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The “Language” Gene and Women’s Wagging Tongues : Guest Blog, Scientific American Blog Network

The “Language” Gene and Women’s Wagging Tongues : Guest Blog, Scientific American Blog Network

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Published by richardus2099
Genes are subject to multiple layers of regulation. An early
regulatory point is transcription. During this process, regulatory
proteins bind to DNA regions
Genes are subject to multiple layers of regulation. An early
regulatory point is transcription. During this process, regulatory
proteins bind to DNA regions

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Published by: richardus2099 on Mar 11, 2013
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05/14/2014

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http://blogs.scientificamerican.com/guest-blog/2013/02/24/the-language-gene-and-womens-wagging-tongues/ 
Stylized rendering of FOXP2 attached to DNA (Wikipedia, Creative Commons License)
The “Language” Gene and Women’s Wagging Tongues
By Athena Andreadis | February 24, 2013
 Aka, How to Twist Science to Reinforce Gender Stereotypes
Genes are subject to multiple layers of regulation. An early regulatory point is transcription. During this process, regulatory proteins bind to DNA regions (promoters and enhancers) that directgene expression. These DNA/protein complexes attract thetranscription apparatus, which docks next to the complex andproceeds linearly downstream, producing the heteronuclear (hn)RNA that is encoded by the gene linked to the promoter. ThehnRNA is then spliced and either becomes structural/regulatory RNA or is translated into protein.Transcription factors are members of large clans that arose fromancestral genes that went through successive duplications and thendiverged to fit specific niches. One such family of about fifty members is called FOX. Their DNA binding portion is shaped like a butterfly, which has given this particular motif the monikers of forkhead box or winged helix. The activities of the FOX proteins extend widely in time and region. One of the FOX family members is FOXP2, as notorious as Fox News – except for different reasons: FOXP2has become entrenched in popular consciousness as “the language gene”. As is the case with all such folklore, there is some truth inthis; but as is the case with everything in biology, reality is far more complex.FOXP2, the first gene found to “affect language” (more on this anon), was discovered in 2001 by several converging observations andtechniques. The clincher was a large family (code name KE), some of whose members had severe articulation and grammatical deficits with no accompanying sensory or cognitive impairment. The inheritance is autosomal dominant: one copy of the mutated gene issufficient to confer the trait. When the researchers definitively identified the FOXP2 gene, they found that the version of FOXP2 carried by the KE affected members has a single point mutation that alters an invariant residue in its forkhead domain, thereby influencing theprotein’s binding to its DNA targets.Like all transcription factors, FOXP2 regulates many promoters. The primary domains of FOXP2 influence are brain and lungdevelopment. Some of its downstream targets are themselves regulators of brain function (most prominently neurexin CNTNAP2). Notsurprisingly, deleting or mutating both FOXP2 copies in mice results in early death, whereas doing so to one copy leads to decreased vocalization and slightly impaired motor learning. FOXP2 is broadly conserved across vertebrates, but its critical functional regionshave tiny but telling differences even between humans and their closest ape relatives. Like other genes that influence human-specificattributes, human FOXP2 seems to have undergone positive selection during the broad intervals of crucial speciation events. Alongrelated lines, Neanderthals and Denisovans apparently had the same FOXP2 allele as contemporary humans, and by this criterion werefully capable of the articulation that makes language possible. Which brings us to the nub of the issue. What does FOXP2 do in brain? Genes don’t encode higher-order functions, let alone behavior. Also recall that the KE family members have a very circumscribed defect, despite its dramatic manifestation. Finally, keep firmly inmind that language in humans includes a complex genetic component that involves many loci and just as many environmentalinteractions. FOXP2 does not encode inherent language ability. Instead, the time and place of its expression as well as studies in cellsystems and other organisms (zebra finches, rodents) indicate that FOXP2 may be involved in neuronal plasticity, which in turnmodulates capacity for learning by forming new synaptic connections. FOXP2 may also be involved in regulation of motor neuron
 
Gender Words. Mark Liberman’s Language Log, Sept. 2006
control in certain brain regions (cortical motor areas, cerebellum, striatum) that affect the ability to vocalize, sing and, in humans, formthe complex sounds of language.Given its connection, however over-interpreted, to “what makes a human” as well as its chromosomal location (in 7q31, which alsoharbors candidates for autism and dementia), it’s not surprising that FOXP2 has acquired quasi-mythic dimensions in the lay imagination. However, careful studies have shown that the genes on 7q31 responsible for autism and dementia are distinct fromFOXP2. Also, as I said earlier, FOXP2 does not code for language ability – and even less for its culturally determined manifestations(many of which are a minefield of confirmation biases, unquestioned assumptions and simply sloppy work).The latest round in the misrepresentation of FOXP2 is the gone-viral variation of “there’s more of this ‘language protein’ in the left hemisphere of 4-year girls andthat’s why women are three times as talkative as men”. This came from the PR pitch of a research team who did a study primarily on rats (which confirmed thelink between FOXP2 levels and vocalization) and then, perhaps attempting to latchonto a catchy soundbite, extended the gender link to humans based on… a singlePCR amplification of ten Broca’s area cortices (from postmortem brains of 4-yearolds, five from each sex; Broca’s area is involved in language processing).To begin with, all studies conducted so far definitively show that women and menutter the same number of words by any metric chosen – and that in fact men talk more than women in mixed-gender conversations (to say nothing of the gender-linked ratio of interruptions). And whereas it’s true that girls develop vocalcompetence slightly earlier than boys and show higher linguistic skills during theearly acquisition window, this difference is transient. Furthermore, the FOXP1control that the authors of the study argue does not show a gender-correlatedchange (unlike FOXP2) in fact is on the verge of doing so, and the relative statisticalsignificances might well change if a larger number of samples were tested. Finally, whereas decrease of FOXP2 reduces vocalizationand increases pitch in male rat pups, it has the opposite effect in female rat pups. In other words, the correlation between FOXP2levels and vocalization/pitch is not straightforward even in rats.In the larger context of expression and reception of vocalizations, the difference is not how much women talk, but how welcome and/or valued their input is. Even trivial zomboid blathering is given higher value if it’s culturally coded as masculine (examples: sportnewscasters; most congressmen). In fairness to the researchers of the study that caused all this rehashing of kneejerk stereotypes andevopsycho Tarzanism, here is the concluding paragraph of their paper. It states something both measured and, frankly, obvious:
“Gender is a purely human construct consisting of both self and others’ perception of one’s sex and is arguably the first and mostsalient of all phenotypic variables. Sex differences in how language is received and processed and how speech is produced has thepotential to influence gender both within and external to an individual. Whether human sex differences in FOXP2, and possibly FOXP1 as well, contribute to gender variation in language is a question for future research.”
Relevant publications and links:
Lai CS,Fisher SE,Hurst JA , Vargha-Khadem F,Monaco AP(2001). A forkhead-domain gene is mutated in a severe speech and language disorder.Nature 413(6855):519-23. White SA, Fisher SE, Geschwind DH, Scharff C, Holy TE (2006).Singing mice, songbirds, and more: models for FOXP2 function anddysfunction in human speech and language.J. Neurosci. 26(41):10376-9.Bowers JM,Perez-Pouchoulen M,Edwards NS,McCarthy MM(2013).FOXP2 mediates sex differences in ultrasonic vocalization by rat pups and directs order of maternal retrieval. J. Neurosci.33(8):3276-83. Mark Liberman.Gabby Guys: The Effect size(Language Log, Sept. 23, 2006)

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