suggests that around 2 Mya H.e/e radiated from somewhere
> between East Asia and Africa and this is in accordance with the
> dates for the earliest H.e/e fossils from both places. In terms of
> parsimony between the two proposals it seems to me to be 'half a
> dozen of one and six of the other'.
As you say, neither proposal provides a satisfactory answer...
> > Something nasty that came out of the sea...
> > History of Malaria Parasite and its Global Spread (2011)
> > http://www.malariasite.com/malaria/history_parasite.htm
> > ___________________________________
> Interesting. Thanks.
> > > You say that the PTERV1 probably changed how the chimpanzee evolved, but
> > > other than leaving a genetic marker, I'm aware of no evidence for this.
> > > Gorillas also carry the PTERV1 marker and AFAIK, there's no evidence for
> > > it having any substantial effect on their evolution either. Likewise with
> > > the later infection of macaques and baboons.....it left a marker and that's
> > > about it. Whatever symptoms that the PTERV1 caused we can reasonably assume
> > > that it had no reproductive repercussions....those who had the disease were
> > > successful enough at reproduction to leave the marker in all descendants.
> > It had the potential to, and may have changed how the ancestor of the
> > extant chimpanzee subsequently evolved . the following quote is from
> > the abstract of the PtERV1 paper;
> > [quote]
> > ".Retroviral infections of the germline have the potential to
> > episodically alter gene function and genome structure during the
> > course of evolution. Horizontal transmissions between species have
> > been proposed, but little evidence exists for such events in the
> > Human/great ape lineage of evolution. Based on analysis of
> > finished BAC chimpanzee genome sequence, we characterize a
> > retroviral element (Pan troglodytes endogenous retrovirus 1
> > [PTERV1]) that has become integrated in the germline of African
> > Great ape and Old World monkey species but is absent from humans
> > and Asian ape genomes."
> Yes, such RVs do have great potential to alter an evolutionary trajectory
> because of the way they can penetrate the genome, but that being said
> there appears to be no evidence at all that this in fact happened with
> the PTERV1 or the baboon C type.
> What does intrigue me is the fact that like every other living thing,
> the virus is first and foremost concerned with survival, then with
> reproduction and proliferation. Viruses that kill their hosts quickly
> are self-limiting in these objectives, while others that don't adversely
> affect their hosts have an advantage in these objectives.
Not certain, that a virus can be defined as living (as apparently they
cannot replicate themselves)
probably they are the real `undead' -
being neither one nor the other.
> This raises the question of why it is that we don't find viruses that
> act to make their hosts healthier with the best chance to reach maximum
> longevity? Surely this would maximise the virus' chances in reproduction
> and proliferation, yet the bloomin' things don't seem to do this....
> why no virus that boosts the immune system, or increases healing
> capacity? I wonder if there are genetic researchers who are trying
> to genetically alter viruses to have positive rather than negative
> consequences. Spontaneous remission of cancer appears to be some sort
> 'delayed' immune system reaction that suddenly recognises the cancer
> cells as 'foreign'....it seems to me that a genetically manipulated
> RV would be able to trigger this reaction.
Probably viruses are the last thing if ever that `scientists' should
ever tamper with... as one mistake could have dire consequences.
Viruses themselves can be likened to parasites, in that they use the
host's cells to reproduce themselves, then when they have finished
they can end up killing the host.
> > > The fact that the later infection also left a marker in Asian macaques is
> > > intriguing given that it did not also get to orangs and gibbons....and both
> > > were in East Asia at that time. IIRC, the oldest Asian macaque fossil dated
> > > at c.3 Mya was found in northern India so maybe they took it there from Africa
> > > and it got no further as an active RV.
> > It would have had to have infected macaques in east Asia, and the
> > baboon in Africa. less than two million years ago - different species
> > on different continents.
> > From the PtERV1 paper;
> > [quote]
> > "...Furthermore, both Asian (macaque) and African (baboon) Old
> > World monkeys show evidence of PTERV1 proviral integrations
> > less than 2 million years ago, indicating that the exogenous
> > source virus is either endemic to both continents or that
> > ancestral populations frequented both continents.'
> Ok, but why did it have to have infected macaques in East Asia rather
> than the marker being carried east from India as the macaques spread
> and diverged?
As far as I know the macaques in Asia diverged into four or five
species some 3 Mya, a million and so years before PtERV1 infected
the Asian macaques. (however there is also a second question, the
question of how the baboons in Africa came to be infected less
than two million years ago and more than a million or so
years after an ancestor of the extant chimpanzee
was infected in Africa?)
It seems that neither the orang, gibbon nor other Asian
> monkeys came into contact with the PTERV1 and while this is not conclusive
> evidence that the RV didn't reach East Asia, it is indicative evidence
> that the RV was never active in eastern Asia.
Seemingly humans, in the shape of the H.erectus also seem to have
evaded that second outbreak less than two million years ago, even
though they were present on both continents when both the baboon
and the macaques would have succumbed to PtERV1.
> > > The fact that an obligate striding bipedal gait was in East Africa c.3.6 Mya
> > > is usually seen as evidence that our ancestors were there c.3.6 Mya and all
> > > they have to do now is deal with the RV evidence in a scientifically rigorous
> > > manner and I for one will readily accept that as the null. But until this
> > > is done I see those prints as evidence of probable common ancestry....a
> > > bipedal A'pith/H/P LCA.
> > The other way of seeing it, would be to say that it is simply evidence that
> > the hominins in east Africa more than 3.6 Mya were obligate bipeds, whether
> > any of the hominins in east Africa at that date were the direct ancestors
> > of Man that would be a different question... though the more that is known
> > about the a'piths, the more it favours that a least one or more a'pith
> > species as being forerunners of genus Homo.
> Yes, I agree....now all they've got to do is deal with the lack of the
> C type baboon RV marker in a scientifically rigorous way and I'll take
> a ride on the A'pith-descent bandwagon toot sweet, but bearing in mind
> that all refuted scientific hypotheses fit all the facts except the one
> that refutes them, I have to consider the A'pith-descent hypothesis as
> refuted. :-)