RE: Language Gene Is Traced to Emergence of Humans

From: Glenn Morton (
Date: Mon Aug 19 2002 - 22:52:43 EDT

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    Shuan wrote:
    >-----Original Message-----
    > According to this link, Language only arose recently and was the major
    >contributor to the emergence of modern humans. This seems a problem for
    >those apologists who argue that modern humam behavior has been around for
    >hundreds of thousands of years. What say those apologists?

    Nah, this isn't a problem. I read the actual article as opposed to the
    press reports and wrote the following to a friend yesterday:

      I just read the article on FOXP2 this morning. Several things concern me
    about his 'dating' of the gene. First we know this gene is involved with
    speech because:

    "A point mutation in FOXP2
    co-segregates with a disorder in a family in which half of the members have
    severe articulation difficulties accompanied by linguistic and grammatical
    impairment. This gene is disrupted by translocation in an unrelated
    individual who has a similar disorder. Thus, two functional copies of FOXP2
    seem to be required for acquisition of normal spoken language. "

      this gene is one of the most conserved genes in the genome. He writes:

    When compared with a collection of 1,880 human-rodent gene pairs, FOXP2 is
    among the 5% most-conserved proteins. The chimpanzee, gorilla and rhesus
    macaque FOXP2 proteins are all identical to each other and carry only one
    difference from the mouse and two differences from the human protein,
    whereas the orang-utan carries two differences from the mouse and three from
    humans. Thus, although the FOXP2 proteins is highly conserved, two of the
    three amino-acid differences between humans and mice occurred on the human
    lineage after the separation from the common ancestor with the chimpanzee.

    Then in 'dating' the gene, the authors use the INTRONS rather than the
    conserved exons for the calcuation. They write:

    If these two changes in amino-acid encoding (or some other feature of the
    human FOXP2 gene) were positively selected recently during human evolution,
    traces of a selective sweep should be detectable in the pattern of variation
    found among humans13, 14. To investigate this possibility, we sequenced a
    segment of 14,063 base pairs (bp) covering introns 4, 5 and 6 of the FOXP2
    gene in seven individuals from Africa, four from Europe, one from South
    America, five from mainland Asia and three from Australia and Papua New
    Guinea. In addition, we sequenced the same segment in a chimpanzee from
    central Africa, a chimpanzee from western Africa and an orang-utan (Table
    1). One hallmark of a recent selective sweep is that more low-frequency
    alleles should be observed than expected under a neutral model of a
    random-mating population of constant size. To test this prediction, we
    calculated Tajima's D statistic15. The value is -2.20 for our sample,
    indicating a sharp excess of rare alleles. Under the standard neutral model
    outlined above, the probability of such an excess by chance is 0.002.
    Population growth can also lead to negative D values throughout the genome.
    However, the value of D at FOXP2 is unusually low compared with other loci.
    For example, among 313 human genes16 sequenced in a sample of 164
    chromosomes, only one has a more negative value (-2.25). A second prediction
    for a selective sweep at a recombining locus is that more derived (that is,
    non-ancestral) alleles at high frequency are expected than under the
    standard neutral model, a feature reflected in a negative H value17. To
    estimate H, we inferred the ancestral states of variable positions seen
    among the humans by using the chimpanzee and orang-utan DNA sequences. The H
    value of -12.24 deviates significantly from the neutral expectation of zero
    (P = 0.042) and would be even less likely by chance under a model with
    population growth13. The strongly negative D and H reflect an extreme skew
    in the frequency spectrum of allelic variants at FOXP2 towards rare and
    high-frequency alleles. Because we considered a worldwide sample of humans,
    population structure might contribute to the negative D value. However, this
    type of sampling scheme is highly unlikely to produce a significantly
    negative H value. In contrast to demographic explanations, a selective sweep
    affecting the FOXP2 gene can account for both aspects of the frequency
    spectrum. We do not observe a reduced diversity at human FOXP2 relative to
    its divergence from the chimpanzee, as expected under a simple
    selective-sweep model. However, the magnitude of the reduction in
    variability expected after a selective sweep depends crucially on the rate
    of recombination. Estimates of recombination between intronic polymorphisms
    taken from a study of FOXP2 (ref. 4) suggest that this region of the gene
    experiences rates of genetic exchange roughly five times the genome-wide
    average. If we assume that a selective sweep at a linked site does account
    for the patterns of variability recovered at FOXP2, it is noteworthy that
    the next gene is located 286 kilobases (kb) away from the sequenced segment.
    A selective sweep is not expected to lead to an excess of high-frequency
    derived alleles at sites that are 286 kb distant from the target of
    selection13, 17. Thus, the best candidates for the selected sites are the
    two amino-acid substitutions specific to humans in exon 7.
    The effective population size was taken to be 10^4, on the basis of
    estimates for other loci29. We tried three different values for the
    selection coefficient: s = 5%, 1% and 0.5%. For these parameters, an s of 1%
    resulted in the highest likelihoods, so we reported the results for s = 1%.
    If we use the chi-squared approximation with one degree of freedom for the
    log-likelihood ratio statistic 2ln(Lik(&tcirc;)/Lik(T)), we obtain an
    approximate 95% confidence interval for T of [0, 4,000 generations].
    However, this approximation may not be appropriate in this context. Thus, we
    also ran 100 simulations to examine the distribution of &tcirc; when the
    true T is equal to our maximum likelihood estimate of T = 0 (here, n = 5
    10^5 and = 0.2). These simulations suggested an approximate 95% confidence
    interval of [0, 6,000 generations]. We assumed a generation time of 20 years
    for converting T into years.

    It seems to me that what they have dated is the time it takes for the gene
    to become fixed given the selection coefficient they chose. Thus, what they
    have is a floating chronology. They can't really say WHEN the gene occurred,
    just how long it took when it happened.

    NOTE ADDED TO SHUAN: Very simplified, the usual way genes are dated is to
    measure the number of mutations in the gene along different lineages and
    divide by the mutation rate. More accurately, they calculate the time it
    would take for all the mutations observed within the human population to
    coalesce (or arise) from a single ancestral sequence. With genes like FOXP2,
    there are too few mutations and too much homogeneity among modern humans to
    use this method. Thus, this date, while it is sure to be widely cited, is
    very uncertain, and in my opinion, meaningless.


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