First 'language gene' discovered 
Author Message
 First 'language gene' discovered
http://www.***.com/

It's apparently associated with {*filter*} movements.  A 2-letter difference
produces severe speech defects in humans.  Other mammals (mice, monkeys,
apes) have the "defective version".  The 2-letter difference is universal in
all humans except those with the defect.  Approximate age of the human
variant is 200 ka.  There are presumed to be other genes to find.

--
Dave Timpe

dtimpe at new dot rr dot com



Mon, 31 Jan 2005 03:18:22 GMT
 First 'language gene' discovered
  Could it be the difference between Neanderthal and man?         Otter
*******************************************            
First 'language gene' discovered  

Group: sci.anthropology.paleo Date: Wed, Aug 14, 2002, 7:18pm (EDT+4)

http://www.***.com/
It's apparently associated with {*filter*} movements. A 2-letter difference
produces severe speech defects in humans. Other mammals (mice, monkeys,
apes) have the "defective version". The 2-letter difference is universal
in all humans except those with the defect. Approximate age of the human
variant is 200 ka. There are presumed to be other genes to find.
--
Dave Timpe
dtimpe at new dot rr dot com



Mon, 31 Jan 2005 12:19:37 GMT
 First 'language gene' discovered

Quote:

>   Could it be the difference between Neanderthal and man?         Otter
> *******************************************            

It's probably _a_ difference. The dating is interesting--about the same
time as the emergence of complex social structures in African hominids,
and also about the same as the appearence of advanced paleolithic
industries in central Africa. There is a suspicion that there was a
climate-caused ecological bottleneck in Africa (like the Grande Coupure
in the Oligocene) at about that time.

The neuroscience of language is interesting, too. To understand complex
language, it looks like you have to be able to produce a complexly
varying sequence of neural attractors in an area of neocortex. Those
attractors participate in a match/mismatch process (c.f., Hebb-Marr
autoassociation) and feed back into other areas of the cortex that do
the semantic decoding. Sure, bats do something like this, but only for
fairly simple dynamics. It now seems that complex attractor dynamics
(think of productive speech or complex plans) may be rather hard to
generate neurally. If the autoassociative connectivity is too sparse, no
association takes place, but if the connectivity is a little too dense
or if the local inhibitory connections are a bit inefficient, you get
overlap between the attractors, and the whole network ignites. You have
tune the system to operate in a narrow band for it to work well. Some
{*filter*} appear to affect the tuning. Caffeine, thiophylline, and
thiobromine seem to increase the sensitivity of this system to patterns,
and some anti-anxiety medicines seem to be able to take the edge off.
This is the sort of thing that would be sensitive to genetic details.

Yes, there's probably a connection to epilepsy, creativity, mood
disorders, and intelligence.

Quote:
> First 'language gene' discovered  

> Group: sci.anthropology.paleo Date: Wed, Aug 14, 2002, 7:18pm (EDT+4)

> http://www.***.com/
> It's apparently associated with {*filter*} movements. A 2-letter difference
> produces severe speech defects in humans. Other mammals (mice, monkeys,
> apes) have the "defective version". The 2-letter difference is universal
> in all humans except those with the defect. Approximate age of the human
> variant is 200 ka. There are presumed to be other genes to find.

--
Harry Erwin < http://www.***.com/ ~herwin/>


Mon, 31 Jan 2005 21:33:26 GMT
 First 'language gene' discovered


Absent genetic evidence from Neanderthals, it's hard to
say. Given the uncertainty in genetic dating, it's hard to
distinguish 200ky from the 450ky for "Mitochrondal Eve."
So if Neanderthals split off before then, most likely they
didn't have it. If they split off later, then they most likely
did.

More research is clearly needed. Don't get in the way
of the researcher stampede.

