FOXP2 - wikipedia FOXP2 FOXP2 Available structures PDB Human UniProt search : PDBe RCSB List of PDB id codes 2AS5, 2A07 Identifiers Aliases FOXP2, CAGH44, SPCH1, TNRC10, forkhead box P2 External IDs OMIM : 605317 HomoloGene : 33482 GeneCards : FOXP2 Gene location ( Human ) Chr. Chromosome 7 ( human ) Band 7q31. 1 Start 114,086,327 bp End 114,693,772 bp RNA expression pattern More reference expression data Gene ontology Molecular function DNA binding sequence - specific DNA binding protein homodimerization activity transcription factor activity, sequence - specific DNA binding metal ion binding RNA polymerase II core promoter proximal region sequence - specific DNA binding transcriptional repressor activity, RNA polymerase II core promoter proximal region sequence - specific binding protein binding protein heterodimerization activity RNA polymerase II transcription factor activity, sequence - specific DNA binding androgen receptor binding identical protein binding Cellular component nucleus Biological process positive regulation of epithelial cell proliferation involved in lung morphogenesis regulation of transcription, DNA - templated lung development positive regulation of epithelial cell proliferation negative regulation of transcription from RNA polymerase II promoter post-embryonic development transcription, DNA - templated cerebellum development putamen development vocal learning positive regulation of mesenchymal cell proliferation smooth muscle tissue development cerebral cortex development caudate nucleus development camera - type eye development lung alveolus development righting reflex negative regulation of transcription, DNA - templated skeletal muscle tissue development forebrain development response to testosterone innate vocalization behavior anatomical structure morphogenesis cell differentiation growth Sources : Amigo / QuickGO Orthologs Species Human Mouse Entrez 93986 n / a Ensembl ENSG00000128573 n / a UniProt O15409 Q75MZ5 Q0PRL4 Q8N6B6 n / a RefSeq ( mRNA ) NM_001172766 NM_001172767 NM_014491 NM_148898 NM_148899 NM_148900 n / a RefSeq ( protein ) NP_001166237 NP_001166238 NP_055306 NP_683696 NP_683697 NP_683698 NP_001166237. 1 NP_683697. 2 n / a Location ( UCSC ) Chr 7 : 114.09 -- 114.69 Mb n / a PubMed search n / a Wikidata View / Edit Human FOXP2 gene is located on the long ( q ) arm of chromosome 7 at position 31. Forkhead box protein P2 ( FOXP2 ) is a protein that, in humans, is encoded by the FOXP2 gene, also known as CAGH44, SPCH1 or TNRC10, and is required for proper development of speech and language. Initially identified as the genetic factor of speech disorder in KE family, its gene is the first gene discovered associated with speech and language. The gene is located on chromosome 7 ( 7q31, at the SPCH1 locus ), and is expressed in fetal and adult brain, heart, lung and gut. FOXP2 orthologs have also been identified in other mammals for which complete genome data are available. The FOXP2 protein contains a forkhead - box DNA - binding domain, making it a member of the FOX group of transcription factors, involved in regulation of gene expression. In addition to this characteristic forkhead - box domain, the protein contains a polyglutamine tract, a zinc finger and a leucine zipper. The gene is more active in females than in males, to which could be attributed better language learning in females. In humans, mutations of FOXP2 cause a severe speech and language disorder. Versions of FOXP2 exist in similar forms in distantly related vertebrates ; functional studies of the gene in mice and in songbirds indicate that it is important for modulating plasticity of neural circuits. Outside the brain FOXP2 has also been implicated in development of other tissues such as the lung and gut. FOXP2 is popularly dubbed the `` language gene '', but this is only partly correct since there are other genes involved in language development. It directly regulates a number of other genes, including CNTNAP2, CTBP1, and SRPX2. Two amino acid substitutions