為什么人類(lèi)能夠說(shuō)話而黑猩猩不能呢,？研究人員現(xiàn)在找到了答案。他們認(rèn)為,，人類(lèi)和黑猩猩身上都擁有的FOXP2基因不僅“長(zhǎng)相”不同,，而且產(chǎn)生的氨基酸也不一樣，這些差異造成了人類(lèi)區(qū)別于黑猩猩的獨(dú)特語(yǔ)言能力,。相關(guān)研究發(fā)表在11月12日的《自然》雜志上,。
人類(lèi)和黑猩猩有95%到98.5%的基因一樣。美國(guó)加州大學(xué)洛杉磯分校的丹·格施溫德團(tuán)隊(duì)使用人類(lèi)和黑猩猩的大腦組織分析了FOXP2的功能和工作情況,。他們發(fā)現(xiàn),，F(xiàn)OXP2基因在人類(lèi)語(yǔ)言功能形成過(guò)程中發(fā)揮著核心作用。這個(gè)基因會(huì)指導(dǎo)合成一種特殊蛋白質(zhì),，該蛋白質(zhì)又會(huì)與DNA（脫氧核糖核酸）結(jié)合,，對(duì)其他基因的功能造成影響。因此,，雖然實(shí)驗(yàn)顯示這個(gè)基因的人類(lèi)版本與黑猩猩版本只有兩處氨基酸不同,，但在同樣的培養(yǎng)環(huán)境下，該基因的人類(lèi)版本會(huì)增強(qiáng)61個(gè)基因的作用,，同時(shí)抑制另外51個(gè)基因的作用,。
在這些受影響的基因中，一些與大腦發(fā)育有關(guān),，F(xiàn)OXP2基因可以通過(guò)它們影響大腦中的語(yǔ)言功能區(qū)域和神經(jīng)網(wǎng)絡(luò),。另一些受影響的基因與咽喉部位的軟組織發(fā)育有關(guān)，F(xiàn)OXP2基因可以通過(guò)它們來(lái)影響與語(yǔ)言功能有關(guān)的器官結(jié)構(gòu),。
研究人員認(rèn)為,，這表明在人類(lèi)獲得語(yǔ)言交流能力的進(jìn)化歷程中，F(xiàn)OXP2基因發(fā)揮了重要作用,。這些發(fā)現(xiàn)有助于解釋為什么人類(lèi)的大腦天生帶著說(shuō)話和語(yǔ)言環(huán)路,，而黑猩猩卻沒(méi)有。研究人員將進(jìn)行深入研究,，進(jìn)一步揭示人類(lèi)掌握語(yǔ)言的機(jī)制,。（生物谷Bioon.com）
有關(guān)語(yǔ)言能力研究：
Cell：將人類(lèi)語(yǔ)言基因植入老鼠體內(nèi)
Science：將線路植入大腦解析語(yǔ)言系統(tǒng)工作機(jī)理
Neuropsychologia：男孩女孩用不同大腦區(qū)域處理語(yǔ)言信息
PNAS：語(yǔ)言與顏色認(rèn)知有直接關(guān)系
PNAS：不同語(yǔ)言失讀癥患者腦構(gòu)造不同
Current Biology：誦讀困難癥在不同語(yǔ)言中表現(xiàn)各異
生物谷推薦原始出處：
Nature 462, 213-217 (12 November 2009) | doi:10.1038/nature08549
Human-specific transcriptional regulation of CNS development genes by FOXP2
Genevieve Konopka1,3, Jamee M. Bomar1,3, Kellen Winden1,3, Giovanni Coppola3, Zophonias O. Jonsson5, Fuying Gao3, Sophia Peng3, Todd M. Preuss6, James A. Wohlschlegel5 & Daniel H. Geschwind1,2,3,4
1 Program in Neurogenetics,
2 Semel Institute and Department of Psychiatry,
3 Departments of Neurology,
4 Human Genetics, and,
5 Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA
6 Division of Neuroscience and Center for Behavioral Neuroscience, Yerkes National Primate Research Center, and Department of Pathology & Laboratory Medicine, Emory University School of Medicine, Atlanta, Georgia 30329, USA
7 Correspondence to: Genevieve Konopka1,3Daniel H. Geschwind1,2,3,4 Correspondence and requests for materials should be addressed to G.K. or D.H.G.
The signalling pathways controlling both the evolution and development of language in the human brain remain unknown. So far, the transcription factor FOXP2 (forkhead box P2) is the only gene implicated in Mendelian forms of human speech and language dysfunction1, 2, 3. It has been proposed that the amino acid composition in the human variant of FOXP2 has undergone accelerated evolution, and this two-amino-acid change occurred around the time of language emergence in humans4, 5. However, this remains controversial, and whether the acquisition of these amino acids in human FOXP2 has any functional consequence in human neurons remains untested. Here we demonstrate that these two human-specific amino acids alter FOXP2 function by conferring differential transcriptional regulation in vitro. We extend these observations in vivo to human and chimpanzee brain, and use network analysis to identify novel relationships among the differentially expressed genes. These data provide experimental support for the functional relevance of changes in FOXP2 that occur on the human lineage, highlighting specific pathways with direct consequences for human brain development and disease in the central nervous system (CNS). Because FOXP2 has an important role in speech and language in humans, the identified targets may have a critical function in the development and evolution of language circuitry in humans.