John Roth

 Could it be the difference between Neanderthal and man?         Otter
*******************************************
First 'language gene' discovered

Group: sci.anthropology.paleo Date: Wed, Aug 14, 2002, 7:18pm (EDT+4)

http://www.***.com/
It's apparently associated with {*filter*} movements. A 2-letter difference
produces severe speech defects in humans. Other mammals (mice, monkeys,
apes) have the "defective version". The 2-letter difference is universal
in all humans except those with the defect. Approximate age of the human
variant is 200 ka. There are presumed to be other genes to find.
--
Dave Timpe
dtimpe at new dot rr dot com



Mon, 31 Jan 2005 22:49:31 GMT
 First 'language gene' discovered

Re: First 'language gene' discovered  

Group: sci.anthropology.paleo Date: Thu, Aug 15, 2002, 2:33pm (EDT+5)

??????Could it be the difference between Neanderthal and
man? ? ? ? ? Otter
*******************************************
It's probably _a_ difference. The dating is interesting--about the same
time as the emergence of complex social structures in African hominids,
and also about the same as the appearence of advanced paleolithic
industries in central Africa. There is a suspicion that there was a
climate-caused ecological bottleneck in Africa (like the Grande Coupure
in the Oligocene) at about that time.
The neuroscience of language is interesting, too. To understand complex
language, it looks like you have to be able to produce a complexly
varying sequence of neural attractors in an area of neocortex. Those
attractors participate in a match/mismatch process (c.f., Hebb-Marr
autoassociation) and feed back into other areas of the cortex that do
the semantic decoding. Sure, bats do something like this, but only for
fairly simple dynamics. It now seems that complex attractor dynamics
(think of productive speech or complex plans) may be rather hard to
generate neurally. If the autoassociative connectivity is too sparse, no
association takes place, but if the connectivity is a little too dense
or if the local inhibitory connections are a bit inefficient, you get
overlap between the attractors, and the whole network ignites. You have
tune the system to operate in a narrow band for it to work well. Some
{*filter*} appear to affect the tuning. Caffeine, thiophylline, and
thiobromine seem to increase the sensitivity of this system to patterns,
and some anti-anxiety medicines seem to be able to take the edge off.
This is the sort of thing that would be sensitive to genetic details.
Yes, there's probably a connection to epilepsy, creativity, mood
disorders, and
intelligence*****************************************************************************************************So
a highly caffeinated beverage would probably put those in the dense or
inefficient catagory" over the edge "(so to speak)
~otter*********************************************************
First 'language gene' discovered
Group: sci.anthropology.paleo Date: Wed, Aug 14, 2002, 7:18pm (EDT+4)

http://www.***.com/ 's apparently
associated with {*filter*} movements. A 2-letter difference produces severe
speech defects in humans. Other mammals (mice, monkeys, apes) have the
"defective version". The 2-letter difference is universal in all humans
except those with the defect. Approximate age of the human variant is
200 ka. There are presumed to be other genes to find.
--
Harry Erwin < http://www.***.com/ ~herwin/>



Mon, 31 Jan 2005 22:43:02 GMT
 First 'language gene' discovered
On Thu, 15 Aug 2002 10:49:31 -0400, "John Roth"

Quote:



>Absent genetic evidence from Neanderthals, it's hard to
>say. Given the uncertainty in genetic dating, it's hard to
>distinguish 200ky from the 450ky for "Mitochrondal Eve."
>So if Neanderthals split off before then, most likely they
>didn't have it. If they split off later, then they most likely
>did.

This is not true in the way which you have said
it. The basic problem with mtDNA dating is the
calibration, the C/H LCA may be in error. The
basis of error in mtDNA divergences over 100,000
ky is the calibration, all other sources of error
only fractionally decrease confidence.

  Because of this the relative difference between
N and human increases if the basis of error
shifts. I find that Neandertal branched about 4 to
5 times earlier than humans from the line that
leads to humans. If humans radiated 250 kya then
this means that neadertals are about 1 - 1.25 mya
branching from the protolineage that lead to this.
OTOH if humans brnached 450 ky then the
protolineage branched with neadertals around 1.8 -
2.25 mya (or about the time of the early erectoid
radiation).