distinguish the human FOXP2 protein from that found in chimpanzees, but only one of these two changes is unique to humans. Evidence from genetically manipulated mice and human neuronal cell models suggests that these changes affect the neural functions of FOXP2. Contents 1 Discovery 2 Function 3 Clinical significance 4 Evolution 5 Interactions 6 Mice 7 Birds 8 See also 9 References 10 External links Discovery FOXP2 and its gene were discovered as a result of investigations on an English family known as the KE family, half of whom ( fifteen individuals across three generations ) suffered from a speech and language disorder called developmental verbal dyspraxia. Their case was studied at the Institute of Child Health of University London College. In 1990 Myrna Gopnik, Professor of Linguistics at McGill University, reported that the disorder - affected KE family had severe speech impediment with incomprehensible talk, largely characterized by grammatical deficits. She hypothesized that the basis was not of learning or cognitive disability, but due to genetic factors affecting mainly grammatical ability. ( Her hypothesis led to a popularised existence of `` grammar gene '' and a controversial notion of grammar - specific disorder. ) In 1995, the University of Oxford and the Institute of Child Health researchers found that the disorder was purely genetic. Remarkably, the inheritance of the disorder from one generation to the next was consistent with autosomal dominant inheritance, i.e., mutation of only a single gene on an autosome ( non-sex chromosome ) acting in a dominant fashion. This is one of the few known examples of Mendelian ( monogenic ) inheritance for a disorder affecting speech and language skills, which typically have a complex basis involving multiple genetic risk factors. In 1998, Oxford University geneticists Simon Fisher, Anthony Monaco, Cecilia S.L. Lai, Jane A. Hurst, and Faraneh Vargha - Khadem identified an autosomal dominant monogenic inheritance that is localized on a small region of chromosome 7 from DNA samples taken from the affected and unaffected members. The chromosomal region ( locus ) contained 70 genes. The locus was given the official name `` SPCH1 '' ( for speech - and - language - disorder - 1 ) by the Human Genome Nomenclature committee. Mapping and sequencing of the chromosomal region was performed with the aid of bacterial artificial chromosome clones. Around this time, the researchers identified an individual who was unrelated to the KE family, but had a similar type of speech and language disorder. In this case the child, known as CS, carried a chromosomal rearrangement ( a translocation ) in which part of chromosome 7 had become exchanged with part of chromosome 5. The site of breakage of chromosome 7 was located within the SPCH1 region. In 2001, the team identified in CS that the mutation is in the middle of a protein - coding gene. Using a combination of bioinformatics and RNA analyses, they discovered that the gene codes for a novel protein belonging to the forkhead - box ( FOX ) group of transcription factors. As such, it was assigned with the official name of FOXP2. When the researchers sequenced the FOXP2 gene in the KE family, they found a heterozygous point mutation shared by all the affected individuals, but not in unaffected members of the family and other people. This mutation is due to an amino - acid substitution that inhibits the DNA - binding domain of the FOXP2 protein. Further screening of the gene identified multiple additional cases of FOXP2 disruption, including different point mutations and chromosomal rearrangements, providing evidence that damage to one copy of this gene is sufficient to derail speech and language development. Function Foxp2 is expressed in the developing cerebellum and the hindbrain of the embryonic day 13.5 mouse. Allen Brain Atlases FOXP2 is required for proper brain and lung development. Knockout mice with only one functional copy of the FOXP2 gene have significantly reduced vocalizations