  BTW its very easy to distinguish humans from
neandertals with the D-loop region. The most
divergent alleles easily track through less
divergent alleles all the way back to african stem
sequences of east and western africa. Even the LM3
has identicle substitutions at positions were the
base east african sequence varies from the
concensus, suggesting even the most divergent
human mtDNAs are simply random (or selective)
increases along a clockable path.
  Neandertal DNA does not track any known human
pattern back to the concensus. While Neandertal
sequences coalesce recently, they share the most
homology with the human concensus (the anceint
possible sequence of Eve) which means that Ns are
most closely related to the tap-root of human
divergence and not any of the stems.

  BTW paabos 450 kya date is incorrect, if you
want to compare it to humans you have to compare
it to the incorrect date presented by stoneking et
al, back in the late 80's of 150kya.
Philip
[pdeitik at bcm.tmc.edu]
http://home.att.net/~DNAPaleoAnthro



Mon, 31 Jan 2005 23:56:51 GMT
 First 'language gene' discovered

Quote:


>>> David Timpe wrote (at bottom of page):

>>   Could it be the difference between Neanderthal and man?        
>> *******************************************            

>It's probably _a_ difference. The dating is interesting--about the
same
>time as the emergence of complex social structures in African
hominids,
>and also about the same as the appearence of advanced paleolithic
>industries in central Africa. There is a suspicion that there was a
>climate-caused ecological bottleneck in Africa (like the Grande
Coupure
>in the Oligocene) at about that time.

>The neuroscience of language is interesting, too. To understand
complex
>language, it looks like you have to be able to produce a complexly
>varying sequence of neural attractors in an area of neocortex. Those
>attractors participate in a match/mismatch process (c.f., Hebb-Marr
>autoassociation) and feed back into other areas of the cortex that do
>the semantic decoding. Sure, bats do something like this, but only
for
>fairly simple dynamics. It now seems that complex attractor dynamics
>(think of productive speech or complex plans) may be rather hard to
>generate neurally. If the autoassociative connectivity is too sparse,
no
>association takes place, but if the connectivity is a little too
dense
>or if the local inhibitory connections are a bit inefficient, you get
>overlap between the attractors, and the whole network ignites. You
have
>tune the system to operate in a narrow band for it to work well. Some
>{*filter*} appear to affect the tuning. Caffeine, thiophylline, and
>thiobromine seem to increase the sensitivity of this system to
patterns,
>and some anti-anxiety medicines seem to be able to take the edge off.
>This is the sort of thing that would be sensitive to genetic details.

>Yes, there's probably a connection to epilepsy, creativity, mood
>disorders, and intelligence.

>> First 'language gene' discovered  

>> It's apparently associated with {*filter*} movements. A 2-letter
difference
>> produces severe speech defects in humans. Other mammals (mice,
monkeys,
>> apes) have the "defective version". The 2-letter difference is
universal
>> in all humans except those with the defect. Approximate age of the
human
>> variant is 200 ka. There are presumed to be other genes to find.

I appreciate these posts very much.
How is talking wired to singing?
It seems different but very closely related.
Babies hear patterns of speech which probably
sound like music or melody (which maybe has something to do with
the mind's attempt to find patterns ...i am guessing).

I would think if a few folks had this speech variation
and traveled into a group without it they would sound
interesting and lovely to the ears of folks who couldn't
form speech sounds as well. And i would think you could make it even
more impressive if you could sing or carry a tune as a group together.
Its always an awesome experience to hear a group of women singing work
songs together or a medicine man shaking the rattle and repeating the
songs and throwing the bad stuff out with physical gestures.
All human ears quiet and focus attention into the music.
Especially children.
What happens with chimps and bonobos and gorillas?
Do they like music?

ejudy



Tue, 01 Feb 2005 00:29:33 GMT
 First 'language gene' discovered


Quote:
>This is not true in the way which you have said
>it. The basic problem with mtDNA dating is the
>calibration, the C/H LCA may be in error. The
>basis of error in mtDNA divergences over 100,000
>ky is the calibration, all other sources of error
>only fractionally decrease confidence.

Actually I wonder what's the confidence interval for their 200kya
estimate.  From the text on the page in question it appears that
        a) distance between H and C alleles is 2
        b) that locus is under strong selective pressure in H
        c) frequency of wild allele in H is nearly 1.

From http://www.***.com/
        d) it's autosomal
        e) these guys had observed an allele at distance 1 from H.  Said
allele shows simple {*filter*} inheritance and gives speech problems.

How does one make an estimate in such situation?  All possible outgroups
had diverged at least an order of magnitude earlier (except N, but as far
as I understand there's no autosomal data on N).  Moreover, estimates
on the frequency of replacements in these positions other primates will
be pretty much worthless, since selective pressure in humans is obviously
different.  Since for all we know the system could be in equilibrum for
hell knows how long...

Philip, any comments?  IIRC you were quite sceptical about estimates based
on autosomal loci and here we have not just autosomal, but one obviously
not neutral...

--
"You're one of those condescending Unix computer users!"
"Here's a nickel, kid.  Get yourself a better computer" - Dilbert.



Tue, 01 Feb 2005 01:51:52 GMT
 First 'language gene' discovered


Fri, 19 Jun 1992 00:00:00 GMT
 First 'language gene' discovered
On 15 Aug 2002 13:51:52 -0400,

Quote:



>>This is not true in the way which you have said
>>it. The basic problem with mtDNA dating is the
>>calibration, the C/H LCA may be in error. The
>>basis of error in mtDNA divergences over 100,000
>>ky is the calibration, all other sources of error
>>only fractionally decrease confidence.

>Actually I wonder what's the confidence interval for their 200kya
>estimate.  From the text on the page in question it appears that
>    a) distance between H and C alleles is 2

The defect in the gene probably shows up in the
protein structure; however you can tract
synonymous mutations as part of a molecular clock,
also intronic and downstream sequence. Here again
I don't know what Paabo did, I looked for the
literature reference this morning. I am
_EXTREMELY_ (add a few !!!!!!) dubious of
prepublish press releases and I have given a
number of critiques of Paabo here. I am however
hopeful that Paabo is consistent in the direction
of error and if so his results seem to be
consistent with my previous expectations. I really
need to see the sequence info and do some
alignments.

Quote:
>    b) that locus is under strong selective pressure in H

Think about it though, such a gene would have
expanded WITH the population or shortly their
after (by my estimates ~125 kya) and reached an
equilibrium level of .99999 or so in the
population. The 'gene' as functionally defined
could have quasi-equivilent alleles that randomly
diverged after that initial burst and
quasi-fixation.

Quote:
>    d) it's autosomal

Definitely, and here again I have to defer to the
MRCA of others since there is no firm basis for
MRCA ing of any gene based on good variant
genetics in apes or chimpanzees. This is a
definite problem. If you go to my site and see the
calibration page

http://home.att.net/~dnapaleoanth/MoleCalib.html

"
Using Autosomal gene mutations to figure out
relatedness of groups
DNA mutations can be compared across families, and
a relative distance put between them based on
accumulated DNA differences. This says nothing
about selection or neutrality, and does not
attempt to explain how the method works; it is an
empirical, observable fact, and can be used
without explaination. Eastall and Herbert, in 1997
counted the mutations (substitution rates) at
"fourfold degenerate sites" of "nuclear
genome-coding DNA"
Abstract- "Evolutionary divergence times can be
inferred from molecular distances if a molecular
clock can be assumed and if the substitution rate
can be estimated. We present new evidence from
relative rate tests that the rate of substitution
at fourfold degenerate sites of nuclear
genome-coding DNA is uniform in primate and rodent
lineages. We also review recent relative rate test
results showing substitution rate uniformity in
the nuclear genome of simian primates. DNA
distances between a range of mammalian taxa shows
that a molecular clock is inconsistent with many
assumed divergence times irrespective of the
assumed substitution rate. We find that the
substitution rate that 'implies' the best
'compromise' fit with divergence times across the
range of taxa is 2.0-2.25 x 10(-9). This range of
substitution rates 'implies' a divergence time of
humans and chimpanzees of 4.0-3.6 million years
ago. This postdates the occurrence of Ardipithecus
ramidus and the earliest occurrence of
Australopithecus afarensis, suggesting that the
common ancestor of humans and chimpanzees was
bipedal and that the trait has been lost in
chimpanzees rather than gained in humans." In a
conference report in 2001, Goodman reported the
work of his group and others in studying the
phylogentic relationships of humans and other
members of the primate order using non-coding non
functional nuclear DNA loci.. The substitution
rate of these sequences is relatively fast,
allowing Goodman and collaborators to draw up a
phylogentic tree up using their primate data sets
(41 of 60 primate genera, comprising 65 primate
species in total.) He used fossil evidence to
'anchor' the calibration rate. From his own
(Goodman et al 1998) and previously published work
(Shoshani et al., 1996) he determined that "The
phylogenetic evidence from these datasets
representing different nuclear loci were mainly
congruent with each other as well as with extant
and fossil osteological evidence".