as pups. Knockout mice with no functional copies of FOXP2 are runted, display abnormalities in brain regions such as the Purkinje layer, and die an average of 21 days after birth from inadequate lung development. FOXP2 is expressed in many areas of the brain including the basal ganglia and inferior frontal cortex where it is essential for brain maturation and speech and language development. A knockout mouse model has been used to examine FOXP2 's role in brain development and how mutations in the two copies of FOXP2 affect vocalization. Mutations in one copy result in reduced speech while abnormalities in both copies cause major brain and lung developmental issues. The expression of FOXP2 is subject to post-transcriptional regulation, particularly micro RNA, which binds to multiple miRNA binding - sites in the neocortex, causing the repression of FOXP2 3'UTR. Clinical significance There are several abnormalities linked to FOXP2. The most common mutation results in severe speech impairment known as developmental verbal dyspraxia ( DVD ) which is caused by a translocation in the 7q31. 2 region ( t ( 5 ; 7 ) ( q22 ; q31. 2 ) ). A missense mutation causing an arginine - to - histidine substitution ( R553H ) in the DNA - binding domain is thought to be the abnormality in KE. A heterozygous nonsense mutation, R328X variant, produces a truncated protein involved in speech and language difficulties in one KE individual and two of their close family members. R553H and R328X mutations also affected nuclear localization, DNA - binding, and the transactivation ( increased gene expression ) properties of FOXP2. Although DVD associated with FOXP2 disruptions are thought to be rare ( ~ 2 % by one estimate ), a faulty copy of FOXP2 in individuals always causes speech and language problems. Several cases of developmental verbal dyspraxia in humans have been linked to mutations in the FOXP2 gene. Such individuals have little or no cognitive handicaps but are unable to correctly perform the coordinated movements required for speech. fMRI analysis of these individuals performing silent verb generation and spoken word repetition tasks showed underactivation of Broca 's area and the putamen, brain centers thought to be involved in language tasks. Because of this, FOXP2 has been dubbed the `` language gene ''. People with this mutation also experience symptoms not related to language ( not surprisingly, as FOXP2 is known to affect development in other parts of the body as well ). Scientists have also looked for associations between FOXP2 and autism, and both positive and negative findings have been reported. There is some evidence that the linguistic impairments associated with a mutation of the FOXP2 gene are not simply the result of a fundamental deficit in motor control. For examples, the impairments include difficulties in comprehension. Brain imaging of affected individuals indicates functional abnormalities in language - related cortical and basal / ganglia regions, demonstrating that the problems extend beyond the motor system. Evolution Human FOXP2 gene and evolutionary conservation is shown in a multiple alignment ( at bottom of figure ) in this image from the UCSC Genome Browser. Note that conservation tends to cluster around coding regions ( exons ). The FOXP2 gene is highly conserved in mammals. Human gene differs from non-human primates by the substitution of two amino acids, threonine to asparagine substitution at position 303 ( T303N ) and asparagine to serine substitution at position 325 ( N325S ). In mice it differs from that of humans by three substitutions, and in zebra finch by seven amino acids. One of the two amino acid difference between human and chimps also arose independently in carnivores and bats. Similar FOXP2 proteins can be found in songbirds, fish, and reptiles such as alligators. DNA sampling from Homo neanderthalensis bones indicates that their FOXP2 gene is a little different, though largely similar to those of Homo sapiens ( i.e. humans ). The FOXP2 gene showed indications of recent positive selection. Some researchers have speculated that positive selection is crucial for the evolution of language in humans. Others, however, have been unable to find a clear association between species with learned vocalizations and similar mutations in FOXP2. Insertion of both human mutations into mice, whose version of FOXP2 otherwise differs from the human and chimpanzee versions in only one additional base pair, causes changes in vocalizations as well as other behavioral changes, such as a reduction in exploratory tendencies. A reduction in dopamine levels and changes in the morphology of certain nerve cells are also observed. However, FOXP2 is extremely diverse in echolocating bats. Twenty - two sequences of non-bat eutherian mammals revealed a total number of 20 nonsynonymous mutations in contrast to half that number of bat sequences, which showed 44 nonsynonymous mutations. Interestingly, all cetaceans share three amino acid substitutions, but no differences were found between echolocating toothed whales and non-echolocating baleen cetaceans. Within bats, however, amino acid variation correlated with different echolocating types. Interactions FOXP2 interacts with a regulatory gene CTBP1. It also downregulates CNTNAP2 gene, a member of the neurexin family found in neurons. The target gene is associated with common forms of language impairment. It regulates the repeat - containing protein X-linked 2 ( SRPX2 ), which is an epilepsy and language - associated gene in humans, and sound - controlling gene in mice. Mice In a mouse FOXP2 knockout study, loss of both copies of the gene caused severe motor impairment related to cerebellar abnormalities and lack of ultrasonic vocalisations normally elicited when pups are removed from their mothers. These vocalizations have important communicative roles in mother - offspring interactions. Loss of one copy was associated with impairment of ultrasonic vocalisations and a modest developmental delay. Male mice on encountering female mice produce complex ultrasonic vocalisations that have characteristics of song. Mice that have the R552H point mutation carried by the KE family show cerebellar reduction and abnormal synaptic plasticity in striatal and cerebellar circuits. Birds In songbirds, FOXP2 most likely regulates genes involved in neuroplasticity. Gene knockdown of FOXP2 in Area X of the basal ganglia in songbirds results in incomplete and inaccurate song imitation. Overexpression of FoxP2 was accomplished through injection of adeno - associated virus serotype 1 ( AAV1 ) into Area X of the brain. This overexpression produced similar effects to that of knockdown ; juvenile zebra finch birds were unable to accurately imitate their tutors. Similarly, in adult canaries higher FOXP2 levels also correlate with song changes. Levels of FOXP2 in adult zebra finches are significantly higher when males direct their song to females than when they sing song in other contexts. `` Directed '' singing refers to when a male is singing to a female usually for a courtship display. `` Undirected '' singing occurs when for example, a male sings when other males are present or is alone. Studies have found that FoxP2 levels vary depending on the social context. When the birds were singing undirected song, there was a decrease in of FoxP2 expression in Area X. This downregulation was not observed and FoxP2 levels remained stable in birds singing directed song. Differences between song - learning and non-song - learning birds have been shown to be caused by differences in FOXP2 gene expression, rather than differences in the amino acid sequence of the FOXP2 protein. FOXP2 also has possible implications in the development of bat echolocation. See also Chimpanzee genome project Evolutionary linguistics FOX proteins Origin of language Vocal learning References ^ Jump up to : GRCh38 : Ensembl release 89 : ENSG00000128573 - Ensembl, May 2017 Jump up ^ `` Human PubMed Reference : ''. ^ Jump up to : 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. doi : 10.1038 / 35097076. PMID 11586359. Jump up ^ Nudel R, Newbury DF ( 2013 ). `` FOXP2 ''. Wiley Interdiscip Rev Cogn Sci. 4 ( 5 ) : 547 -- 560. doi : 10.1002 / wcs. 1247. PMC 3992897. 