Accordingly he constructed a phylogeny based on
Hennig (1966) ideas, where-
1.each taxon held all species descended from a
common ancestor (a monophyletic group or clade)
2.heirachic grouping of lower ranked taxa into
higher  taxa ought to follow the phylogenetic
relationship
3.taxa of the same evolutionary age within a given
taxon should be 'ranked' equally

    Goodman acknowledges that the fossil record is
so poor that it allows only a scattering of branch
points in primate evolution to be identified and a
time depth estimated. The solution used by Goodman
and many other workers (Goodman, 1986; Bailey et
al., 1991, 1992; Porter et al., 1997a, b, 1999;
Barroso et al., 1997; Goodman et al., 1998;
Meireles et al., 1999; Page et al., 1999; Chaves
et al., 1999) was to develop models of 'local
molecular clocks'. These clocks 'adjusted' the
rate of molecular evolution (nucleotide base
substituion) making it slower or faster -
according to whether workers identified a
particular non coding DNA  lineage as being slower
evolving than others or not. Differences between
primate lineages in the rate of neutral nucleotide
substitution has been detected by various workers.
The rate has been identified as nearly twice as
fast in loriforms vs lemuriforms (Bonner et al.,
1980, 1981; Koop et al.,1989; Porter et al.,
1997a). Among monkeys, those that have a more
complex feeding ecology (i.e. frugivory/omnivory
vs. leaf browsing) have larger brains (Allman,
1999) and live longer (Rowe, 1996). They
apparently also have a slower rate of noncoding
DNA mutation (Meireles et al., 1999; Page et al.,
1999; Page and Goodman, 2001 , contra Estall &
Herbert 1997, above ).  Hominids have been
identified as having the slowest rates in
primates.
"

Basically what they are saying is that autosomal
mutation rates vary (between loci) for any given
species and even if they didn't there is the
possible problem of interspecific mutation rate
variation.
  To be quite frank at this point, because this
becomes now an important issue, I have created a
model of intragenic rate variation and then
applied that to the interspecific variation and I
don't think that one can statistically resolve
interspecific from intergenic if one concludes
that the intergenic rates are subject to variation
as a result of evolution. Thus I think some of
what is said in the above quote is optimistic.
  The other issue is whether one can use any
coding loci to clock anything.
  But underlying all of these is the curses of all
molecular clocking curses, a topic I have pointed
to many times which is very infrequently discussed
in the human molecular evolution literature. That
issue is bleed through variation.