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PMID 1461156. Jump up ^ Li G, Wang J, Rossiter SJ, Jones G, Zhang S ( 2007 ). `` Accelerated FoxP2 evolution in echolocating bats ''. PLoS ONE. 2 ( 9 ) : e900. doi : 10.1371 / journal. pone. 0000900. PMC 1976393. PMID 17878935. Jump up ^ Li S, Weidenfeld J, Morrisey EE ( 2004 ). `` Transcriptional and DNA binding activity of the Foxp1 / 2 / 4 family is modulated by heterotypic and homotypic protein interactions ''. Mol. Cell. Biol. 24 ( 2 ) : 809 -- 22. doi : 10.1128 / MCB. 24.2. 809 - 822.2004. PMC 343786. PMID 14701752. Jump up ^ Vernes SC, Newbury DF, Abrahams BS, Winchester L, Nicod J, Groszer M, Alarcón M, Oliver PL, Davies KE, Geschwind DH, Monaco AP, Fisher SE ( 2008 ). `` A functional genetic link between distinct developmental language disorders ''. N. Engl. J. Med. 359 ( 22 ) : 2337 -- 45. doi : 10.1056 / NEJMoa0802828. PMC 2756409. PMID 18987363. Jump up ^ Sia GM, Clem RL, Huganir RL ( 2013 ). `` The human language - associated gene SRPX2 regulates synapse formation and vocalization in mice ''. Science. 342 ( 6161 ) : 987 -- 91. doi : 10.1126 / science. 1245079. PMC 3903157. PMID 24179158. Jump up ^ Holy TE, Guo Z ( 2005 ). `` Ultrasonic songs of male mice ''. PLoS Biol. 3 ( 12 ) : e386. doi : 10.1371 / journal. pbio. 0030386. PMC 1275525. PMID 16248680. ^ Jump up to : Teramitsu I, White SA ( 2006 ). `` FoxP2 regulation during undirected singing in adult songbirds ''. J. Neurosci. 26 ( 28 ) : 7390 -- 4. doi : 10.1523 / JNEUROSCI. 1662 - 06.2006. PMC 2683919. PMID 16837586. Jump up ^ Heston, Jonathan B. ; White, Stephanie A. ( 2015 - 02 - 18 ). `` Behavior - linked FoxP2 regulation enables zebra finch vocal learning ''. The Journal of Neuroscience. 35 ( 7 ) : 2885 -- 2894. doi : 10.1523 / JNEUROSCI. 3715 - 14.2015. ISSN 1529 - 2401. PMC 4331621. PMID 25698728. Jump up ^ Jarvis, E.D. ; Scharff, C. ; Grossman, M.R. ; Ramos, J.A. ; Nottebohm, F. ( 1998 - 10 - 01 ). `` For whom the bird sings : context - dependent gene expression ''. Neuron. 21 ( 4 ) : 775 -- 788. doi : 10.1016 / s0896 - 6273 ( 00 ) 80594 - 2. ISSN 0896 - 6273. PMID 9808464. Jump up ^ Teramitsu, Ikuko ; White, Stephanie A. ( 2006 - 07 - 12 ). `` FoxP2 regulation during undirected singing in adult songbirds ''. The Journal of Neuroscience. 26 ( 28 ) : 7390 -- 7394. doi : 10.1523 / JNEUROSCI. 1662 - 06.2006. ISSN 1529 - 2401. PMC 2683919. PMID 16837586. Jump up ^ Wilbrecht L, Nottebohm F ( 2003 ). `` Vocal learning in birds and humans ''. Ment Retard Dev Disabil Res Rev. 9 ( 3 ) : 135 -- 48. doi : 10.1002 / mrdd. 10073. PMID 12953292. External links Wikimedia Commons has media related to FOXP2. Gene information at NCBI Gene information at Genetic Home Reference Language and Genetics Research at the Max Planck Institute for Psycholinguistics The FOXP2 story Revisiting FOXP2 and the origins of language FOXP2 and the Evolution of Language FactorBook FOXP2 PDB gallery 2a07 : Crystal Structure of Foxp2 bound Specifically to DNA. 2as5 : Structure of the DNA binding domains of NFAT and FOXP2 bound specifically to DNA. Transcription factors and intracellular receptors ( 1 ) Basic domains ( 1.1 ) Basic leucine zipper ( bZIP ) Activating transcription factor AATF 5 6 7 AP - 1 c - Fos FOSB FOSL1 FOSL2 JDP2 c - Jun JUNB JunD BACH BATF BLZF1 C / EBP α β γ δ ε ζ CREB L1 CREM DBP DDIT3 GABPA GCN4 HLF MAF NFE L1 L2 L3 NFIL3 NRL NRF XBP1 ( 1.2 ) Basic helix - loop - helix ( bHLH ) ATOH1 AhR AHRR ARNT ASCL1 BHLH 9 ARNTL ARNTL ARNTL2 CLOCK EPAS1 FIGLA HAND HES 5 6 HEY HES1 HIF 1A 3A ID LYL1 MESP2 MXD4 MYCL1 MYCN Myogenic regulatory factors MyoD Myogenin MYF5 MYF6 Neurogenins NeuroD NPAS OLIG Pho4 Scleraxis SIM TAL Twist USF1 ( 1.3 ) bHLH - ZIP AP - 4 MAX MXD3 MITF MNT MLX MXI1 Myc SREBP ( 1.4 ) NF - 1 NFI X SMAD R - SMAD 5 9 I - SMAD 