  Let us imagine that we are trying to establish a
local clock, say the clock is based on human
molecular variation. If we assume that all human
variation was focused by a constriction, and
assume fixation, in about 30-40% of genes that
assumption maybe right, but many other genes
'bleed though' variation, the HLA loci 'poured'
through variation. OK so we shouldn't use human
coalescence as an anchor, how about chimpanzee,
same problem.
  Basically what has happened is that some genes
MRCA to mtDNA fixation, some genes MRCA to
probably about the time of erectoid divergence,
some even may have variation carried all the way
back to chimps. So if, for example you assume the
alleles between humans and chimp will anchor at
the MRCA, there is a chance at some loci,
especially certain variably selective loci that
assumption could be wrong (See 'Myth about Eve'
Ayala, 1995. Science)  
  Therefore where do we anchor genes for setting
up the calibration, particularly if the MRCA are
circularly defined? The answer is that you need to
look at literally hundreds of genes, thousands of
genes to see where there is nodalities in the
fixation times, that will give a rough guage of
when constrictions have occurred in the past, and
then you need to find some means of externally
anchoring those constrictions. Once you've done
that you can go about estimating the substitution
rate, and if your 'anchoring' informatics (fossil
information) is accurate all the 'pools' of rate
estimations (based on nodality) should overlay
each other.

 What if they are not? One of the basic problems
is that bleedthrough variation when it occurs is
not similar. One loci may have 2 major branches
bleed through, or 3 or 4 or 2 majors and 2 minor
offshoots or whatever. Apriori this might not seem
all that important but now lets add in
recombination, less also addin that during the end
of constrictions and during expansions some
alleles, even ancient alleles are lost. What this
means is that the source of recombination can be
lost, but not the recombinants. With recombination
and GOOD and THOROUGH population studies such
recombinatorial events may leave notable hints for
a studious observer; however with the generally
'ignored' process of gene conversion, no hints of
the parent template may be left except those
absolutely disguised in the convertants. Therefore
the 'apparent' rate of evolution of a loci might
be variation x geneconversion + the real rate of
point mutations. And since variation differs per
gene, some might the rate of evolution.
Notice also that this rate will differ between
species more or less dependent on the population
dynamic. As far as I know, noone has ever
attempted to statistically reconcile the affect
that variation will have on the rate of
recombination and statistically modulate the
substitution rate. Therefore ...

read more »



Tue, 01 Feb 2005 03:55:07 GMT
 First 'language gene' discovered


Fri, 19 Jun 1992 00:00:00 GMT
 First 'language gene' discovered


Quote:
> On Thu, 15 Aug 2002 10:49:31 -0400, "John Roth"



>> Absent genetic evidence from Neanderthals, it's hard to
>> say. Given the uncertainty in genetic dating, it's hard to
>> distinguish 200ky from the 450ky for "Mitochrondal Eve."
>> So if Neanderthals split off before then, most likely they
>> didn't have it. If they split off later, then they most likely
>> did.

> This is not true in the way which you have said
> it. The basic problem with mtDNA dating is the
> calibration, the C/H LCA may be in error. The
> basis of error in mtDNA divergences over 100,000
> ky is the calibration, all other sources of error
> only fractionally decrease confidence.

This would be the case if there were a LINEAR relationship between the
differences that you look at and the passage of time.  Get the "K" factor
and you can count the differences and calculate the years.

Of course if the relationship is NOT linear, if there are some forces (dont
know what it might be) that retard or accelerate the accumulation of genetic
"differnces" you have a bit more of a problem with that "confidence
interval".  

As an example, if you "know" that a given species of tree puts on 1/4 inch
of wood every year you might be able to calculate the age based on the
diameter of the tree.  On the other hand, wet years might make for more wood
an dry years make for less! Trees in damp marshy soil might never show the
"dry years" events, trees in poor soil might never hit the growth spurts!
With trees of course you have another option and you can count the "rings"
with a certain degree of accuracy.  You have a high "confidence" since you
are looking for the start and stops of groth that mark a years seasons.  In
the case of "diameter" you have a nonlinearity, in the case of tree rings
you have a pretty much hard and fast linear relationship.

Which is the case with the "genetic clock"?

I suspect I know which one you would claim, but with  the papers coming out
talking about the "newfound" importance of the "unexpressed portions", how
CONFIDENT are you of the linearity!

Regards
bk



Tue, 01 Feb 2005 05:50:48 GMT
 First 'language gene' discovered

Quote:

> http://www.***.com/

> It's apparently associated with {*filter*} movements.  A 2-letter difference
> produces severe speech defects in humans.  Other mammals (mice, monkeys,
> apes) have the "defective version".  The 2-letter difference is universal in
> all humans except those with the defect.  Approximate age of the human
> variant is 200 ka.  There are presumed to be other genes to find.

> --
> Dave Timpe

> dtimpe at new dot rr dot com

It should be possible, although perhaps the first step down a path many will not
wish to travel, to insert this allele into a chimp embryo.   My guess would be,
that a chimp with this allele would be worse, rather than better, at tasks
involving movements of the face, lips, and tongue.    FOXP2 (the gene) produces
a transcription factor - a sort of flag that gets set during brain development
which the developing neurons can use to coordinate their development.
Although transcription factors 'control' development, I think it's a mistake to
think of them as blueprints for brain development; each cell contains all the
blueprints it needs - the transcription factor just tells them which page of the
blueprints to look at, and when.

A scenario for adaptation by the mutation of a transcription factor goes like
this: an animal is in an environment for which it is not well adapted, but is
lucky enough not to go extinct.    In some small population, a mutation occurs
in a transcription factor gene.   This throws a monkey-wrench into the
development process, producing a severe defect.   But by chance those with the
defect survive.   For those with the mutation, fetal brain cells are not getting
the signal they need to turn on development, so they don't develop.    But in
this situation, further mutations, which allow the fetal cells to recognize the
mutated transcription factor, are adaptive.   So the result is a reorganized
system of signals.    Occasionally, the reorganized system works better for the
animal than the original one.

If at some point, the world contained only a single population of a few hundred
hominids, the chance that these mutations would happen in that population is
tiny.   If there were hundreds of such small populations, then there is a much
better chance that these mutations would happen in some one of the hundreds of
populations.    But then there would be a process where the mutated population
grew, and interbred with the non-mutated hominids, producing hybrids with
defects.   The new allele could be lost in this process, but there is a fair
chance it would survive.

So I don't think the human allele of FOXP2 is a gene 'for' better {*filter*}
control, and I think a chimp with the human allele would have a defect in {*filter*}
control, not an improvement.   The chimp's fetal brain cells are expecting the
chimp allele of FOXP2 as the signal to turn on; if they get the human allele,
they won't develop.   That at any rate is my guess.

Some further information is online at:
 Scientists Identify a Language Gene

------- -- ---- - --- -- --------- -----
Sandy Hodges / Alameda,  California,   USA



Tue, 01 Feb 2005 23:56:43 GMT
 First 'language gene' discovered

Quote:

> http://www.***.com/

> It's apparently associated with {*filter*} movements.  A 2-letter difference
> produces severe speech defects in humans.  Other mammals (mice, monkeys,
> apes) have the "defective version".  The 2-letter difference is universal in
> all humans except those with the defect.  Approximate age of the human
> variant is 200 ka.  There are presumed to be other genes to find.

> --
> Dave Timpe

> dtimpe at new dot rr dot com

Also
 Functional abnormalities associated with the FOXP2 gene mutation in the KE
family: a covert language fMRI study

Quote: "When group averaged activation maps were compared, it was observed that
the FOXP2 mutation was associated with significant underactivation in several
brain regions, mainly in Broca's area (left inferior frontal gyrus), but also
the right putamen, and the right inferior frontal gyrus. These results indicate
that the FOXP2 mutation results in abnormal functioning of language regions,
even when speech output is not required."
------- -- ---- - --- -- --------- -----
Sandy Hodges / Alameda,  California,   USA



Wed, 02 Feb 2005 00:12:24 GMT
 First 'language gene' discovered

| Yes, there's probably a connection to epilepsy, creativity, mood
| disorders, and intelligence.

You anticipated my question.  Epilepsy and mood disorders are the price we
pay for the good things, I suppose.  Somebody came out the other day with
the a study that said autism was related to "geek genes" (a very high
concentration of autistic children is found in Silicon Valley).  Were
Neandertals geeks, Leif?

--
Dave Timpe

dtimpe at new dot rr dot com



Wed, 02 Feb 2005 06:47:49 GMT
 
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