6 7 4 ) ( 1.5 ) RF - X RFX 5 6 ANK ( 1.6 ) Basic helix - span - helix ( bHSH ) AP - 2 α β γ δ ε ( 2 ) Zinc finger DNA - binding domains ( 2.1 ) Nuclear receptor ( Cys ) subfamily 1 Thyroid hormone α β CAR FXR LXR α β PPAR α β / δ γ PXR RAR α β γ ROR α β γ Rev - ErbA α β VDR subfamily 2 COUP - TF ( I II Ear - 2 HNF4 α γ PNR RXR α β γ Testicular receptor TLX subfamily 3 Steroid hormone Androgen Estrogen α β Glucocorticoid Mineralocorticoid Progesterone Estrogen related α β γ subfamily 4 NUR NGFIB NOR1 NURR1 subfamily 5 LRH - 1 SF1 subfamily 6 GCNF subfamily 0 DAX1 SHP ( 2.2 ) Other Cys GATA 5 6 MTA TRPS1 ( 2.3 ) Cys His General transcription factors TFIIA TFIIB TFIID TFIIE TFIIF TFIIH 2I 3A 3C1 3C2 ATBF1 BCL 6 11A 11B CTCF E4F1 EGR ERV3 GFI1 GLI - Krüppel family REST S1 S2 YY1 HIC HIVEP IKZF ILF KLF 5 6 7 8 9 10 11 12 13 14 15 17 MTF1 MYT1 OSR1 PRDM9 SALL SP 7 8 TSHZ3 WT1 Zbtb7 7A 7B ZBTB 11 16 17 20 32 33 40 zinc finger 7 9 10 19 22 24 33B 34 35 41 43 44 51 74 143 146 148 165 202 217 219 238 239 259 267 268 281 295 300 318 330 346 350 365 366 384 423 451 452 471 593 638 644 649 655 ( 2.4 ) Cys HIVEP1 ( 2.5 ) Alternating composition AIRE DIDO1 GRLF1 ING JARID 1A 1B 1C 1D JMJD1B ( 2.6 ) WRKY WRKY ( 3 ) Helix - turn - helix domains ( 3.1 ) Homeodomain ARX CDX CRX CUTL1 DBX DLX 5 EMX EN FHL HESX1 HHEX HLX Homeobox A1 A2 A3 A4 A5 A7 A9 A10 A11 A13 B1 B2 B3 B4 B5 B6 B7 B8 B9 B13 C4 C5 C6 C8 C9 C10 C11 C12 C13 D1 D3 D4 D8 D9 D10 D11 D12 D13 HOPX IRX 5 6 MKX LMX 1A 1B MEIS MEOX2 MNX1 MSX NANOG NKX 2 - 1 2 - 2 2 - 3 2 - 5 3 - 1 3 - 2 6 - 1 6 - 2 NOBOX PBX PHF 6 8 10 16 17 20 21A PHOX 2A 2B PITX POU domain PIT - 1 BRN - 3 : A Octamer transcription factor : 1 3 / 4 6 7 11 OTX PDX1 SATB2 SHOX2 SIX 5 VAX1 ZEB ( 3.2 ) Paired box PAX 5 6 7 8 9 PRRX RAX ( 3.3 ) Fork head / winged helix E2F 5 FOX proteins A1 A2 A3 C1 C2 D3 D4 E1 E3 F1 G1 H1 I1 J1 J2 K1 K2 L2 M1 N1 N3 O1 O3 O4 P1 P2 P3 P4 ( 3.4 ) Heat shock factors HSF ( 3.5 ) Tryptophan clusters ELF 5 EGF ELK ERF ETS ERG SPIB ETV 5 6 FLI1 Interferon regulatory factors 5 6 7 8 MYB MYBL2 ( 3.6 ) TEA domain transcriptional enhancer factor ( 4 ) β - Scaffold factors with minor groove contacts ( 4.1 ) Rel homology region NF - κB NFKB1 NFKB2 REL RELA RELB NFAT C1 C2 C3 C4 5 ( 4.2 ) STAT STAT 5 6 ( 4.3 ) p53 p53 TBX 5 19 21 22 TBR1 TBR2 TFT MYRF TP63 ( 4.4 ) MADS box Mef2 SRF ( 4.6 ) TATA - binding proteins TBP TBPL1 ( 4.7 ) High - mobility group BBX HMGB HMGN HNF 1A 1B LEF1 SOX 5 6 8 9 10 11 12 13 14 15 18 21 SRY SSRP1 TCF TOX ( 4.9 ) Grainyhead TFCP2 ( 4.10 ) Cold - shock domain CSDA YBX1 ( 4.11 ) Runt CBF CBFA2T2 CBFA2T3 RUNX1 RUNX2 RUNX3 RUNX1T1 ( 0 ) Other transcription factors ( 0.2 ) HMGI ( Y ) HMGA HBP1 ( 0.3 ) Pocket domain Rb RBL1 RBL2 ( 0.5 ) AP - 2 / EREBP - related factors Apetala 2 EREBP B3 ( 0.6 ) Miscellaneous ARID 1A 1B 3A 3B 4A CAP IFI 16 35 MLL T1 MNDA NFY Rho / Sigma see also transcription factor / coregulator deficiencies Animal communication Concepts Animal training Animal language Animal cognition Bioacoustics Deception in animals Ethology Evolutionary linguistics FOXP2 FOXP2 and human evolution Talking animals Origin of language Human -- animal communication Animal - specific Bird vocalization Talking birds Alex Great ape language ( Yerkish ) Whale song Dog communication Cat communication Related topics Category : Talking birds Category : Apes from language studies Retrieved from `` https://en.wikipedia.org/w/index.php?title=FOXP2&oldid=809837685 '' Categories : Genes on human chromosome 7 Forkhead transcription factors Human genes Evolution of language Genetic diseases and disorders Speech and language pathology Hidden categories : Use dmy dates from July 2013 Talk Contents About Wikipedia Català Deutsch Eesti Español Français Italiano Nederlands 日本 語 Português Русский Slovenčina Svenska தமிழ் Українська 中文 Edit links This page was last edited on 11 November 2017, at 19 : 30. 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Question: the foxp2 sequences of mice were most different from those of
Answer: humans